Atlas of Renal Ultrasonography

CONTENTS
SECTION I ANATOMY AND SONOGRAPHY OF

THE KIDNEYS
CHAPTER 1
Perirenal anatomy .......................................................................................................... 3
CHAPTER 2
Sonography of the normal kidney .............................................................................. 11
CHAPTER 3
Developmental variants ................................................................................................ 21
CHAPTER 4
Percutaneous renal biopsy .................................................................................. 35
SECTION 11
RENAL PARENCHYMAL DISEASE
39
CHAPTER 5
Chronic renal failure ................................................................................. 41
CHAPTER 6
Glomerular disease ................................................................................... 45
CHAPTER 7
Acute tubular necrosis ....................................................................................... 53
CHAPTER 8
Tubulointerstitial disease ..................................................................................... 57
CHAPTER 9
Infectious disease ....................................................................................... 65
Deborah A. Baumgarten and W Charles O'Neill
SECTION III CYSTS AND CYSTIC DISEASE
79
CHAPTER 1 0
Sporadic cysts ............................................................................................................... 81
CHAPTER 1 1
Autosomal dominant polycystic disease ............................................................. 93
xi
xii
CONTENTS
CHAPTER 1 2
Other multicystic disorders ................................................................................................... 99
SECTION IV THE COLLECTING SYSTEM AND DISTAL

URINARY TRACT
1 07
CHAPTER 1 3
Hydronephrosis .................................................................................................................... 109
CHAPTER 1 4
Obstruction of the lower urinary tract .......................................................................... 119
CHAPTER 1 5
Nephrolithiasis .................................................................................................................... 129
CHAPTER 1 6
Catheters and stents ............................................................................................................ 135
SECTION V NEOPLASTIC DISEASE
139
CHAPTER 1 7
Renal epithelial tumors ...................................................................................................... 141
CHAPTER 1 8
Pelvocalyceal tumors ......................................................................................................... 151
CHAPTER 1 9
Angiomyolipomas .............................................................................................................. 155
CHAPTER 2 0
Metastases and hematologic malignancies ................................................................. 161
SECTION VI VASCULAR DISORDERS
1 65
CHAPTER 2 1
Anatomy of the renal vessels ........................................................................................... 167
CHAPTER 2 2
Arterial disorders ................................................................................................................. 171
CHAPTER 2 3
Venous disorders ....................................................................................................... 179
SECTION VII RENAL TRAUMA
185
CHAPTER 2 4
Renal trauma ....................................................................................................................... 187
W Charles O'Neill, John P McGahan, and John R. Richards
CONTENTS
SECTION VIII SONOGRAPHY OF RENAL ALLOGRAFTS
1 97
CHAPTER 2 5
Sonography of the normal allograft ............................................................ 199
CHAPTER 2 6
Parenchymal disease ............................................................................... 207
CHAPTER 2 7
Urinary obstruction in renal allografts ....................................................... 213
CHAPTER 2 8
Perinephric fluid collections ...................................................................... 221
CHAPTER 2 9
Vascular complications in renal allografts ................................................... 233
Deborah A. Baumgarten
INDEX
243
xiii
ANATOMY
AND
SONOGRAPHY
OF THE
KIDNEYS
Perirenal Anatomy
SONOGRAPHY
he relationship of the kidneys to other structures is shown in Figures 1-1 and
1-2. The liver overlies much of the right kidney and the spleen is adjacent to
the left kidney, with a peritoneal reflection between the kidney and each organ. Adjacent to the superior pole of the kidney is the adrenal gland. The renal
vessels course medially to the vena cava (adjacent to the right kidney) and aorta
(adjacent to the left kidney). The psoas muscle lies medial and posterior to the kidney, whereas the quadratus lumborum muscle is posterior. In patients with spinal
cord injuries, psoas atrophy causes medial displacement of the kidneys.' Diagnostic sonography is performed with the patient supine or in the lateral decubitus
position. Although kidneys can be visualized via a dorsal approach, the image
quality is impaired by sound attenuation from muscle and fascia. The probe is positioned so that on sagittal or coronal scanning, caudal structures are placed on the
righthand side of the image. Overlying bowel often prohibits a sagittal view of the
kidney, with longitudinal views usually obtained in a more coronal plane. The
right kidney is best imaged in the anterior axillary line or midaxillary line using
the liver as an accoustic window. This can often be accomplished in the supine position with the left lateral decubitus position required in certain cases. The spleen
is usually too small to displace overlying bowel and stomach and serve as an accoustic window. Thus, adequate visualization of the left kidney usually requires
i maging in the midaxillary or posterior axillary line. Ribs frequently overlie the
upper pole, particularly on the left, because that kidney is more superior. When
adequate images cannot be obtained through intercostal spaces, several maneuvers can be helpful. Often, a deep inspiration will bring the kidney down below
the costal margin. If not, ensuring that the head of the bed or stretcher is flat, removing any pillows from under the patient's head, and placing the patient's ipsilateral upper extremity over the patient's head will usually move the ribs superiorly and enlarge the intercostal spaces. This effect can be maximized by placing
the patient in the lateral decubitus position and placing a pillow under the patient's contralateral flank.
ATLAS OF RENAL ULTRASONOGRAPHY
L adrenal gland
Liver
FIGURE 1-1
Perirenal anatomy, anterior view.
L kidney
Superior
Mesenteric
Artery
R kidney
L ureter
Vena cava
Aorta
Psoas muscle
Vena cava
Aorta
FIGURE 1-2
Perirenal anatomy, transverse section.
R renal
Vein
R kidney
Spleen
L kidney
Ureter
Psoas muscle
INTERPRETATION
he proximity of the kidneys to the liver and spleen is quite apparent on
sonography (Figs. 1-3 and 1-4). Normal adrenal glands are rarely seen in
standard views of the kidney but can mimic renal masses when enlarged
(Fig. 1-5). 2 Accessory spleens (Fig. 1-6) and masses in the tail of the pancreas can
be mistaken for left renal masses. 3-5 Adjacent bowel can usually be identified on
the basis of its gas content and peristalsis, but edematous bowel can appear as a
mass (Fig. 1-7). Occasionally, this presents as a "pseudokidney," with the edematous wall and echogenic lumen mimicking the parenchyma and sinus fat, respectively (Fig. 1-8). Additional causes of a pseudokidney are lymphoma, carcinoma,
and diverticulitis. 6 The psoas muscle is often visible immediately adjacent to the
kidney (Fig. 1-9). A variety of retroperitoneal abnormalities can be responsible for
lateral displacement of the kidneys, including aortic aneurysms (see Fig. 22-3), enlarged lymph nodes, and tumors/
Quadratus
lumborum
muscle
PERIRENAL ANATOMY
FIGURE 1- 3
Sagittal scan showing the liver (L) immediately adjacent to
and overlying the kidney (arrowheads). The space between
the kidney and liver is very thin.
FIGURE 1 -4
Coronal scan of the left kidney (K) showing the adjacent
spleen (S).
FIGURE 1 - 5
Adrenal hyperplasia. Longitudinal view of right kidney (K)
with an enlarged adrenal gland (arrows) adjacent to the
upper pole. (From Bryan PJ, Caldamone AA, Morrison SC,
et al: Ultrasound findings in the Adreno-genital Syndrome
[Congenital Adrenal Hyperplasia]. J Ultrasound Med
1988;7:675, with permission.)
FIGURE 1 -6
Accessory spleen. On longitudinal view of upper pole of left kidney (K),
accessory spleen appears as an exophytic mass (white arrow). Black arrows
show blood supply from splenic artery. S, spleen. (From Subramanyam
BR, Balthazar EJ, Horii SC: Sonography of the accessory spleen. AIR
FIGURE 1 -7
Pseudomembranous colitis appearing as perirenal mass.
Longitudinal view of right kidney (arrowheads) showing
edematous colon (C) adjacent to the lower pole.
FIGURE 1 - 8
Pseudokidney. Longitudinal view of left kidney (cursors)
with adjacent edematous bowel having the appearance of a
kidney (arrowheads). The hypoechoic bowel wall surrounds
echogenic material in the lumen.
PERIRENAL ANATOMY
FIGURE 1-9
Transverse view of right kidney (arrowheads) at the level of
the pelvis showing psoas muscle (arrows) medial to kidney.
Striations are visible in the muscle.
Peritoneal
space
Anterior
pararenal
space
Posterior
peritoneum
Posterior
pararenal
fascia
Perirenal
space
Transversalis
fascia
Posterior
pararenal
space
Anterior
pararenal
fascia
FIGURE 1 - 1 0
Diagram of transverse section through the
abdomen showing the pararenal fascia and
spaces. The spaces have been enlarged for
ease of identification. K, kidney; L, liver;
P, pancreas.
The tissue compartments surrounding the kidneys are diagrammed in Figure

1-10. The kidney is invested by the anterior and posterior pararenal fascia, also
known as Gerota's fascia, forming the perirenal space. Between the anterior
pararenal fascia and the posterior peritoneum is the anterior pararenal space, and
the posterior pararenal space lies between the posterior pararenal fascia and the
transversalis fascia." The perirenal space together with the two pararenal spaces
comprise the retroperitoneum. The fascia cannot be discerned by sonography, so
the perirenal and pararenal spaces appear as a single fat-filled compartment. 8 The
fat is variable in amount and is usually echogenic, but it is occasionally hypoechoic when the water content of the fat tissue is low,") appearing as a hypoechoic
rim (Fig. 1-11) mimicking perirenal fluid. 11 ' 12 Lastly, there is a peritoneal reflection
between the kidneys and the liver and spleen. The space between the right kidney
and the liver is normally 1-6 mm thick, being Ls. 1 mm in about 50% of patients.
Obesity accounts for the higher values. 8 Ascites is a common cause of widening of
this space (Fig. 1-12). An aberrant vein (Fig. 1-13) is a rare cause of fluid in this
space. 13 Widening and increased echogenicity of the anterior pararenal space (Fig.
1-14A) occurs with acute abdominal inflammation." Carcinoma (Fig. 1-14B),
lymphoma (see Fig. 20-5), 14 and chronic inflammation can also enlarge this space
but without an increase in echogenicity. 9 Perirenal fluid collections are discussed
in Chapter 24.
FIGURE
1 -11
Hypoechoic perirenal fat. Longitudinal image of right kidney
with adjacent hypoechoic fat (arrowheads) mimicking perirenal
fluid. The parenchyma is thin and there is a small simple cyst
(arrow), consistent with chronic renal failure.
FIGURE 1-12
Ascites. Longitudinal view of right kidney showing fluid
(arrows) in the peritoneal reflection between the kidney and
the liver (L).
FIGURE 1-13
Anomolous perirenal vein. Transverse image of right kidney
(K) showing a fluid collection (arrows) betweeen the kidney

and the liver (L) that was found to be an aberrant vein
joining the right renal vein. (From Baker JA, Carroll BA: The
sonographic appearance of anomalous circumrenal vein
mimicking perirenal fluid collection. J Ultrasound Med
PERIRENAL ANATOMY
FIGURE 1-14
Enlargement of the anterior
pararenal space. Longitudinal
views of the right kidney. The
pararenal space (arrows) between
the right kidney (K) and liver (L) is
increased in (A) acute pancreatitis
and (B) gastric carcinomatosis.
Note the increased echogenicity of
this space in acute pancreatitis.
(From Chen J-J, Changchien C-S,
Kuo C-H: Causes of increasing
width of right anterior extrarenal
space seen in ultrasonographic
examinations. J Clin Ultrasound
REFERENCES
1. Karasick D, Karasick S, Brennan R: Renal positional changes in spinal-cord-injured patients. AIR
1982;140:521.
2. Bryan PJ, Caldamone AA, Morrison SC, et al: Ultrasound findings in the Adreno-genital Syndrome
(Congenital Adrenal Hyperplasia). J Ultrasound Med 1988;7:675.
3. Subramanyam BR, Balthazar EL Horii SC: Sonography of the accessory spleen. AIR 1984;143:47.
4. Baker MK, Kopecky KK, Wass JL: Perirenal pancreatic pseudocysts: Diagnostic management. AIR
1983;140:729.
5. Kiser JW, Fagien M, Clore FF: Splenosis mimicking a left renal mass. AIR 1996;167:1508.
6. Bluth EI, Merritt CRB, Sullivan MA: Ultrasonic evaluation of the stomach, small bowel, and colon.
Radiology 1979;133:677.
7. Silverman PM, Kelvin FM, Korobkin M: Lateral displacement of the right kidney by the colon: An
anatomic variation demonstrated by CT. AJR 1983;140:313.
8. Belli A-M, Joseph AEA: The Renal Rind Sign: A new ultrasound indication of inflammatory disease in the abdomen. Br J Radiol 1988;61:806.
9. Chen J-J, Changchien C-S, Kuo C-H: Causes of increasing width of right anterior extrarenal space
seen in ultrasonographic examinations. J Clin Ultrasound 1995;23:287.
10. Behan M, Kazam E: The echographic characteristics of fatty tissues and tumors. Radiology
1978;129:143.
11. Brammer HM, Smith WS, Lubbers PR: Septated hypoechoic perirenal fat on sonograms: a pitfall in
renal ultrasonography. I Ultrasound Med 1992;11:361.
12. Heinz-Peer G, Oettl C, Mayer G, et al: Hypoechoic perirenal fat in renal transplant recipients. Radiology 1994;193:717.
13. Baker JA, Carroll BA: The sonographic appearance of anomalous circumrenal vein mimicking
perirenal fluid collection. J Ultrasound Med 1995;14:244.
14. Horii SC, Bosniak MA, Megibow AJ, et al: Correlation of CT and ultrasound in the evaluation of
renal lymphoma. Urol Radiol 1983;5:69.
C H .A P
Sonography of the
Normal Kidney
SONOGRAPHY
he kidneys should first be imaged in the longitudinal axis until a maximal

length is obtained. The probe should then be rotated 90 to obtain a transverse image through the renal pelvis and then moved or angled to obtain
transverse images of the upper and lower poles. At least one view of the right kidney should include the liver at the same depth as the kidney to allow comparison
of echogenicity. The same should be done on the left side using the spleen instead
of the liver. The height of particularly short or tall patients should be noted to aid
in interpreting renal length.
INTERPRETATION
ntrarenal anatomy is shown in Figure 2-1. The kidney consists of multiple lobules, each consisting of a rim of cortex surrounding a medullary pyramid that
terminates in a papilla protruding into a minor calyx. In adults, the lobules are
fused and usually not apparent. The minor calyces converge into major calyces
that then join to form the renal pelvis and proximal ureter. The space between the
calyces and the parenchyma is the renal sinus, which contains blood vessesls, lymphatics, and fat. The vascular pedicle that supplies the kidney is known as the
hilum and is adjacent to the renal pelvis but outside the sinus. Sonographically the
normal kidney has a characteristic oval appearance in the sagittal plane (Fig.
2-2A) that makes it readily distinguishable from other organs and structures. The
sinus fat produces a brightly echogenic center, obscuring the collecting system
and blood vessels, and is surrounded by a hypoechoic rim consisting of cortex and
medulla. In the coronal plane, there is a discontinuity in the rim of parenchyma at
the level of the renal pelvis and hilum (Fig. 2-2B). Because the coronal width is
27% greater than the sagittal width,' the kidney appears plumper on coronal
views. This explains why the right kidney, which is usually viewed in a more
sagittal plane, often appears thinner than the left left kidney, which is often
viewed more coronally. The calyceal system is not visible unless filled with urine
(Fig. 2-3). The intrarenal vessels are not usually seen because of their small size
and obscuration by sinus fat. An exception is the arcuate vessels, which can occasionally be seen as hyperechoic dots at the outer border of the medullary pyramids (Fig. 2-4). A longitudinal view of maximal length should have an even rim
of parenchyma surrounding the sinus fat, although the cortex is usually a bit
12
Papilla
Column of
Bertin
Major calyx
Hilum
Cortex
Pelvis
Medulla
Sinus
Arcuate
artery
Ureter
Intralobular
artery
Minor calyx
Interlobular
artery
FIGURE 2 - 2
Longitudinal images of the right kidney. A. On sagittal
scanning, the renal parenchyma appears as a relatively
hypoechoic, oval rim around the echogenic sinus fat.
Medullary pyramids, which are not very distinct in this
kidney, appear as regularly spaced structures (arrows)
slightly less echogenic than the cortex, which is less
echogenic than the liver (L). B. Coronal scan showing the
discontinuity of the parenchyma (arrow) at the level of the
renal pelvis and hilum. The coronal width is greater than
the sagittal width. L, liver.
FIGURE 2 - 1
Intrarenal anatomy, midline coronal section.
(From O'Neill WC: Sonographic evaluation
of renal failure. Am I Kidney Dis 2000;35:1021,
with permission.)
SONOGRAPHY OF THE NORMAL KIDNEY
13
FIGURE 2-3
Intrarenal anatomy. A. Oblique image of right kidney with
mild hydronephrosis. B. Diagram of image identifying
structures. M, medullary pyramid; C, cortex; B, column of A
Bertin; I, infundibulum of a minor calyx.
Minor calyx
Major calyx
FIGURE 2-4
Arcuate vessels. Longitudinal view of left kidney showing two
arcuate arteries in cross-section (arrows), each at the corticomedullary junction. A segmental vein is also visible (curved
arrow).
thicker at the poles. An uneven rim indicates that the kidney has been imaged
obliquely. An imaging plane off the midline can result in medullary pyramids being imaged in cross-section, appearing as sinus masses (Fig. 2-5). In the transverse
plane the kidney appears circular at the poles and C-shaped at the level of the renal pelvis (Fig. 2-6). The kidneys of neonates differ substantially from the kidneys
of older children and adults (Fig. 2-7). Not only are they smaller but the cortex is
echogenic and lobulated and the medullary pyramids are very prominent.
14
FIGURE 2-5
Off center longitudinal scan of right kidney. A medullary
pyramid is viewed in cross-section (arrow), appearing as a
sinus mass.
FIGURE 2-6
Transverse images of the kidney. A. The kidney appears circular in transverse scanning through a renal pole, with
parenchyma completely surrounding sinus fat. B. The kidney appears C-shaped at the level of the renal pelvis and hit =
where the renal vein is visible (arrow) entering the sinus. L, liver.
FIGURE 2-7
Normal neonatal kidney. Longitudinal scan of right kidney (arrowheads)
showing accentuated lobulation (arrows) and prominent medullary
pyramids. L, liver.
SONOGRAPHY OF THE NORMAL KIDNEY 15
Kidney Size
The best measure of renal size is volume, which corrleates well with glomerular filtration rate. 2 Volume can be determined directly by the the stepped section method,'
but this is cumbersome, and calculating volume on the basis
of the formula for an
3.4
ellipsoid is far simpler and yields equally reliable values. On the basis of correlation with true volume, the best formula is V = 0.49 X L X W7 X W2 where L is length,
and W, and W2 are the widths in the the two transverse dimensions. 4 For adults, median renal volumes are 146 cm 3 for the left kidney and 134 cm 3 for the right kidney.'
However, calculation of volume is prone to significant error because three independent measurements are used.' In practice, measurement of maximum renal length
has become the clinical standard because it is simple, more accurate, and correlates
well with renal volume."' The interobserver and intraobserver variability in this measurement is about 5% 7 but may be greater in childrenas much as 2-3 years in the
relationship between age and renal length.' Kidney length correlates with body
height"-" in both adults (Fig. 2-8) and children (Fig. 2-9) and, after correction for
body height, there is no sex difference in kidney length. As with kidney volume, the
length is slightly greater (1.8%-2.8 %) in the left kidney. 5'93 ' 12 Another parameter that
correlates with kidney length is age. In children, this is best described by two nomograms (Fig. 2-10), reflecting the more rapid growth in the first year. 11 ' 12 The correlation with age is poorer than the correlation with body length, 1 " indicating that the
former is probably a manifestation of the latter. In adults, there is a gradual reduction
in renal length that becomes more precipitous after age 50 years (Fig. 2-11) that is due
entirely to loss of parenchyma. The variability between repeat measurements of a
normal kidney is approximately 5%; indicating that size differences of up to 1 cm
may not be significant. This variability is likely to be greater in abnormal kidneys. Renal length averages about 11 cm in adults,' so that 10-12 cm is a useful range for normal renal length (with correction for particularly tall or short patients). Discrepancy
in size between the two kidneys is not abnormal, provided that the smaller kidney is
not less than 37% of the total renal volume.13
Physiologic enlargement occurs in solitary kidneys and during pregnancy. Renal length is 12% above normal in 5-year-old children with congenitally solitary
kidneys, 14 and renal volume is increased 80%-90% in congenitally or surgically
solitary kidneys in children. 14-16 Much less compensatory hypertrophy is seen in
adults after nephrectomy. This varies with time, with a maximum of 30% after 1
year,'" decreasing to a permanent increase in length of approximately 5%. 17' 18 There
is a progressive increase in renal size during pregnancy that resolves by 12 weeks
postpartum (Fig. 2-12). 19 This is primarily due to parenchymal enlargement, although some pelvocalyceal enlargement occurs, particularly in the right kidney.19
Cortical Thickness
Because some of the renal volume is not occupied by parenchyma, indices of
parenchymal size may correlate better with renal function, 6 but there are no
140
c 130
FIGURE 2-8
Correlation between kidney length and body height in adults.
Solid lines, analysis of variance; dotted line, 95% confidence
limits. (From Miletic D, Fuckar Z, Sustic A, et al: Sonographic
measurement of absolute and relative renal length in adults.
J Clin Ultrasound 1998;26:185, with permission.)
o E 120
E
0
-J 4)
rn
110
100
al
'2 Or
4) 90
80
150 155 160
165 170 175

Body Height (cm)
180 185 190 195
16
12
10
le
FIGURE 2 - 9
Nomogram showing 95% confidence limits for
maximum length of left kidney as a function of
body height in children. (Adapted from Dinkel E,
Ertel M, Dittrich M, et al: Kidney size in childhood:
Sonographical growth charts for kidney length
and volume. Pediatr Radiol 1985;15:38, with
permission.)
_c 8
0-)
a)
6
-0
2
4
2
40
60
80
120
100
Body height (cm)
180
160
140
13
12
11
10
9
FIGURE 2 - 1 0
Nomogram of 95% confidence limits for
kidney length versus age in children.
(From O'Neill WC: sonographic evaluation
of renal failure. Am J Kid Dis 2000;35:1021,
with permission.)
8
_c 7
0)
6
5
4
3
2
6
Months
10
12
10
15
Years
14
13
E
_c 12
FIGURE 2 - 1 1
Reduction in kidney length with age in adults.
Mean (dashed line) 2 SD (solid lines). (From
O'Neill WC: sonographic evaluation of renal
failure. Am J Kid Dis 2000;35:1021, with
permission.)
iT
9
8
20
30
40
60
50
Age (years)
70
80
90
SONOGRAPHY OF THE NORMAL KIDNEY 17
15
13
FIGURE 2 - 1 2
Renal enlargement during pregnancy. Mean
(dashed line) and 95% confidence limits (solid lines)
of right kidney length in pregnancy as a function
of gestational age and time postpartum. (Data
from Cietak KA, Newton JR: Serial quantitative
maternal nephrosonography in pregnancy. Br J
Radiol 1985;58:405.)
5
0
10
20
30
Weeks
established nomal ranges. The thickness of the renal cortex is measured from either the outer border of the medullary pyramids or the arcuate arteries to the renal capsule. On the basis of arteriography, normal values of 7.5-9.5 mm 2 ' and 5-8
mm 22 have been proposed. By sonography, a value of 9.3 1.1 mm was obtained
in 23 renal transplant donors (mean age, 36 years) with normal renal function.23
The combined thicknesses of the cortex and medullae (parenchymal thickness),
measured as the distance between the sinus fat and the renal capsule, was found
to be 15-16 mm in adults; but a normal range has not been established. Another
index that has been used is the ratio of cortical thickness to the length of the
medullary pyramid, the corticomedullary ratio. A mean value of 0.97 with a range
of 0.5-1.4 was obtained in renal transplant donors, 23 whereas a range of 0.81-1.0
has been determined by arteriography. 21 This corticomedullary ratio may be of
limited value because the size of both the cortex and medulla are often reduced in
parallel in chronic renal disease.21
Cortical Echogenicity
The echogenicity of the renal cortex should be carefully compared to that of
the liver or spleen. This must be done at similar depths to avoid artifact related
to time-gain compensation. Transmission artifacts related to overlying fluid
(Fig. 2-13) or ribs (Fig. 2-14) must also be avoided, and care must also be taken
to distinguish cortex from medulla. Finally, one must be aware of increases in
hepatic echogenicity due to steatosis, cirrhosis, or other disorders. In particular, the liver appears to be a poor reference structure in neonates. 24 There have
been no studies of renal cortical echogenicity in subjects in whom normal renal function has been documented, and no studies in which echogenicity has
been quantified. In a commonly cited study of patients between the ages of 19
and 82 years undergoing sonography for indications other than renal disease,
renal cortex and liver had the same echogenicity in a large proportion. 25 However, a large number of these patients undoubtedly had renal impairment, because the only criterion of normal renal function was a serum creatinine of 1.4
mg/ dL or less. In a random population study, equal echogenicities were found
in one third of 30-year-old subjects. 26 Because this is substantially higher than
the expected prevalence of renal disease, it is reasonable to assume that the
echogenicity of the normal renal cortex is usually less than that of the liver but
occasionally may be the same. Cortical echogenicity varies with age. The renal
cortex is less echogenic than the liver in only 5% of infants up to 6 months of
age, with increased echogenicity in 30%. 27 Renal cortical echogenicity increases
with decreasing birth weight and is greater than the liver in over 80% of
neonates under 1,000 g. 28 After 6 months of age, normal cortex is never more
10
18
FIGURE 2-13
Artifactual increase in echogenicity due to ascites. Longitudinal
view of right kidney showing increased echogenicity of the
lower pole (arrowhead) due to overlying ascites (A).
Echogenicity decreases in more cephalad portions of the
kidney as the amount of overlying ascites decreases, with
normal echogenicity in the extreme upper pole (arrow).
FIGURE 2-14
Shadowing artifact. Longitudinal view of right kidney with a
band of apparent decreased echogenicity due to an acoustic
shadow from an overlying rib (arrows). The parenchyma in
the shadow is artifactually enlarged, giving the appearance
of a mass (arrowheads).
echogenic than the liver and there is a progressive decrease in echogenicity so

that the cortex is less echogenic than the liver in 90% of kidneys by age 7
years. 27 In adults the proportion of kidneys less echogenic than the liver increases with age. 26 This is probably due to an increase in liver echogenicity
rather than a decrease in renal cortical echogenicity since echogenicity in relationship to the spleen does not change. Greater echogenicity of the renal cortex as compared with the liver is clearly abnormal past age 6 months and indicates renal disease.2'
Medulla
The medulla is a densely packed array of tubules that converges into a papilla at
the tip of each lobule. It has a pyramidal shape (with the papilla being the apex)
and less sound attenuation than the cortex, appearing as a hypoechoic triangle beneath the cortex of each lobule. The degree of sound attenuation depends on fluid
content, so that the pyramids beome more echogenic during antidiuresis and less
echogenic during diuresis. 29 However, the pyramids are often indistinct in deep
SONOGRAPHY OF THE NORMAL KIDNEY
kidneys and at low sound frequencies, and their visibility depends on the
echogenicity of the cortex. They should be easily seen and well defined in all
neonates, 27 ' 28 with visibility decreasing to about 10% of kidneys between the ages
of 10 and 15 years. 27 This age dependence is undoubtedly related to the progressive decrease in cortical echogenicity during childhood. The visibility of the
medullary pyramids decreases with age in adults, 3 undoubtedly due to progressive medullary fibrosis. The height of medullary pyramids determined by sonography is 9.7 0.8 mm, 23 corresponding closely to the 8.5-11 mm range determined
by arteriography.21
REFERENCES
1. Brandt TD, Neiman HL, Dragowski MJ, et al: Ultrasound assessment of normal renal dimensions.
J Ultrasound Med 1982;1:49.
2. Troell S, Berg U, Johansson B, et al: Comparison between renal parenchymal sonographic volume,
renal parenchymal urographic area, glomerular filtration rate and renal plasma flow in children.
Scand J Urol Nephrol 1988;22:207.
3. Jones TB, Riddick LR, Harpen MD, et al: Ultrasonographic determination of renal mass and renal
volume. J Ultrasound Med 1983;2:151.
4. Hricak H, Lieto RP: Sonographic determination of renal volume. Radiology 1983;148:311.
5. Emamian SA, Nielsen MB, Pedersen JF, et al: Kidney dimensions at sonography: correlation with
age, sex, and habitus in 665 adult volunteers. AIR 1993;160:83.
6. Troell S, Berg U, Johansson B, et al: Renal parenchymal volume in children. Acta Radiol 1988;29:127.
7. Emamian SA, Nielsen MB, Pedersen JF: Intraobserver and interobserver variations in sonographic
measurements of kidney size in adult volunteers. Acta Radiol 1995;36:399.
8. Sargent MA, Long G, Karmali M, et al: Interobserver variation in the sonographic estimation of renal volume in children. Pediatr Radiol 1997;27:663.
9. Miletic D, Fuckar Z, Sustic A, et al: Sonographic measurement of absolute and relative renal length
in adults. J Clin Ultrasound 1998;26:185.
10. Dinkel E, Ertel M, Dittrich M, et al: Kidney size in childhood: Sonographical growth charts for kidney length and volume. Pediatr Radiol 1985;15:38.
11. Han BK, Babcock DS: Sonographic measurements and appearance of normal kidneys in children.
AIR 1985;145:611.
12. Rosenbaum DM, Korngold E, Teele RL: Sonographic assessment of renal length in normal children. AIR 1984;142:467.
13. Rasmussen SN, Haase L, Kjeldsen H, et al: Determination of renal volume by ultrasound scanning.
J Clin Ultrasound 1978;6:160.
14. Rottenberg GT, De Bruyn R, Gordon I: Sonographic standards for a single functioning kidney in
children. AIR 1996;167:1255.
15. Dinkel E, Britscho J, Dittrich M, et al: Renal growth in patients nephrectomized for Wilms' tumour
as compared to renal agenesis. Eur J Pediatr 1988;147:54.
16. Gudinchet F, Meuli R, Regazzoni B: Compensatory renal growth in children and adults studied by
Doppler sonography. I Clin Ultrasound 1994;22:11.
17. Prassopoulos P, Gourtsoyiannis N, Cavouras D, et al: CT evaluation of compensatory renal growth
in relation to postnephrectomy time. Acta Radiol 1992;33:566.
18. Tapson JS, Owen JP, Robson RA, et al: Compensatory renal hypertrophy after donor nephrectomy.
Clin Radiol 1985;36:307.
19. Cietak KA, Newton JR: Serial quantitative maternal nephrosonography in pregnancy. Br J Radiol
1985;58:405.
20. Roger SD, Beale AM, Cattell WR, et al: What is the value of measuring renal parenchymal thickness before renal biopsy? Clin Radiol 1994;49:45.
21. Khademi M: Angiographic measurement of renal compartments. Radiology 1974;113:51.
22. Abrams HL: Quantitative derivates of renal radiologic studies. An overview. Invest Radiol
1972;7:240.
23. Raj DSC, Hoisala R, Somiah S, et al: Quantitation of change in the medullary compartment in renal allograft by ultrasound. J Clin Ultrasound 1997;25:265.
24. Lamont AC, Pelmore JM, Thompson JR, et al: Ultrasound assessment of liver and kidney brightness in infants: Use of the gray-level histogram. Invest Radiol 1994;30:232.
25. Platt JF, Rubin JM, Bowerman RA, et al: The inability to detect kidney disease on the basis of
echogenicity. AIR 1988;151:317.
26. Emamian SA, Nielsen MB, Pedersen JF, et al: Sonographic evaluation of renal appearance in 665
adult volunteers. Acta Radiol 1993;34:482.
27. Vade A, Lau P, Smick J, et al: Sonographic renal parameters as related to age. Pediatr Radiol
1987;17:212.
28. Erwin BC, Carroll BA, Muller H: A sonographic assessment of neonatal renal parameters. J Ultrasound Med 1985;4:217.
29. Hricak H, Cruz C, Eyler WR, et al: Acute post-transplantation renal failure: Differential diagnosis
by ultrasound. Radiology 1981;139:441.
30. Marchal G, Verbeken E, Oyen R, et al: Ultrasound of the normal kidney: A sonographic, anatomic
and histologic correlation. Ultrasound Med Biol 1986;12:999.
19
CHAPTER
Developmental Variants
SONOGRAPHY
evelopmental variants are common and usually of no clinical significance

other than being mistaken for pathology. They must be considered during
the examination so that additional images are obtained to avoid this pitfall.
In particular, the failure to visualize a kidney should raise the suspicion of ectopia
and prompt a search of the pelvis as well as careful examination for fusion with
the contralateral kidney.
DUPLICATION
uplication of the collecting system is a common abnormality that arises

from division of the ureteric bud during embryogenesis) Most cases involve only the very proximal ureter and are of no clinical significance to
the patient. Duplications involving the entire ureter are usually associated with
ectopic attachment of the distal ureter draining the superior collecting system,
which frequently results in chronic reflux or obstruction)
Interpretation
On longitudinal views, duplication appears as a relatively hypoechoic band separating the sinus fat into two compartments (Fig. 3-1). This band of cortex joins the
outer cortex between medullary pyramids and is indisinguishable from it in terms
of echogenicity. In some cases, the two renal segments may not be in the same
plane and the duplication appears quite irregular, often mimicking a sinus mass
(Fig. 3-2) or a parenchymal mass (Fig. 3-3). Duplications are slightly asymetric
rather than being midline, and transverse images will show two separate compartments of sinus fat. Hydronephrosis of one of the collecting systems, usually
the result of obstruction or reflux in the upper unit, appears as segmental calicectasis but with a dilated ureter (Fig. 3-4). Obstruction in utero can lead to multicystic dysplasia in one of the segments. 2 When a diseased segment involutes, it
can appear as a small mass at one end of the remaining segment (Fig. 3-5), the socalled nubbin sign.3
text continued on pg. 24
22
FIGURE 3-1
Duplication. Longitudinal view of left kidney showing a
band of tissue (arrow) demarcating two separate renal
sinuses. The band is contiguous with the cortex, has the
same echogenicity, and is slightly eccentric.
FIGURE 3-2
Duplication. A. Longitudinal view of right kidney showing
a sinus mass that appears contiguous with the cortex. B.
The duplication is more apparent in another longitudinal
view that has the appearance of two kidneys stacked side
by side. Arrows indicate the two separate renal sinuses.
DEVELOPMENTAL VARIANTS
23
FIGURE 3 - 3
Partial duplication. Oblique longitudinal view of left kidney
(arrowheads) showing a mass (arrows) protruding from kidney. The mass exhibits normal renal architecture, including
cortex, a medullary pyramid, and sinus fat. Whether "extra
poles" such as this arise from partial duplication or from
fusion of supernumerary kidneys is unclear.
FIGURE 3 4
Hydronephrosis in a duplicated collecting system. Longitudinal scan
of right kidney (arrowheads) showing dilated calyces (C) in the upper
pole. The dilated upper pole ureter is an important clue to the
diagnosis. (Photo courtesy of Dr. B. Gay.)
FIGURE 3 5
Atrophic duplication (nubbin sign). Longitudinal view of
right kidney (K) showing a small inferior duplication
(straight arrows). The curved arrow indicates the sinus of the
atrophic duplication. (From Blair D, Rigsby C, Rosenfield AT:
The Nubbin Sign on computed tomography and sonography.
Urol Radiol 1987;9:149, with permission.)
24
Differential Diagnosis
Hypertrophied column of Bertin (see Fig. 3-6) is a related variant in which the cortex
extends into the sinus but does not bisect the kidney. The distinction between this
and duplication is unimportant. Duplication, particularly when irregular, must be
distinguished from other causes of split sinus echoes. Masses within the renal sinus such as transitional cell carcinoma (Chapter 18) are usually not continuous with
the cortex and not necessarily interposed between medullary pyramids. In hydronephrosis, the calyces are anechoic and converge into a dilated pelvis.
HYPERTROPHIED COLUMN OF BERTIN

ypertrophied column of Bertin is another common defect found in approximately 15% of studies, 4 that is closely related to duplication. It is not
true enlargement of the cortex as its name implies; rather, it is a partial duplication s Both kidneys are affected in 20% of patients with the defect.4
Interpretation
This variant appears as a mass extending into the sinus fat centered between two
medullary pyramids (Fig. 3-6). The column should be continuous with and have
the same echogenicity as the cortex, and, as with duplication, it is slightly eccentric. There may be a junctional cortical defect or junctional line marking the line of
duplication s ; otherwise, there should be no distortion of the renal architecture.
The duplicated collecting system (Fig. 3-1) has a similar appearance, but the
parenchyma completely bridges the sinus. Neoplasms usually distort the renal architecture. A transitional cell carcinoma (see Chapter 18) usually has sinus fat separating it from parenchyma. A calyx dilated with clotted blood can exhibit an
echogenicity similar to that of cortex (see Fig. 24-5). None of these should be in direct continuity with a column of Bertin.
FIGURE 3 - 6
Hypertrophied column of Bertin. Longitudinal image of
renal allograft showing cortex (C) protruding into the renal
sinus between two medullary pyramids (arrows).
JUNCTIONAL FUSION DEFECT
functional fusion defect results from incomplete lobular fusion and has no
clinical significance.' Because of continued fusion of the renal lobules during childhood, this anomaly is rarely observed in adults.'
Interpretation
In its full form, the junctional defect appears as a hyperechoic line extending from
the renal sinus and terminating as a small, echogenic, wedge-shaped defect in the
outer cortex (Fig. 3-7). This appearance probably results from the extension of sinus fat to the renal capsule along the line of incomplete fusion.' Either the line or
the cortical defect may be seen in isolation, and occasionally, the fat tissue will cast
an accoustic shadow (Fig. 3-8). Like other variants, it occurs between the middle
third and either the lower or upper third of the kidney.
A
FIGURE 3-7
Junctional parenchymal defect. A. Longitudinal view of right
kidney with a fat-filled, wedge-shaped parenchymal defect
extending to the sinus (arrow). B. Same view in a different
patient showing a more subtle defect (arrowhead) connected
to the sinus by a thin, echogenic line (arrow).
FIGURE 3-8
Junctional parenchymal defect. Longitudinal view of right
kidney with wedge-shaped defect filled with fat (arrow) that
casts an acoustic shadow (arrowheads).
25
26
Cortical scars (see Figs. 13-1, 22-6, 22-7) are not as sharply demarcated and tend to
be larger. Stones (see Chapter 15) are not found in the outer cortex, are rarely
wedge shaped, and usually cast stronger shadows. Angiomyolipomas (see Chapter
19) can also present as hyperechoic areas in the cortex but are not linear or wedge
shaped.
FETAL LOBULATION
he kidney contains more than a dozen lobes, and these are quite prominent
before they fuse during late gestation and in early childhood. 6 Occasionally,
the lobulation persists into adulthood and is of no clinical importance, except for the possible misidentification of a lobe as a mass, or the indentations as
scars.
Interpretation
Multiple lobulations are easily recognized as regularly spaced convexities, each
overlying a medullary pyramid (Fig. 3-9). Each lobulation should contain one
medullary pyramid and its cortex should be of normal thickness and continuous
with the cortex of the other lobules. Occasionally lobulations can be particularly
prominent and mimic a mass (Fig. 3-10).
FIGURE 3-9
Fetal lobulation. Longitudinal view of left kidney showing
accentuated lobules (arrows). Note the medullary pyramid
centered within each lobule (arrowheads).
FIGURE 3 - 1 0
Fetal lobulation. Longitudinal scan of left kidney showing a
prominent lobule (arrowhead). Additional lobulation (arrows)
is present.
27
FIGURE 3 1 1
BardetBiedl syndrome. Longitudinal view of left kidney
showing lobulation (arrowheads), caliectasis (curved arrows),
and a small calyceal cyst (straight arrow). (Cramer B,
Green J, Harnett J, et al: Sonographic and urographic
correlation in Bardet-Biedl Syndrome (formerly LaurenceMoon-Biedl Syndrome). Urol Radiol 1988;10:176.)
FIGURE 3 1 2
Fused medullary pyramid. Longitudinal view of right
kidney with prominent pyramids secondary to chronic
renal failure. The fused pyramid (arrow) is Y shaped. The
echogenic focus just below the arrow is an arcuate artery at
the corticomedullary junction.
Cortical atrophy can accentuate lobulation (see Fig. 5-3), but the cortex is thin. Lobulation is a prominent feature of BardetBiedl syndrome,' usually accompanied by
calyceal cysts and diverticula (Fig. 3-11). Neoplasms can distort the renal contour
but do not contain normal architecture (medullary pyramids and columns of
Bertin). Scarring (see Figs. 13-1, 22-6, 22-7) also alters the renal contour, but it is irregular and there is cortical thinning. The cortical thickness is normal throughout
in a lobulated kidney.
FUSED MEDULLARY PYRAMID

lso known as compound renal pyramid, fused medullary pyramid is a
8
very common finding resulting from fusion of two adjacent papillae. This
finding is also of no clinical importance but should not be mistaken for a
dilated calyx or a mass.
Interpretation
A fused pyramid appears as a heart-shaped or Y-shaped hypoechoic area located
at the same depth and spacing as the other pyramids (Fig. 3-12). If there is an underlying calyx, it should be a single one. There should be no other distortion of renal anatomy.
28
A dilated minor calyx (see Fig. 2-3A) should be deeper, just below a medullary pyramid, and should be anechoic. Small neoplasms are usually circular and unlikely to be
spaced evenly with respect to the other pyramids.
DROMEDARY HUMP
dromedary hump is seen in the left kidney and is of no clinical importance

other than its potential for being misdiagnosed as a renal mass.
Interpretation
The dromedary hump is a bulge in the kidney just inferior to the spleen (Fig.
3-13), consistent with the kidney being distorted by the spleen. The underlying
architecture should be normal and the contour of the kidney should be smooth.
Lobulation is more abrupt and centered on a medullary pyramid (Figs. 3-9, 3-10),
but the distinction is not clinically important. Neoplasms usually produce more
distortion of both the contour and architecture. Scarring (see Figs. 13-1, 22-7) is irregular, without a smooth contour, and with cortical thinning.
EXTRARENAL PELVIS
ccasionally, the renal pelvis is located or extends outside the kidney, where
it is no longer obscured by sinus fat. This is of no clinical significance other
than being confused with hydronephrosis.
Interpretation
Extrarenal pelvis appears as a short dilation of the initial proximal ureter without
any calyceal dilation or other abnormalities within the renal sinus (Fig. 3-14).
In obstructive uropathy, the calyces should be dilated as well and dilation of the
ureter extends distally. In pregnancy, the ureter is enlarged to the pelvic brim and
caliectasis is usually present (Fig. 13-7).
29
FIGURE 3-1 3
Dromedary hump. Longitudinal view of left kidney showing
bulge in kidney (arrow) just inferior to spleen (S). The renal
architecture is otherwise normal.
'. -= 111111 A
4
FIGURE 3-14
Extrarenal pelvis. A. Longitudinal and (B) transverse views
of left kidney showing an apparent dilated proximal ureter
(arrowhead). The major calyces (A, arrows) can be seen converging on the renal pelvis.
30
ECTOPIAS AND FUSIONS

Interpretation
Ectopic location of the kidney can range from the pelvis (Fig. 3-15) to the thorax"
(Fig. 3-16). Occasionally, the ectopia is crossed, with both kidneys being on the
same side and usually fused."'" Fused kidneys appear longer than normal, with
the site of fusion usually
marked by notches (Fig. 3-17), and the contralateral re12
nal fossa is empty.' 1 ' A rare anomaly is a supernumerary kidney, which is usually
diminutive and located more inferiorly' but may also be fused with the normal
kidney." In this case, a contralateral kidney is present. Fusion without ectopia produces a horseshoe kidney with attachment usually at the lower poles."'" Clues
to the diagnosis include poorly defined (Fig. 3-18) or elongated and tapered (Figs.
3-19A, 3-19B) inferior margin, low-lying kidneys; malrotation with anteriorly directed pelvis; and excess curvature in the longitudinal axis." The isthmus can be
difficult to visualize because of overlying bowel or because it may be only a thin
band of fibrous tissue." It can be detected overlying the aorta (Fig. 3-19C) in a majority of patients in whom a midline longitudinal scan is performed." Ureteral abnormalities are common in fused kidneys, usually manifested as hydronephrosis
or multicystic dysplasia' in one of the kidneys" 2 (Fig. 3-20).
FIGURE 3-15
Pelvic kidney. Sagittal scan of pelvis showing a kidney
(arrowheads) posterior to the bladder (B). (Photo courtesy of
Dr. D. Baumgarten.)
31
FIGURE 3 - 1 6
Intrathoracic kidney. Longitudinal image of kidney showing
it to be posterior and superior to the spleen (S) and separated
from it by the diaphragm (D). (From Sumner TE, Volberg FM,
Smolen PM: Intrathoracic kidneydiagnosis by ultrasound.
Pediatr Radiol 1982;12:78, with permission.)
FIGURE 3 - 1 7
Fused supernumerary kidneys. Longitudinal view of the
right renal fossa showing the two fused kidneys (arrowheads)
separated by a notch (arrow). (From Lubat E, HernanzSchulman M, Genieser NB, et al: Sonography of the simple
and complicated ipsilateral fused kidney. J Ultrasound Med
FIGURE 3 - 1 8
Horseshoe kidney. Coronal view of right kidney (cursors).
The lower pole cannot be demarcated and fuses medially
with the lower pole of the left kidney (arrows).
32
FIGURE 3-19
Horseshoe kidney in a patient with abdominal aortic
aneurysm. Transverse scans of the (A) right and (B) left
kidneys showing elongation and tapering of the kidney
(arrows) extending over the aneurysmal aorta. C. Midline
longitudinal scan showing the isthmus (arrows) overlying
the aorta. The isthmus has a typical renal appearance of
hypoechoic parenchyma surrounding echogenic sinus fat.
FIGURE 3-20
Crossed fused ectopia with obstruction of one ureteropelvic
junction. Coronal view showing two right kidneys (arrowheads)

that are fused, with hydronephrosis (C) of the superior
kidney. The site of fusion is indicated by the arrows. A, aorta.
(From Lubat E, Hernanz-Schulman M, Genieser NB, et al:
Sonography of the simple and complicated ipsilateral fused
kidney. J Ultrasound Med 1989;8:109, with permission.)
Kidneys with a duplicated collecting system (see Fig. 3-1) are normal-sized or only
slightly enlarged 12 and have a normal contour, and the contralateral kidney is present. Fusions are easily confused with neoplasms, but normal renal architecture is
present and the contralateral renal fossa is usually empty (or the contralateral kidney is similarly abnormal in the case of a horseshoe
kidney). However, further
11,12
particularly when one of the kidimaging is often required for confirmation,
neys is hydronephrotic and appears as a multiloculated mass.
REFERENCES
1. Davidson AJ, Hartman DS, Choyke PL, et al: Davidson's Radiology of the Kidney and Genitourinary
Tract. Philadelphia, WB Saunders, 1999, pp 59-65.
2. Levine, E, Hartman DS, Meilstrup JW, et al: Current concepts and controversies in imaging of renal cystic diseases. Urol Clin North Am 1997;24:523.
3. Blair D, Rigsby C, Rosenfield AT: The Nubbin Sign on computed tomography and sonography.
Urol Radio! 1987;9:149.
4. Lafortune M, Constantin A, Breton G, et al: Sonography of the hypertrophied Column of Bertin.
AIR 1986; 146:53.
5. Yeh H-C, Halton KP, Shapiro RS, et al: Junctional parenchyma: Revised definition of hypertrophic
Column of Bertin. Radiology 1992;185:725.
6. Patriquin H, Lefaivre J-F, Lafortune M, et al: Fetal lobation: An anatomo-ultrasonographic correlation. I Ultrasound Med 1990;9:191.
7. Cramer B, Green J, Harnett J, et al: Sonographic and urographic correlation in Bardet-Biedl Syndrome (formerly Laurence-Moon-Biedl Syndrome). Urol Radio! 1988;10:176.
8. Jones BE, Hoffer FA, Littlewood Teele R, et al: The compound renal pyramid: A normal hypoechoic
region on the pediatric sonogram. I Ultrasound Med 1987;6:515.
9. Sumner TE, Volberg FM, Smolen PM: Intrathoracic kidneydiagnosis by ultrasound. Pediatr Radio! 1982;12:78.
10. N'Guessen G, Stephens FD, Pick J: Congenital superior ectopic (thoracic) kidney. Urology 1984;
224:219.
11. Lubat E, Hernanz-Schulman M, Genieser NB, et al: Sonography of the simple and complicated ipsilateral fused kidney. I Ultrasound Med 1989;8:109.
12. McCarthy S, Rosenfield AT: Ultrasonography in crossed renal ectopia. I Ultrasound Med 1984;3:107.
13. Strauss S, Dushnitsky T, Peer A, et al: Sonographic features of horseshoe kidney: review of 34 patients. I Ultrasound Med 2000;19:27.
33
Percutaneous Renal
Biopsy
SONOGRAPHY
onography has revolutionized percutaneous renal biopsy, making it a far

safer and more reliable procedure, and it has become the method of choice for
guiding biopsy. Recent studies have documented close to 100% success rate
with few, if any serious complications.' Diagnostic sonography of both kidneys
should be performed, or a recent study should be reviewed, to identify any
pathology that might influence the decision of whether to biopsy and which kidney to use. For biopsy, the patient is placed prone, with the back flat and level.
Proper positioning of the patient is extremely important, so the back should be as
level as possible without the normal concavity. This is accomplished by placing
pillows under the abdomen just superior to the iliac crests (Fig. 4-1). All subsequent imaging is done with the probe perpendicular to the back with a minimal
amount of pressure. Proper handling of the probe is critical because deviation
from perpendicular orientation can cause misalignment with a deep kidney and
excessive pressure can lead to large underestimates of kidney depth. Once the
lower pole is identified, its respiratory excursion is studied to determine the timing of the biopsy. The location of the lower pole is confirmed in both the sagittal
and transverse planes and the depth is recorded. Sonographic guidance for percutaneous biopsy of renal allografts is covered in Chapter 25.
INTERPRETATION
he biopsy site should be centered over the tip of the lower pole in both the
sagittal and transverse planes (Fig. 4-2). Use of the lower pole maximizes
the amount of cortex obtained and minimizes the chance of puncturing the
collecting system or a large vessel. Usually the biopsy is performed at end inspiration but can be performed at end expiration on kidneys that are particularly
deep. The depth recorded by sonography is only an approximation; the biopsy
depth is often as much as 2 cm greater. This is probably due to pressure on the skin
and subcutaneous tissue by the ultrasound probe and to depression of the kidney
by anesthetic and the biopsy needle. Some authors advocate real-time guidance of
the biopsy needle 2 '3 using a guide attached to the probe (Fig. 4-3) but excellent results can be obtained without this technique.' With biopsy of native kidneys, the
overlying tissue consists entirely of subcutaneous tissue, muscle, and fascia and
there are no intervening structures that need to be avoided.
36
FIGURE 4-1
Patient position for percutaneous renal biopsy.
A A. Normal prone position showing natural
lordosis of the lower back. B. A pillow is placed
underneath the lower abdomen to flatten the
back, and the patient is positioned so that the
back is level with the bed.
FIGURE 4-2
Location of the native kidney for percutaneous biopsy. A. Sagittal and (B) transverse views of left kidney, prone position,
showing the lower pole (arrows) centered under the probe.
PERCUTANEOUS RENAL BIOPSY
37
FIGURE 4 3
Sonographic guidance of
biopsy needle. Sagittal images
of kidney, prone position, (A)
just before and (B) during
biopsy. The needle (arrows) can
be seen touching the kidney
prior to biopsy and then entering the lower pole of the kidney during the biopsy. (From
Cozens NJA, Murchison JT,
Allan PL, et al: Conventional
15G needle technique for renal
biopsy compared with ultrasound-guided spring-loaded
18G needle biopsy. Br J Radiol
COMPLICATIONS
he most common complication is hemorrhage, which is easily diagnosed by

sonography. Small perirenal hematomas are common after biopsy and are
usually asymptomatic. 4,5 Occasionally, they can be quite large (see Chapter
24) and produce pain and hypotension. Sizable hematomas may also occur in the
musculature and appear as heterogeneous masses containing both clotted and unclotted blood, posterior to the kidney (Fig. 4-4). Hemorrhage into the collecting
system (see Fig. 24-5) is a rarer but more serious complication that can lead to
bladder outflow obstruction due to blood clots (see Fig. 14-21). Arteriovenous fistulas and pseudoaneurysms (see Figs. 29-6, 29-7) can appear almost immediately
after biopsy or can develop gradually.6
FIGURE 4-4
Hemorrhage into the posterior musculature after percutaneous renal biopsy. Sagittal scan in the prone position
showing a large heterogeneous hematoma (small arrowheads)
displacing the left kidney (large arrowheads) anteriorly.
There is no blood in the perirenal space.
38
REFERENCES
1. Nass K, O'Neill WC: Bedside renal biopsy: Ultrasound guidance by the nephrologist. Am J Kidney
Dis 1999;34:1.
2. Cozens NJA, Murchison JT, Allan PL, et al: Conventional 15G needle technique for renal biopsy
compared with ultrasound-guided spring-loaded 18G needle biopsy. Br J Radiol 1992;65:594.
3. Donovan KL, Thomas DM, Wheeler DC, et al: Experience with a new method for percutaneous renal biopsy. Nephrol Dial Transplant 1991;6:731.
4. Feneberg R, Schaefer F, Zieger B, et al: Percutaneous renal biopsy in children: A 27-year experience.
Nephron 1998;79:438.
5. Riehl J, Maigatter S, Kierdorf H, et al: Percutaneous renal biopsy: Comparison of manual and automated puncture techniques with native and transplanted kidneys. Nephrol Dial Transplant
1994;9:1568.
6. Hubsch PJS, Mostbeck G, Barton PB, et al: Evaluation of arteriovenous fistulas and pseudoaneurysms in renal allografts following percutaneous needle biopsy: Color-coded Doppler Sonography versus Duplex Doppler Sonography. J Ultrasound Med 1990;9:95.
RENAL
PARENCHYMAL
DISEASE
CHAPTER
Chronic Renal Failure
SONOGRAPHY
he natural history of many renal diseases converges on a final common state

of cortical atrophy and fibrosis. Although this finding is not helpful in identifying the underlying disease, it is extremely useful in identifying patients
with irreversible disease in whom further costly or invasive diagnostic measures
can be avoided. In cases of known disease, the finding of cortical atrophy or
fibrosis can be useful in assessing prognosis and in decisions concerning continuation of treatment, particularly immunosuppressive therapy. Sonography is therefore indispensable in the workup of chronic renal failure. If a kidney appears
small, it is important to ensure that it is not being viewed in a tangential or oblique
plane and that it is not related to a small body size. The sonographer must be
aware of liver disease or artifacts that affect interpretation of renal cortical
echogenicity.
INTERPRETATION
he sonographic appearance of chronic renal failure is easily recognized12

and consists of a decrease in renal size, thinning of the parenchyma (particularly the cortex), and increased echogenicity of the cortex reflecting fibrosis
and sclerosis. In some cases, the cortex is so echogenic that it cannot be distinguished from the sinus fat and the kidney is diffusely echogenic (Fig. 5-1). In other
cases, the cortex is not as echogenic and its thinness is easily appreciated (Fig.
5-2). Unfortunately, there are not extensive data on normal cortical thickness, but
a value <7 mm is probably abnormal. 3 When cortical thickness cannot be determined because the medullary pyramids are not visible, thinning of the cortex can
still be appreciated as thinning of the entire parenchyma. Again, there are limited
data, but a cutoff of 12 mm may be appropriate. 4 Although cortical thinning can
be seen in many disorders, it is more commonly observed with vascular disease
(nephrosclerosis and renal arterial insufficiency) than with glomerular disease.
Another manifestation of cortical thinning is accentuated lobulation (Fig. 5-3) due
to loss of cortex in the columns of Bertin between the medullary pyramids. Of the
characteristics of cortical atrophy, the most reliable is cortical thinning. Renal size
varies with body size so that a small kidney can be normal and atrophy can be present in a "normal-size" kidney (Fig. 5-4). Increased echogenicity is a subjective
determination that can be influenced by artifacts and does not always indicate fibrosis or sclerosis, because it can also be produced by cellular infiltrates. Thus,
caution should be exercised in diagnosing irreversible renal damage solely by kidney size or echogenicity. The frequency of simple cysts increases with progression
42
FIGURE 5 - 1
Chronic renal failure. Longitudinal image of right kidney
(cursors) with a length of 9.8 cm and a simple cyst at the
extreme lower pole. The cortex is echogenic compared with
the liver and cannot be distinguished from the sinus fat.
Several small medullary pyramids are visible (arrows).
(From O'Neill WC: Sonographic evaluation of renal failure.
Am J Kidney Dis 2000;35:1021, with permission.)
FIGURE 5 - 2
Chronic renal failure. Longitudinal view of left kidney
showing a thin rim of parenchyma (arrowheads) surrounding
the sinus fat. Despite its thinness, the parenchyma is less
echogenic than the spleen (S). Kidney length is 9.5 cm.
FIGURE 5 - 3
Chronic renal failure. Longitudinal view of right kidney
(cursors) showing accentuated lobulation (arrows) due to
thinning of the cortex, which is not echogenic.
CHRONIC RENAL FAILURE
FIGURE 5 -4
Chronic renal failure. Longitudinal image of a right kidney
that, despite a maximum length of 11.1 cm, has thinning of
the parenchyma (arrowheads) and an increase in echogenicity.
of renal disease s and therefore provides another indication of chronic renal damage (Fig. 5-1). Occasionally, the findings of chronic renal disease are unilateral, indicative of vascular disease (see Fig. 22-1), urologic disorders, or congenital
atresia.
DIFFERENTIAL DIAGNOSIS
espite the fact that many disorders can lead to a similar sonographic appearance of chronic renal failure, there are some differences that suggest
specific diagnoses. Cortical thinning in the presence of caliectasis suggests
obstructive uropathy (see Figs. 13-9 through 13-11) or reflux nephropathy (see Fig.
13-1) with segmental involvement and irregularities in the renal contour related to
scarring often seen in the latter. Cortical thinning is often most noticable in renovascular disease (see Fig. 22-1) and hypertensive nephrosclerosis, whereas in glomerular disorders, particularly diabetic nephropathy, cortical thickness is often preserved
even late in the disease (see Figs. 6-7, 6-8). Unilateral cortical atrophy is very suggestive of renovascular disease (see Fig. 22-1).
REFERENCES
1. Paivansalo M, Huttunen K, Suramo I: Ultrasonographic findings in renal parenchymal diseases.
2. Hricak H, Cruz C, Romanski R, et al: Renal parenchymal disease: Sonographic-histologic correlation. Radiology 1982;144:141.
3. Raj DSC, Hoisala R, Somiah S, et al: Quantitation of change in the medullary compartment in renal
allograft by ultrasound. J Clin Ultrasound 1997;25:265.
4. Emamian SA, Nielsen MB, Pedersen JF, et al: Kidney dimensions at sonography: Correlation with
age, sex, and habitus in 665 adult volunteers. AIR 1993;160:83.
5. Ravine D, Gibson RN, Donlan J, et al: An ultrasound renal cyst prevalence survey: Specificity data
for inherited renal cystic diseases. Am J Kidney Dis 1993;22:803.
43
Glomerular Disease
SONOGRAPHY
he diagnosis of glomerular disease is often apparent from the clinical presentation; sonography is performed principally as a prelude to percutaneous
biopsy. In these cases, the purpose is to rule out irreversible renal damage
and to detect abnormalities that might affect the biopsy. When correlated with
other clinical findings, sonographic findings can suggest particular diagnoses but
cannot provide specific diagnostic infomation. In some cases, the indication for
sonography is hematuria, in which case nephrolithiasis, tumors, and papillary
necrosis need to be ruled out.
ACUTE GLOMERULONEPHRITIS
Interpretation
Although sonographic findings can be normal in glomerulonephritis, there is frequently swelling and increased echogenicity of the cortex (Figs. 6-1, 6-2). Swelling
of the cortex is apparent as increased cortical thickness, rounding of the renal
contour, and expansion of the cortex so that it surrounds the medullary pyramids
and compresses the sinus fat. The changes can be dramatic, resulting in very
echogenic, globular kidneys that bear little resemblance to normal kidneys (Fig.
6-3). Linear or irregular hypoechoic areas can be seen within the echogenic cortex
(Fig. 6-4) and have been ascribed to focal edema.' The sonographic abnormalities
can occur in all forms of glomerulonephritis and presumably represent edema and
cellular infiltration. A normal-size or shrunken cortex with increased echogenicity probably indicates fibrosis and sclerosis 2 -4 and may be of prognostic value.
Renal veins may be prominent, owing to the inflammation or to volume overload
(Fig. 6-5).
Acute interstitial nephritis (see Fig. 8-1) can have identical sonographic findings
and cannot be distinguished from glomerulonephritis by sonography. Renal vein
thrombosis (see Figs. 23-3, 23-4) also results in a swollen and echogenic cortex and
often occurs in the setting of glomerulonephritis. Detection of thrombus or an
acute increase in kidney size can be helpful in making this diagnosis in a patient
with glomerulonephritis and worsening renal function. In acute tubular necrosis
46
FIGURE 6 - 1
Acute glomerulonephritis. Longitudinal view of right kidney
(cursors) in a patient with mesangial proliferative glomerulonephritis. The kidney is globular with diminished sinus fat,
indicating swelling of the cortex. The medullary pyramids
are prominent (arrows), indicating increased cortical
echogenicity. Kidney length is 12.5 cm. (From O'Neill WC:
Sonographic evaluation of renal failure. Am J Kidney Dis
FIGURE 6 - 2
in a patient with antiglomerular basement membrane disease
(Goodpasture's syndrome). The kidney is enlarged (13.0 cm)
and somewhat globular, with increased cortical thickness
and reduced sinus fat, indicating cortical swelling. Two
medullary pyramids are visible (arrows) and highlight the
increase in echogenicity.
FIGURE 6 - 3
in a patient with membranoproliferative glomerulonephritis.
The kidney is enlarged (12.4 cm), globular, and very echogenic
compared to the liver (L), with no detectable internal
architecture. (From O'Neill WC: Sonographic evaluation of
renal failure. Am I Kidney Dis 2000;35:1021, with permission.)
GLOMERULAR DISEASE
47
FIGURE 6 - 4
Acute glomerulonephritis. Longitudinal view of left kidney
in a patient with membranoproliferative glomerulonephritis.
The kidney is swollen with a diffusely enlarged and
echogenic cortex. There are several irregular hypoechoic
areas within the cortex that may represent edema (black
arrows) or compressed medullary pyramids (white arrows).
FIGURE 6 5
Glomerulonephritis with venous engorgement. Longitudinal
view of left kidney in patient with diffuse proliferative lupus
nephritis. The cortex is swollen and echogenic and the renal
vein and its branches are dilated (arrows). A, aorta; IVC,
inferior vena cava. (From O'Neill WC: Sonographic
evaluation of renal failure. Am J Kidney Dis 2000;35:1021,
with permission.)
(see Chapter 7) and in amyloidosis (see below), the kidney usually maintains a normal shape, and although proteinuria occurs in amyloidosis, hematuria is not seen
in either. Leukemic or lymphomatous infiltration (see Figs. 20-4, 20-6) can be indistinguishable from glomerulonephritis by sonography but usually does not produce hematuria or proteinuria.
DIABETIC NEPHROPATHY
Interpretation
Diabetes produces renal enlargement in the absence of nephropathy, 5 and this is reversible with glycemic control. 6 This hypertrophy involves all components, so that
the kidneys maintain their shape and architecture (Fig. 6-6). The enlargement of the
cortex should be distinguished from the cortical swelling that occurs in inflammatory conditions, which results in rounding of the renal contour and compression of
48
FIGURE 6 - 6
Early diabetic nephropathy. Longitudinal scan of right
kidney (cursors) showing generalized enlargement with a
normal shape and architecture. Kidney length is 15 cm and
the cortex is the same echogenicity as the liver (arrow).
FIGURE 6 - 7
Diabetic nephropathy. Longitudinal view of left kidney
showing a cortex of normal thickness but increased
echogenicity compared to the spleen (S). A dromedary hump
is present (arrowhead). (From O'Neill WC: Sonographic
evaluation of renal failure. Am I Kidney Dis 2000;35:1021,
with permission.)
FIGURE 6 - 8
End-stage diabetic nephropathy. Longitudinal image of right
kidney (arrowheads) in patient with diabetic nephropathy and
end-stage renal disease. Aside from a slight increase in
echogenicity, the kidney appears normal with no cortical
thinning.
GLOMERULAR DISEASE
the sinus fat. As nephropathy develops, the cortex becomes more echogenic but
without any thinning (Fig. 6-7). The increase in echogenicity is not extreme, but because only the cortex is involved, the medullary pyramids are often prominent. Cortical thickness remains normal even into end-stage disease (Fig. 6-8), so that cortical
thinning or reduced kidney size in diabetic nephropathy is often a sign of superimposed disease, usually hypertensive nephrosclerosis or renovascular disease.
Differential diagnosis
With most other causes of chronic renal failure, renal size and cortical thickness are
reduced (see Chapter 5). Amyloidosis (see Fig. 6-9) and human immunodeficiency
virus (HIV) nephropathy (see Fig. 6-14) also produce proteinuria and renal failure,
but the kidneys are usually larger and more echogenic. However, early disease
may not be distinguishable from diabetic nephropathy. In acute glomerulonephritis
(Figs. 6-1 through 6-3) and interstitial nephritis (see Fig. 8-1), the kidney is usually
swollen, which does not occur in diabetes. Chronic glomerular disorders such as
membranous nephropathy and immunoglobulin A (IgA) nephropathy may have
a sonographic appearance identical to that of diabetic nephropathy.
AMYLOIDOSIS
myloidosis usually results from multiple myeloma and produces renal failure and nephrotic syndrome. This should be distinguished from myeloma
kidney, which is an acute or subacute form of renal failure due to precipitation of paraprotein in the tubules with tubular necrosis.
Interpretation
The kidneys are usually enlarged with increased cortical thickness but maintain a
normal shape (Fig. 6-9). Echogenicity is increased, often with a fine texture, and
the medullary pyramids can be quite prominent, because amyloidosis primarily
involves the cortex. The changes are not as marked in early disease (Fig. 6-10).
FIGURE 6-9
Amyloidosis. Longitudinal image of right kidney (small
arrowheads) with increased thickness and echogenicity of the
cortex. The texture of the echogenicity is very fine. Large
arrowhead indicates the liver. (From O'Neill WC: '\
Sonographic evaluation of renal failure. Am I Kidney Dis
49
50
FIGURE 6-10
Amyloidosis. Longitudinal image of right kidney in a patient
with newly diagnosed amyloidosis. Size and cortical thickness are normal, and echogenicity is only slightly greater
than that of the liver (L). Medullary pyramids are prominent
(arrows) and there is a simple, exophytic cyst at the extreme
lower pole.
In diabetic nephropathy (Figs. 6-7, 6-8), the increase in echogenicity is not as marked
as in amyloidosis. HIV nephropathy also presents with nephrotic syndrome and
enlarged, echogenic kidneys, but the texture is usually coarser (see Fig. 6-14). In
acute glomerulonephritis (see Figs. 6-1 through 6-3), renal vein thrombosis (see Fig.
23-3), and lymphomatous or leukemic infiltration (see Figs. 20-4, 20-6) the kidneys
are usually swollen, whereas renal shape is maintained in amyloidosis. POEMS
syndrome (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes) presents with enlarged kidneys with echogenic
cortex.' Heavy proteinuria does not occur in POEMS syndrome, leukemia or lymphoma, and renal vein thrombosis (in the absence of glomerulonephritis).
OTHER GLOMERULAR DISORDERS
ncreased echogenicity occurs in hemolytic uremic syndrome and may correlate

with prognosis." Increased cortical echogenicity has also been reported in
preeclampsia, with rapid resolution postpartum w (Fig. 6-11). Findings on renal
sonogram are frequently normal in chronic immune complex disorders such as
membranous nephropathy or IgA nephropathy. An increase in cortical echogenicity
may occur (Fig. 6-12), presumably as a manifestation of glomerular deposits or of
fibrosis and sclerosis. 3 HIV nephropathy is a glomerulopathy associated with infection by HIV, most often a focal, segmental glomerulosclerosis. It produces1 highly
2
echogenic kidneys (Fig. 6-13), often with significant renal enlargement' ' (Fig.
6-14). It is important to remember that there are other causes of renal failure in
HIV-infected patients, including drug toxicity, acute tubular necrosis, infections,
and lymphoma.
GLOMERULAR DISEASE
FIGURE 6- 1 1
Preeclampsia. A. Longitudinal image of right kidney on the
day of delivery showing expanded echogenic cortex and a
length of 11.1 cm. B. Three days postpartum, the cortex is
normal and kidney length is 9.5 cm. (from Schutz K,
Siffring PA, Forrest TS, et al: Serial renal sonographic
changes in preeclampsia. J Ultrasound Med 1990;9:415, with
permission.)
51
FIGURE 6- 1 2
Chronic renal failure secondary to membranous nephropathy.
Longitudinal view of right kidney (cursors) showing a slight
increase in cortical echogenicity compared with the liver (L).
Note the absence of cortical thinning.
52
FIGURE 6-13
Human immunodeficiency virus (HIV) nephropathy. Longitudinal image of right kidney (K) in patient with end-stage
renal disease due to HIV nephropathy. The kidney is very
echogenic compared with the liver (L). Kidney length is
9.7 cm.
FIGURE 6-14
Human immunodeficiency virus nephropathy. Longitudinal
view of right kidney (arrowheads) showing cortical expansion
with increased echogenicity compared with the liver (L).
The hypoechoic regions within the kidney are medullary
pyramids.
REFERENCES
1. Longmaid HE III, Rider E, Tymkiw J: Lupus nephritis: New sonographic findings. I Ultrasound Med
1987;6:75.
4. Rosenfield AT, Siegel NJ: Renal parenchymal disease: Histopathologic-sonographic correlation.
AJR 1981;137:793.
5. Segel MC, Lecky JW, Slasky BS: Diabetes mellitus: The predominant cause of bilateral renal enlargement. Radiology 1984;153:341.
6. Feldt-Rasmussen B, Mathiesen EA, Hegedus L, et al: Kidney function during 12 months of strict
metabolic control in insulin-dependent diabetic patients with incipient nephropathy. N Engl J Med
1986;314:665.
7. Arenson AM, Rubenstein JD, McKee JD: Renal ultrasound in POEMS syndrome. I Clin Ultrasound
1985;13:208.
8. Choyke PL, Grant EG, Hoffer FA, Tina L, Korec S: Cortical echogenicity in the hemolytic uremic
syndrome: Clinical correlation. J Ultrasound Med 1988;7:439.
9. Kenney PJ, Brinsko RE, Patel DV, Spitzer RE, Farrar FM: Sonography of the kidneys in hemolytic
uremic syndrome. Invest Radiol 1986;21:547.
10. Schutz K, Siffring PA, Forrest TS, et al: Serial renal sonographic changes in preeclampsia. J Ultrasound Med 1990;9:415.
11. Yee JM, Raghavendra N, Horii SC, et al: Abdominal sonography in AIDS: A review. J Ultrasound
Med 1989;8:705.
12. Di Fiori JL, Rodrigue D, Kaptein EM, et al: Diagnostic sonography of HIV-associated nephropathy:
New observations and clinical correlation. AIR 1998;171:713.
CHAPTER
Acute Tubular Necrosis
SONOGRAPHY
ubular necrosis is the most common cause of acute renal failure and has a
variety of causes, including ischemia, drugs, and toxins. Sonography is performed primarily to rule out urinary obstruction and therefore is not indicated in all cases.' The patients are often very ill; are unable to be positioned
properly; and have dressings, drains, and catheters, all of which render optimum
studies difficult. Provided that hydronephrosis is ruled out and kidney size can be
determined, the study should be considered adequate for the workup of acute
renal failure. A more thorough examination can be performed at a later date if
further information is required.
INTERPRETATION
fter urinary obstruction has been ruled out, the cause of acute renal failure
is likely to be either acute tubular necrosis (ATN) or functional (prerenal)
failure. It is a common misconception that findings on renal sonogram are
routinely normal in ATN. Experimental studies in animals have clearly shown increases in cortical echogenicity, 2,3 and clinical studies have confirmed this and
have demonstrated enlargement of the cortex as wel1. 45 Sonographic abnormalities would not be expected in functional (prerenal) renal failure and have not been
reported, so the sonogram may be helpful in distinguishing ATN from functional
renal failure. Several sonographic patterns are seen in ATN: enlarged hypoechoic
cortex (Fig. 7-1), increased cortical echogenicity (Fig. 7-2) with or without cortical
enlargement, and norma1. 6-8 Whether the differing sonographic findings are a
function of the cause or severity of the ATN or of the timing of the sonogram is
unknown. A normal or enlarged hypoechoic cortex is frequently observed in ischemic ATN (Fig. 7-1) and presumably represents cortical edema. 2,9 Despite the
cortical enlargement, the kidneys maintain their shape and usually do not appear
swollen. This abnormality may be more common than generally believed when
correlated with the clinical picture. Because ATN occurs predominantly in older
patients, many of whom have some chronic renal insufficiency with cortical thinning, "normal" sonographic findings may actually represent cortical edema. Enlargement may predict clinical
course. 4 Increased cortical echogenicity may be
ATN2'3'5'1
more frequent in nephrotoxic
and is probably a manifestation of cellular
casts and other debris within the tubules. Cortical echogenicity is conspicuous in
ATN associated with myeloma, so-called myeloma kidney, presumably because of
tubular protein casts (Fig. 7-3). Because ATN predominantly involves proximal
54
FIGURE 7- 1
Acute tubular necrosis secondary to ischemia. Longitudinal
view of right kidney showing increased length (14.0 cm)
and enlarged parenchyma without increased echogenicity.
L, liver. (From O'Neill WC: Sonographic evaluation of renal
failure. Am J Kidney Dis 2000;35:1021, with permission.)
FIGURE 7- 2
Acute tubular necrosis in a patient with hypotension and
sepsis. A. Longitudinal view of right kidney demonstrating
an expanded cortex that is echogenic compared with the
liver (L). B. Longitudinal image of left kidney from a
different patient showing expanded, echogenic cortex with
prominent medullary pyramids (arrows).
ACUTE TUBULAR NECROSIS
55
FIGURE 7 3
Acute tubular necrosis secondary to multiple myeloma.
Longitudinal view of right kidney (cursors) in patient with
severe paraproteinemia and acute renal failure. The kidney
is enlarged (14.3 cm) and the cortex is echogenic compared
with the liver (L), with prominent medullary pyramids. The
cortical thickness is increased and the sinus fat is decreased,
indicating swelling of the cortex. Renal function returned
after plasmapheresis.
FIGURE 7 4
Acute renal failure from ethylene glycol ingestion. Longitudinal images of right kidney (arrowheads) (A) at onset of renal
failure and (B) after recovery. The echogenicity of the kidney is markedly increased compared with the liver (L), and the
pyramids are not prominent, indicating medullary involvement as well. Findings on the follow-up sonogram are normal.
(From Walker JT, Keller MS, Katz SM: Computed tomographic and sonographic findings in acute ethylene glycol poisoning.
J Ultrasound Med 1983;2:429, with permission.)
tubules, the medullary pyramids are usually not involved and are often very
prominent (Figs. 7-2, 7-3). Marked increases in echogenicity also occur in ATN
from ethylene glycol ingestion (Fig. 7-4), probably related to deposition of calcium oxalate, but in this case, the medulla is involved as well. 10 Because the sonographic findings of ATN are nonspecific and baseline sonograms are usually not
available for comparison, the diagnosis cannot be made or excluded by ultrasonography alone.
lomerulonephritis (see Figs. 6-1 through 6-3), interstitial nephritis (see Fig.
8-1), and renal vein thrombosis (see Figs. 23-3, 23-4) can produce acute renal
failure with enlarged, echogenic kidneys, but renal enlargement is usually
greater than in ATN and these disorders differ clinically from ATN. There should
56
be no venous engorgement in ATN unless volume overload or right heart failure

is present. Transplant rejection (see Figs. 26-1 through 26-3) and ATN have identical appearances and cannot be reliably distinguished by ultrasonography. Although not a cause of acute renal failure, chronic glomerulopathies such as diabetic
nephropathy (see Fig. 6-7,) can have a sonographic appearance indistinguishable
from that of ATN.
REFERENCES
1. Gottlieb RH, Weinberg EP, Rubens DJ, et al: Renal sonography: Can it be used more selectively in
the setting of an elevated serum creatinine level? Am J Kidney Dis 1997;29:362.
2. Rosenfield AT, Zeman RK, Cicchetti DV, et al: Experimental acute tubular necrosis: US appearance.
Radiology 1985;157:771.
3. Rivers BJ, Walter PA, Holm JC, et al: Gray-scale sonographic characterization of aminoglycosideinduced nephrotoxicosis in a canine model. Invest Radiol 1996;10:639.
4. Nomura G, Kinoshita E, Yamagata Y, et al: Usefulness of renal ultrasonography for assessment of
severity and course of acute tubular necrosis. J Clin Ultrasound 1984;12:135.
5. Pardes JG, Auh YH, Kazam E: Sonographic findings in myoglobinuric renal failure and their clinical implications. J Ultrasound Med 1983;2:391.
6. Jeffrey RB, Federle MP: CT and ultrasonography of acute renal abnormalities. Radiol Clin North Am
1983;21:515.
Tract. Philadelphia, WB Saunders, 1999 pp 162-164.
10. Walker JT, Keller MS, Katz SM: Computed tomographic and sonographic findings in acute ethylene glycol poisoning. J Ultrasound Med 1983;2:429.
Tubulointerstitial Disease
SONOGRAPHY
nterstitial diseases have several presentations, but sonography is usually performed for acute or chronic renal failure. Other indications include pain and
hematuria. More subtle manifestations of tubulointerstitial disease are hypokalemia, polyuria, and renal tubular acidosis. When interstitial disease is being
considered, particular attention should be focused on the medullary pyramids.
ACUTE INTERSTITIAL NEPHRITIS

cute interstitial nephritis is often caused by medications, particularly antibiotics, and can also be idiopathic (presumably autoimmune). It is an uncommon but important cause of acute renal failure, because it is treatable
and usually reversible.
Interpretation
Sonography reveals swollen, echogenic kidneys 1 -3 (Fig. 8-1). The pyramids are not
prominent, presumably because of involvement of both the cortex and medulla.
To what extent this appearance varies and whether sonographic findings can be
normal is unknown.
Swollen, echogenic kidneys are seen in several situations, so the distinction of
cause usually rests on other parameters. Glomerulonephritis and human immunodeficiency virus nephropathy (see Chapter 6) are usually accompanied by substantial
proteinuria. Although proteinuria is present in interstitial nephritis, it is generally
not in the nephrotic range.' The renal enlargement in acute tubular necrosis (see
Chapter 7) is more subtle and the kidneys do not appear swollen. The medullary
pyramids are often prominent. The urine contains granular casts and renal tubular cells as opposed to the hematuria and pyuria frequently seen in interstitial
nephritis.' Transplant rejection (see Figs. 26-1 through 26-3) has the same sonographic appearance as acute interstitial nephritis. Differentiation of interstitial
nephritis from renal vein thrombosis (see Fig. 23-3) rests on venous dilatation and
visualization of thrombus in the vein.
58
FIGURE 8-1
Acute interstitial nephritis. Transverse view of right kidney
(arrowheads) showing an enlarged, echogenic cortex without
prominent medullary pyramids. Note the lack of sinus fat,
indicating significant cortical swelling.
CHRONIC INTERSTITIAL NEPHRITIS

variety of disorders can lead to chronic interstitial nephritis, including
analgesic abuse, sickle hemoglobinopathies, Sjogren's syndrome, chronic
hypokalemia, and chronic lithium therapy. The pathology is localized primarily to the medulla and can eventuate in papillary necrosis, particularly in analgesic nephropathy. Papillary necrosis can also occur in diabetes mellitus, chronic
pyelonephritis, and obstructive uropathy.
Interpretation
The hallmark of chronic interstitial nephritis is increased echogenicity of the
medulla, although the cortex can also be involved. The appearance depends on
the relative involvement of the two, ranging from loss of corticomedullary differentiation 45 to hyperechoic medullary pyramids (Fig. 8-2), a reversal of the normally hypoechoic medulla. 4' 6' 7 In some cases of analgesic nephropathy, the
pyramids become quite prominent (Fig. 8-3), with the echogenicity being greatest
along the outer margins of the pyramids. 8 In other cases, the increase in echogenicity is localized to the papillae (Fig. 8-4). The echogenicity results from inflammation and fibrosis with perhaps a minor degree of calcification, so that acoustic
shadowing is never impressive (Fig. 8-4C) and is often absent 4 '" until late in the
disease, when a characteristic garland arrangement of calcifications is seen around
the renal sinus 9-" (Fig. 8-5). Eventually, the papillae necrose and are replaced by
expanded minor calyces (see Figs. 8-3B and 8-4B), with sloughed papillae occasionally visible in the collecting system as echogenic filling defects that can produce obstruction 13 (Fig. 8-6). Cortical scarring may occur in advanced disease.14
Many disorders can produce echogenic kidneys, particularly in the advanced
stage. However, the medulla is often relatively spared and the pyramids remain
relatively hypoechoic and never hyperechoic. Echogenic pyramids are observed
TUBULOINTERSTITIAL DISEASE
59
FIGURE 8-2
Sickle cell nephropathy. Transverse view of right kidney
showing a diffuse increase in medullary echogenicity with
normal cortical echogenicity. (From Zinn D, Haller JO,
Cohen HL: Focal and diffuse increased echogenicity in the
renal parenchyma in patients with sickle hemoglobinopathies: An observation. J Ultrasound Med 1993;4:211, with
permission.)
FIGURE 8 3
Analgesic nephropathy. A. Longitudinal view of left kidney
showing hyperechoic pyramids (arrows) with relative
sparing of the central portions. B. Oblique view of same
kidney (arrowheads) showing the cavities formed by the loss
of papillae (arrows). Note the lack of acoustic shadows.
(From O'Neill WC: Sonographic evaluation of renal failure.
Am J Kidney Dis 2000;35:1021, with permission.)
60
FIGURE 8-4
Papillary necrosis. A. Longitudinal image of left kidney
(arrowheads) demonstrating three echogenic papillae
(arrows). The echogenicities are outside the renal sinus
within medullary pyramids. B. Transverse view of right
kidney (arrowheads) through the pelvis demonstrating an
echogenic papilla (arrow) at the apex of a medullary
pyramid. The loss of medullary tissue has formed a
small cavity into which the remnant papilla protrudes.
C. Oblique longitudinal view of left kidney (arrowheads)
demonstrating a weak acoustic shadow from emanating
from a papilla (arrow).
in nephrocalcinosis (see Fig. 8-8.), but there is usually more acoustic shadowing and
loss of medullary tissue does not occur. Papillary necrosis can be easily confused
with hydronephrosis, but other findings of hydronephrosis, such as dilation of the
major calyces, pelvis, and proximal ureter, are absent. The medullary pyramids
are intact in hydronephrosis except in severe obstructive uropathy. The calyceal
enlargement in chronic pyelonephritis and reflux nephropathy (see Fig. 13-1) is associated with significant cortical
scarring, but scarring can also be seen in advanced
1 14
analgesic nephropathy,' ' and chronic infection can cause papillary necrosis.
Fused medullary pyramids (see Fig. 3-12) can mimic an enlarged minor calyx, with
the intervening column of Bertin masquerading as an echogenic pyramid. When
particulary prominent, hypoechoic pyramids can mimic enlarged minor calyces,
with the arcuate artery (see Fig. 2-4) appearing as an echogenic papillary remnant.
FIGURE 8 5
End-stage analgesic nephropathy. Longitudinal view of
right kidney (arrowheads) showing decreased size, thin,
echogenic cortex, and a garland-like distribution of calcified
pyramids (arrows). (From Weber M, Braun B, Kohler H:
Ultrasonic findings in analgesic nephropathy. Nephron
FIGURE 8 6
Sloughed renal papilla. Longitudinal image of a renal allograft showing an
echogenic papilla (arrow) lodged in a major calyx (arrowhead). (From Shapeero LG,
Vordermark JS: Papillary necrosis causing hydronephrosis in the renal allograft:
Sonographic findings. J Ultrasound Med 1989;8:579, with permission.)
NEPHROCALCINOSIS AND CRYSTAL

NEPHROPATHIES
ephrocalcinosis is seen in renal tubular acidosis, medullary sponge kidney,
and severe hyperparathyroidism. Uric acid has a low solubility in urine
and can precipitate in the tubules and produce acute renal failure when
excretion is high, such as with hematologic malignancies. Chronic deposition occurs in gouty nephropathy. A variety of medications have a very low solubility in
urine and can precipitate in the kidney, producing acute renal failure. 15 The most
common offenders are acyclovir, indinavir, sulfonamides, and methotrexate. The
expected medullary echogenicity has been reported with sulfonamides 16 but not
with other medications.
61
62
FIGURE 8-7
Uric acid deposition. Longitudinal image of right kidney
with echogenic pyramids (arrows) and acoustic shadowing.
FIGURE 8-8
Medullary sponge kidney with nephrocalcinosis.
A. Oblique longitudinal scan of left kidney (arrowheads)
showing calcification of the inner medullae, producing an
acoustic shadow (arrows). B. Longitudinal scan of right
kidney from the same patient, which is obstructed. The
medullary calcifications (arrows) highlight each minor
calyx. (Photos courtesy of Dr. D. Baumgarten.)
63
FIGURE 8 - 9
Nephrocalcinosis. Longitudinal image of left kidney in a
patient with renal tubular acidosis. There is a line of dense
calcification at the corticomedullary junction (arrows) with
distal acoustic shadowing (arrowheads).
FIGURE 8 - 1 0
Sulfadiazine-induced renal failure. Longitudinal image of
left kidney (arrowheads) containing two echogenic foci with
acoustic shadowing. One focus is in the parenchyma
(straight arrow) and presumably represents precipitation in
the medulla. The other is in the renal sinus (curved arrow)
and represents crystals in a calyx. (From Kane D, Murphy
JM, Keating S, et al: Renal ultrasonic findings in sulphadiazine-induced renal failure. Br J Radiol 1996;69:925, with
permission.)
Interpretation
The characteristic finding is increased echogenicity of all or part of the medullary
pyramids, 6' 7,17 ' 18 often with significant acoustic shadowing (Figs. 8-7, 8-8). Distal
portions of the pyramids may not be visible because of sound reflection, and in
some cases all that is visible is a rim of calcification at the corticomedullary junction
with dense shadowing distally (Fig. 8-9). Precipitation of oxalate occurs both in the
cortex and medulla and therefore produces a diffuse increase in echogenicity. This
occurs after ingestion of ethylene glycol 19 (see Fig. 7-4A) and in oxalosis. In the case
of medications, crystals may be visible both in the medulla and in the calyces (Fig.
8-10) but can precipitate throughout the tubules and produce a diffuse increase in
echogenicity, as in the case of acyclovir.
In chronic interstitial nephritis, the medullary echogenicity is usually not as marked
and acoustic shadowing is either absent or subtle unless substantial calcification
has occurred (Figs. 8-3, 8-4). Although nephrolithiasis (see Chapter 15) often coexists with nephrocalcinosis or gouty nephropathy, it is important to distinguish
between the two. Stones occur in the collecting system and not within the medulla.
64
REFERENCES
1. Ten RM, Torres VE, Milliner DS, et al: Acute interstitial nephritis: Immunologic and clinical aspects. Mayo Clin Proc 1988;63:921.
2. Hiraoka M, Hori C, Tsuchida S, et al: Ultrasonographic findings of acute tubulointerstitial nephritis. Am J Nephrol 1996;16:154.
4. Zinn D, Haller JO, Cohen HL: Focal and diffuse increased echogenicity in the renal parenchyma in
patients with sickle hemoglobinopathies: An observation. J Ultrasound Med 1993;4:211.
5. Strauss S, Robinson G, Lotan D, et al: Renal sonography in Bartter Syndrome. J Ultrasound Med
1987;6:265.
6. Toyoda K, Miyamoto Y, Ida M, et al: Hyperechoic medulla of the kidneys. Radiology 1989;173:431.
7. Jequier S, Kaplan BS: Echogenic renal pyramids in children. J Clin Ultrasound 1991;19:85.
8. Braden GL, Kozinn DR, Hampf FE, et al: Ultrasound diagnosis of early renal papillary necrosis.
9. Weber M, Braun B, Kohler H: Ultrasonic findings in analgesic nephropathy. Nephron 1985;39:216.
10. Segasoth M, Abdul Samad S, Zulfiqar A, et al: Computed tomography and ultrasonography: A
comparative study in the diagnosis of analgesic nephropathy. Nephron 1994;66:62.
11. DeBroe ME, Elseviers MM: Analgesic nephropathy. N Engl J Med 1998;338:446.
12. Hoffman JC, Schnur MJ, Koenigsberg M: Demonstration of renal papillary necrosis by sonography.
Radiology 1982;145:785.
13. Shapeero LG, Vordermark JS: Papillary necrosis causing hydronephrosis in the renal allograph:
Sonographic findings. J Ultrasound Med 1989;8:579.
14. Elseviers MM, De Schepper A, Corthouts R, et al: High diagnostic performance of CT scan for analgesic nephropathy in patients with incipient to severe renal failure. Kidney Int 1995;48:1316.
15. Perazella MA: Crystal-induced acute renal failure. Am J Med 1999;106:459.
16. Kane D, Murphy JM, Keating S, et al: Renal ultrasonic findings in sulphadiazine-induced renal failure. Br J Radiol 1996;69:925.
17. Patriquin HB, O'Regan S: Medullary sponge kidney in childhood. AIR 1985;145:315.
18. Glazer GM, Callen PW, Filly RA: Medullary nephrocalcinosis: Sonographic evaluation. AJR
1982;138:55.
19. Walker JT, Keller MS, Katz SM: Computed tomographic and sonographic findings in acute ethylene glycol poisoning. J Ultrasound Med 1983;2:429.
Infectious Disease
Deborah A. Baumgarten and W. Charles O'Neill
SONOGRAPHY
onography is not indicated in acute urinary tract infections unless urinary obstruction is suspected or renal failure occurs. Although renal parenchymal
abnormalities are frequent in acute pyelonephritis, they do not influence disease management. 1 '2 Imaging should be reserved for pyelonephritis that does not
respond to therapy or for other types of infection; in general, computed tomography (CT) is superior to sonography in this setting.'- 3 However, sonography is
often the first imaging study performed and may reveal unanticipated infectious
lesions.
ACUTE PYELONEPHRITIS
cute pyelonephritis is an infection of the renal parenchyma that may involve all or part of a kidney and is described as diffuse or focal, respectively. Sonographic findings may be completely normal even when
obvious abnormalities are visualized by CT or magnetic resonance imaging
(MRI).4
I nterpretation
The classic findings in diffuse pyelonephritis include renal enlargement,5'6
decreased echogenicity, and effacement of the renal sinus fat (Fig. 9-1). The increase in volume can be as much as 75% and may take 3 or more weeks to re56
solve. 5 '6 Decreased echogenicity is an unreliable finding ' ; occasionally, an
increase in echogenicity is seen.' In many cases, the findings are focal and may appear as an ill-defined mass (Fig. 9-2). These areas are of variable echogenicity and
there may be accompanying loss of the differentiation between the cortex and
medulla. The presence of increased echogenicity has been linked to hemorrhagic
pyelonephritis 8 (Fig. 9-3). In some cases, only focal enlargement with normal
echogenicity is encountered.
66
PWR
56d
GAI
TE
FIGURE 9-1
Acute diffuse pyelonephritis. Longitudinal images of the
( A) right and (B) left kidneys demonstrate decreased
echogenicity of the right kidney with effacement of the
renal sinus fat. The left kidney is normal.
PWR
56d B
CAIN
FIGURE 9-2
Focal pyelonephritis. Longitudinal image of the right
kidney reveals a discrete but not sharply demarcated
hypoechoic lesion (arrows) typical of uncomplicated focal
pyelonephritis.
INFECTIOUS DISEASE
FIGURE 9 3
Focal hemorrhagic pyelonephritis. A. Longitudinal image
of the right kidney (K). B. Transverse scan of the right
kidney from a different patient. There are rounded areas of
increased echogenicity (arrows). (From Rigsby CM,
Rosenfield AT, Glickman MG, et al: Hemorrhagic focal
bacterial nephritis: Findings on gray-scale sonography and
CT. AIR 1986;146:1173, with permission.)
Although the sonographic findings in acute pyelonephritis are not specific, the
clinical picture can help to narrow the differential diagnosis. Glomerulonephritis
(see Figs. 6-1, 6-2) and diffuse lymphoma (see Figs. 20-3A, 20-4A) can have the
same appearance as diffuse pyelonephritis but are bilateral. Acute or chronic renal
vein thrombosis (see Figs. 23-3, 23-4) may mimic diffuse pyelonephritis, presenting
in its acute form with an enlarged hypoechoic kidney and in its chronic form with
increased renal echogenicity. Because both entities produce flank pain, the distinction rests on the finding of thrombus in the renal vein or the presence of bacteriuria and pyuria. The differential diagnosis of focal pyelonephritis includes
other masses. Renal cell carcinomas (see Chapter 17) usually have more sharply demarcated borders and often protrude from the surface of the kidney. Like
pyelonephritis, they can range from hypoechoic to hyperechoic. Angiomyolipomas
(see Chapter 18) are generally very echogenic, especially when small. Neoplastic
masses are relatively stable, whereas focal infection either rapidly resolves or progresses to an abscess or more diffuse involvement. Renal infarction (see Fig. 22-5)
may be indistinguishable from focal pyelonephritis.
67
68
RENAL/PERINEPHRIC ABSCESS
cute pyelonephritis can progress to abscess formation, and abscesses may

also result from hematogenous infection. Sonography may underestimate
the extent of disease; CT is the preferred imaging modality.'
Interpretation
Abscesses appear as cystic masses that are often complex, containing both fluid
and internal debris and exhibiting variable wall thickness (Figs. 9-4, 9-5). Occasionally, there is no cystic component, particularly with fungal infections, and the
lesion appears as a mass (Fig. 9-6). Perinephric extension of the abscess or perinephric fluid can be seen but is often underestimated (Fig. 9-7). Occasionally, an
isolated perinephric abscess occurs without a well-formed renal component.
The distinction between focal pyelonephritis (Fig. 9-2) and frank abscess can be subtle and require CT. A simple renal cyst (see Fig. 10-1) is anechoic and has increased
through transmission and an imperceptible wall. An infected cyst (see Fig. 10-13)
is similar to an abscess but usually has thinner walls. The distinction is not clinically important because the treatment is similar. Benign complex cysts (see Fig.
10-16) and cystic renal cell carcinomas (see Figs. 17-15, 17-18) may be difficult to differentiate from an abscess without the clinical history. Perinephric hematomas (see
Figs. 24-1 through 24-4) or urinomas (see Figs. 24-9, 28-16) may mimic a perinephric abscess.
FIGURE 9 4
Renal abscess. Transverse image of the left kidney reveals
a hypoechoic mass (arrow) with internal debris. (From
Baumgarten DA, Baumgartner BR: Imaging and radiologic
management of upper urinary tract infections. Urol Clin
North Am 1997;24:545, with permission.)
FIGURE 9 - 5
Renal abscess. Longitudinal image of the right kidney
shows a complicated cystic mass with a thick septation
(arrow). (From Baumgarten DA, Baumgartner BR: Imaging
and radiologic management of upper urinary tract
infections. Uro Clin North Am 1997;24:545, with permission.)
INFECTIOUS DISEASE
69
FIGURE 9-6
Renal aspergillomas. Longitudinal image of the right kidney
reveals multiple focal hypoechoic masses (arrows). (From Kay
CJ: Renal diseases in patients with AIDS: Sonographic findings.
AIR 1992;159:551, with permission.)
FIGURE 9-7
Renal abscess with perinephric extension. Transverse image of
the right kidney reveals a hypoechoic mass within the posterior
midkidney (arrows). The hypoechoic area posterior to the kidney
represents perinephric extension of the abscess (arrowheads).
EMPHYSEMATOUS PYELONEPHRITIS
AND PYELITIS
mphysematous pyelonephritis is a severe necrotizing infection associated

with gas in the renal parenchyma that is usually seen in patients with diabetes or in immunocompromised individuals. In emphysematous pyelitis,
the gas is limited to the collecting system.
Interpretation
Sonography reveals hyperechoic foci within the parenchyma (representing pockets of gas) with distal acoustic shadowing. 79 If there is a significant amount of
parenchymal air, part or all of the kidney may be obscured by the shadowing
and not seen (Fig. 9-8). In emphysematous pyelitis, the gas is usually more central within the kidney (Fig. 9-9) and may move with a change in patient position.
As with other infectious processes, sonography can underestimate the extent of
disease.1
70
FIGURE 9-8
Emphysematous pyelonephritis. A. Longitudinal image of the left kidney demonstrates a brightly echogenic rim, owing to
parenchymal gas, that casts a diffuse shadow obscuring the entire kidney. B. A corresponding axial computed-tomography
image reveals extensive parenchymal gas in the left kidney (arrowheads). Gas is also noted within the left renal vein (arrow).
FIGURE 9 - 9
Emphysematous pyelitis. Longitudinal image of the left kidney shows
small echogenic foci (arrows) within the collecting system with posterior
acoustical shadowing.
Stones (see Chapter 15) have a similar appearance to emphysematous pyelitis but
cast shadows that are usually denser and without echoes ("clean" shadows).
Nephrocalcinosis (see Figs. 8-8, 8-9) can mimic emphysematous pyelonephritis because it is parenchymal and may cast incomplete ("dirty") shadows. Bowel gas may
obscure part of the kidney but should become apparent when patient's position or
the scanning plane is changed. Gas may also form in a renal tumor that has been embolized. Noninfectious causes of air in the collecting system include penetrating
trauma, fistulas to the gastrointestinal tract, and instrumentation (see Fig. 15-11).
PYONEPHROSIS
yonephrosis describes a condition in which there is grossly purulent material within the collecting system, usually proximal to an obstruction.
Unlike
11,12
other infections, pyonephrosis is best imaged by sonography.
INFECTIOUS DISEASE
71
Interpretation
The most reliable finding is reproducible, persistent low-level echoes within the
dependent portion of a dilated collecting system (Fig. 9-10), often with well-defined layering of the debris (Fig. 9-11). The echogenic debris should be mobile and
shift to dependent areas when the patient is repositioned. Occasionally, a dilated
collecting system is seen without internal echoes, in which case aspiration is performed to document infection.'
FIGURE 9 1 0
Pyonephrosis. Longitudinal image of the left kidney
(arrowheads) reveals a dilated collecting system with
persistent low-level echoes (arrows). (From Baumgarten DA,
Baumgartner BR: Imaging and radiologic management
of upper urinary tract infections. Uro Clin North Am
FIGURE 9 1 1
Pyonephrosis. A. Transverse and (B) longitudinal images of
the right kidney (cursors) demonstrate well-defined fluiddebris levels (arrows) in the dilated collecting system and
proximal ureter. (From Baumgarten DA, Baumgartner BR:
Imaging and radiologic management of upper urinary tract
infections. Uro Clin North Am 1997;24:545, with permission.)
72
Clotted blood (see Figs. 13-17, 24-5) has the same sonographic appearance as infectious debris. Other pelvocalyceal filling defects are more easily distinguished
from pyonephrosis because they appear as distinct masses (stones [see Chapter
15], sloughed papillae [see Fig. 8-6], fungus balls [Fig. 9-12]) or are immobile (transitional cell carcinoma [see Figs. 18-2, 18-3]). Infectious debris should not be as
echogenic as stones or crystals (see Fig. 8-10) and should not cast an acoustic
shadow. Fungus balls are usually more echogenic as well.
FUNGAL INFECTION
ungal infections may produce parenchymal lesions (Fig. 9-6) but are usually
apparent in the collecting system and proximal ureter, particularly with candidal infections. These infections are primarily nosocomial and often related
to diabetes, immunosuppression, malignancy, and broad-spectrum antibiotic
therapy. They are a common cause of ureteral obstruction in premature infants.13
Interpretation
One or more echogenic masses in the collecting system without posterior shadowing is the usual finding 13,14 (Fig. 9-12). Fungus balls have a propensity to obstruct the proximal ureter (Fig. 9-12B). They may also move when the patient is
repositioned.
FIGURE 9 1 2
Fungus balls. A. Longitudinal view of the left kidney from an adult with diabetes shows multiple hyperechoic foci within
the lower pole collecting system (arrows). B. Longitudinal image of a right neonatal kidney (arrowheads) demonstrates multiple
dilated calyces (C), a dilated renal pelvis (P), and an echogenic mass within the renal pelvis (arrows). (From Stuck KJ, Silver
TM, Jaffe MH, et al: Sonographic demonstration of renal fungus balls. Radiology 1981;142:473, with permission.)
INFECTIOUS DISEASE
Pyonephrosis (Figs. 9-10, 9-11) generally presents with low-level echoes or a fluiddebris level and not an echogenic mass. Blood clots (see Figs. 13-17, 24-5) and
sloughed papillae (see Fig. 8-6) can mimic fungus balls. Transitional cell carcinoma
(see Figs. 18-2, 18-3) should not move when the patient is repositioned.
XANTHOGRANULOMATOUS
PYELONEPHRITIS
anthogranulomatous pyelonephritis (XGP) is a chronic, indolent infection,
usually associated with an obstructing calculus, that is characterized by
parenchymal destruction and replacement with lipid-laden histiocytes
(xanthoma cells). 15 XGP may be focal or diffuse.?,"
Interpretation
Typical findings in diffuse XGP include
renal enlargement with multiple hypo16
echoic or anechoic cystic areas 7 ' representing the collections of xanthoma ells
(Fig. 9-13). A thin rim of cortex may be seen. The obstructing calculus is often visible as a central area of echogenicity with or without distal acoustic shadowing.16
Rarely, the sonographic appearance is atypical and mimics pyonephrosis. 16 In
these cases, there is collecting system dilation with fluid-debris levels and no
staghorn calculus. 15 XGP can be segmental, presenting as a hypoechoic, irregular
mass.
Chronic hydronephrosis (see Figs. 13-10, 13-11) may look similar to diffuse XGP, but
the dilated calyces should be anechoic and interconnected with a branching pattern. Atypical XGP can mimic pyonephrosis (Figs. 9-10, 9-11), and in these cases,
CT correlation is particularly helpful. Autosomal-dominant polycystic kidney disease
(see Chapter 11) is bilateral and the cysts are normally anechoic. Lymphoma (see
Fig. 20-2) can simulate XGP' whensevere but is generally bilateral and associated
with extrarenal disease. Renal cell carcinoma (see Figs. 17-16, 17-17) may mimic focal XGP, so additional imaging or surgery may be necessary to differentiate
the two.
FIGURE 9-1 3
Xanthogranulomatous pyelonephritis. The kidney is
enlarged and contains multiple hypoechoic areas that
resemble cysts. (From Hayes WS, Hartman DS, Sestebenn
IA: Xanthogranulomatous pyelonephritis. Radiographics
73
74
TUBERCULOSIS
enitourinary
involvement accounts for about 20% of extrapulmonary tu12,17,18
berculosis.
As with other infectious processes, ultrasonography is
rarely used for definitive diagnosis and as such, the sonographic manifestations of tuberculosis have not been extensively described.
Interpretation
Findings associated with renal tuberculosis include focal parenchymal masses,
focal calcifications, segmental and diffuse calyceal dilation (presumably from infundibular and renal pelvic stenoses, respectively), and sloughed calyceal
walls. 17' 18 The focal masses have a variable appearance depending on size, with
small lesions (5-15 mm) being uniformly echogenic or hypoechoic with an
echogenic border (Fig. 9-14A) and larger lesions having mixed echogenicity and
poor definition. 18 Sloughed calyceal walls appear as an echogenic flap adjacent to
the calyceal wall (Fig. 9-14B).
FIGURE 9 - 1 4
Renal tuberculosis. A. Longitudinal image of the right kidney
reveals an echogenic tuberculoma (arrow) within the anterior upper
pole. B. Oblique image of the right kidney shows a dilated calyx
containing an echogenic flap (arrow) indicative of sloughing of the
calyceal wall. (From Das KM, Indudhara R, Vaidyanathan S:
Sonographic features of genitourinary tuberculosis. AIR
INFECTIOUS DISEASE
The findings in tuberculosis are not specific, so that clinical correlation and other
diagnostic studies important. A renal abscess (Figs. 9-4, 9-5) may look very similar
to a tuberculoma and aspiration may be necessary for differentiation. Renal cell
carcinoma (see Figs. 17-2A, 17-4) and angiomyolipoma (see Chapter 19) may also
mimic a tuberculoma and CT or MRI may be necessary. Diffuse or focal hydronephrosis from a variety of noninfectious causes can mimic the calyceal abnormalities seen in tuberculosis.
OPPORTUNISTIC INFECTIONS
ycobacterium avium-intercellulare, Pneumocystis carinii, histoplasmosis, and
cytomegalovirus occur primarily in association with acquired immuno-
deficiency syndrome. They rarely produce renal dysfunction and are

M
usually an incidental finding.
Interpretation
Any of these entities can cause small focal hyperechoic areas in the renal cortex or
medulla because of calcification (Fig. 9-15) and cannot be distinguished from one
another by sonography. 19 ' 2 These foci can be diffuse or may be confined to a particular segment.
The differential diagnosis includes other small echogenic foci. Nephrocalcinosis (see
Figs. 8-8 through 8-10) is limited to the renal medulla and is usually more extensive. Papillary necrosis (see Figs. 8-4, 8-5) is also limited to the medulla. Arcuate arteries (see Fig. 2-4) are at the corticomedullary junction and usually not as
echogenic. Very small angiomyolipomas (see Fig. 19-1) can have an identical appearance but are rarely multiple. Stones (see Chapter 15) and vascular calcifications
(see Fig. 22-2) are located in the renal sinus rather than the parenchyma.
FIGURE 9-15
Pneumocystis carinii. Longitudinal image of the left kidney
reveals multiple punctate hyperechoic foci (arrows)
reflecting the presence of parenchymal calcification.
(From Baumgarten DA, Baumgarten BR: Imaging and
radiologic management of upper urinary tract infections.
Uro Clin North Am 1997;24:545, with permission.)
75
76
HYDATID DISEASE
enal involvement is a rare manifestation of echinococcal infection.
R
Interpretation
Generally, a multiloculated cystic structure with curvilinear septations and internal echoes is seen. 21 '22 The septa may represent detached membranes (Fig. 9-16A)
or the walls of daughter cysts (Fig. 9-16B). An early lesion may be unilocular and
anechoic, mimicking a simple cyst. 22 In some cases, the cyst may be completely
filled with material, appearing solid, u,23 with occasional peripheral cysts.
Renal abscesses (Figs. 9-4, 9-5), infected cysts (see Fig. 10-13), and hemorrhagic cysts
(see Fig. 10-11) are generally unilocular. Localized cystic disease and septated cysts
(see Fig. 10-18) usually have thinner walls. A cystic renal cell carcinoma (see Figs.
FIGURE 9 - 1 6
Hydatid disease. A. Transverse image of the lower pole of the left
kidney demonstrates a large hytatid cyst containing detached
membranes (arrows). (From Schoeneich G, Heimbach D, Buszello
H, et al: Isolated echinococcal cyst of the kidney. Scand J Urol
Nephrol 1997;31:95, with permission.) B. Longitudinal image of
the left kidney (K) from a different patient reveals a large hydatid
cyst with multiple daughter cysts. (From Afsar H, Yagci F,
Aybasti N, et al: Hydatid disease of the kidney. Br J Urol 1994;
73:17, with permission.)
INFECTIOUS DISEASE
17-16, 17-18) may have more solid-appearing areas or nodularity of the wall. A
multilocular cystic nephroma (see Fig. 17-14) can have a very similar appearance but
may herniate into the renal collecting system. Additional studies are required to
confidently differentiate hydatid disease from any of these entities.
REFERENCES
1. Soulen MC, Fishman EK, Goldman SM, et al: Bacterial renal infection: Role of CT. Radiology
1989;171:703.
2. Baumgarten DA, Baumgartner BR: Imaging and radiologic management of upper urinary tract infections. Urology Clin North Am 1997;24:545.
3. Lowe LH, Zagoria RJ, Baumgartner BR, et al: Role of imaging and intervention in complex infections of the urinary tract. AIR 1994;163:363.
4. Talner LB, Davidson AJ, Lebowitz RL, et al: Acute pyelonephritis: Can we agree on terminology?
(Review). Radiology 1994;192:297.
5. Dinkel E, Orth S, Dittrich M, et al: Renal sonography in the differentiation of upper from lower urinary tract infection. AIR 1986;146:775.
6. Johansson B, Troell S, Berg U: Renal parenchymal volume during and after acute pyelonephritis
measured by ultrasonography. Arch Dis Child 1988;63:1309.
7. Piccirillo M, Rigsby CM, Rosenfield AT: Sonography of renal inflammatory disease. Urol Radio!
1987;9:66.
8. Rigsby CM, Rosenfield AT, Glickman MG, et al: Hemorrhagic focal bacterial nephritis: Findings on
gray-scale sonography and CT. AIR 1986;146:1173.
9. Allen HA III, Walsh JW, Brewer WH, et al: Sonography of emphysematous pyelonephritis. J Ultrasound Med 1984;3:533.
10. Evanoff GV, Thompson CS, Foley R, et al: Spectrum of gas within the kidney: Emphysematous
pyelonephritis and emphysematous pyelitis. Am J Med 1987;83:149.
11. Jeffrey RB, Liang FC, Wing VW, et al: Sensitivity of sonography in pyonephrosis: A reevaluation.
AJR 1985;144:71.
12. Kenney PJ: Imaging of chronic renal infections. AIR 1990;155:485.
13. Cohen HL, Haller JO, Schechter S, et al: Renal candidiasis of the infant: Ultrasound evaluation.
Urol Radio! 1986;8:17.
14. Stuck KJ, Silver TM, Jaffe MH, et al: Sonographic demonstration of renal fungus balls. Radiology
1981;142:473.
15. Hayes WAS, Hartman DS, Sestebenn IA: Xanthogranulomatous pyelonephritis. Radiographics
1991;11:485.
16. Hartman DS, Davis CJ, Goldman SM, et al: Xanthogranulomatous pyelonephritis: Sonographicpathologic correlation of 16 cases. J Ultrasound Med 1984;3:481.
17. Premkumar A, Lattimer J, Newhouse JH: CT and sonography of advanced urinary tract tuberculosis. AIR 1987;148:65.
18. Das KM, Indudhara R, Vaidyanathan S: Sonographic features of genitourinary tuberculosis. AIR
1992;158:327.
19. Kay CJ: Renal diseases in patients with AIDS: Sonographic findings. AIR 1992;159:551.
20. Miller FH, Parikh S, Gore RM, et al: Renal manifestations of AIDS. Radiographics 1993;13:587.
21. Afsar H, Yagci F, Aybasti N, et al: Hydatid disease of the kidney. Br J Urol 1994;73:17.
22. Migaleddu V, Conti M, Canalis GC, et al: Imaging of renal hydatid cysts. AIR 1997;169:1339.
23. Schoeneich G, Heimbach D, Buszello H, et al: Isolated echinococcal cyst of the kidney. Scand J Urol
Nephrol 1997;31:95.
77
Sporadic Cysts
SONOGRAPHY
ysts are almost always incidental discoveries because they are rarely symptomatic and almost never affect renal function. It is important to obtain the
maximum dimensions of any fluid collection suspected of being a cyst,
thereby ensuring that it is imaged through its center rather than tangentially. Clear
i mages of the distal wall should be obtained to document its enhancement. Fluid
collections should be imaged completely to detect internal echoes, abnormalities
in the wall, or interconnection with other structures. Internal echoes should be
confirmed in another plane to rule out the possibility of reverberation artifact and
to demonstrate layering. Tenderness over a cyst should be noted.
SIMPLE CORTICAL CYSTS
i mple cysts are class I cysts in the Bosniak classification scheme,' and because
they are rarely if ever associated with underlying malignancy, further diagnostic imaging is not indicated. The frequency of cysts increases with age
(Table 10-1) and renal impairment, and cysts are twice as frequent in males as in
females. 2,3 This is important in differentiating isolated cysts from multicystic disorders. In individuals with normal renal function, single cysts are extremely rare
below age 30 years and are very suggestive of a multicystic disorder.
Interpretation
Simple cysts appear as circular or nearly circular anechoic masses within (Fig.
10-1) or protruding from (Fig. 10-2) the renal cortex. The walls should be thin and
smooth, with enhancement of the distal wall (Fig. 10-3). The enhancement often
extends distally, particularly in larger cysts, in a radial orientation (so-called
through-transmission) that is reminiscent of a comet tail (Fig. 10-4). This enhancement results from the lack of sound attenuation by the cyst fluid compared
with adjacent tissues. Simple cysts may exhibit irregular borders and luminal
echogenicity when imaged in a tangential plane (Fig. 10-5) and be misidentified
as complex cysts or masses. Simple cysts are almost always of no clinical significance despite sometimes attaining very large sizes (Fig. 10-5). Rarely, a cyst can
obstruct the renal pelvis (Fig. 10-6).
82
TABLE 10-1
PREVALENCE OF CYSTS IN INDIVIDUALS WITH NORMAL RENAL FUNCTION
Number of Cysts
15-29 y ( %)
30-49 y ( %)
50-69 y ( %)
1
0
1.1
9.7
2 (unilateral)
0
0
0.4
2 (bilateral)
0
0
0.7
3 (unilateral)
0
0
0
3 (bilateral)
0
0.6
0.7
2 in each kidney
0
0
0
70 y (%)
10.4
5.0
2.2
1.3
3.2
1.9
( Adapted from Ravine D, Gibson RN, Donlan J, et al: An ultrasound renal cyst prevalence survey: Specificity data for inherited renal cystic
diseases. Am J Kidney Dis 1993;22:803, with permission.)
FIGURE 1 0 1
Simple cyst. Longitudinal view of right kidney showing a
circular mass (arrow) with a smooth, thin wall and no
internal echoes. There is some enhancement of the sinus fat
distal to the cyst .
FIGURE 10 2
Simple, exophytic cyst. Oblique longitudinal image of right
kidney with an exophytic cyst extending from lower pole
(arrow).
FIGURE 10-3
Distal wall enhancement in a simple cyst. Longitudinal
view of right kidney with a 2.5-cm simple cyst extending
from upper pole (cursors). The distal wall (arrows) is
brightly echogenic because of the overlying fluid. There is
also acoustic enhancement of distal tissue.
SPORADIC CYSTS
83
FIGURE 1 0-4
Distal enhancement by a simple cyst. Longitudinal view of
left kidney (cursors) containing a simple cyst (arrow). There
is distal enhancement (through-transmission) extending
radially from the cyst (arrowheads).
FIGURE 10-6
Cyst obstructing the renal pelvis. Transverse view of left
kidney with a cyst (arrowhead) impinging on the renal
pelvis (arrow), which is slightly dilated.
FIGURE 10-5
Large simple cyst. A. Longitudinal view of left kidney with
an irregular mass in the upper pole (arrowheads) with
internal echoes and a poorly defined wall. B. Repositioning
of the probe reveals that the mass is actually a large simple
cyst. The remainder of the kidney is not visible in this view.
Figure A was produced by scanning the cyst in a tangential
plane.
84
FIGURE 1 0 7
Simple cyst in a hydronephrotic kidney. Transverse view of
left kidney showing a simple cyst (arrowhead) and two
dilated calyces (arrows). Note the thicker, echogenic walls of
the calyces.
Caliectasis can be mistaken for cortical cysts (see Fig. 13-9), but calyces are located
in the renal sinus, have thicker walls, and usually can be seen to connect with
other calyces (Fig. 10-7). Medullary pyramids are not anechoic or round, do not exhibit distal enhancement, and are regurlarly arrayed. Neoplasms can be round and
hypoechoic (see Figs. 17-1,17-2) but are not anechoic and do not exhibit distal enhancement. Cystic or necrotic regions within neoplasms usually appear as complex cysts rather than simple cysts as a result of wall thickening and luminal
irregularities. Arteriovenous fistulas (see Fig. 29-7) can be pulsatile but otherwise
are indistinguishable from cysts by gray-scale imaging.
FIGURE 1 0 8
Parapelvic cyst. A. Longitudinal view of right kidney showing simple cyst (arrow) protruding from the parenchyma into the
sinus. Note the absence of sinus fat between the cyst and the parenchyma. B. Oblique view confirming that the cyst arises
from the parenchyma.
SPORADIC CYSTS
FIGURE 1 0 - 9
Peripelvic cysts. A. Longitudinal and (B) transverse views
of right kidney (arrowheads) showing a large collection of
interconnected cysts in the renal sinus. Note the absence of
any dilation of the minor calyces or proximal ureter.
PERIPELVIC CYSTS
eripelvic cysts originate in the sinus and are actually dilated lymphatic vessels (lymphangiectasia) rather than being of tubular origin." These unusual
cysts should be distinguished from parapelvic cysts, which are parenchymal
cysts that protrude into the sinus (Fig. 10-8). Peripelvic cysts are of no clinical importance other than their propensity to mimic hydronephrosis. In the past,
peripelvic cysts were incorrectly identified as hypoechoic sinus fat, so-called sinus
lipomatosis.7
Interpretation
Peripelvic cysts are located exclusively in the renal sinus and do not extend into
the renal parenchyma. They can appear either as a collection of contiguous cysts"-5
(Fig. 10-9) or as a single cystic mass occupying a portion of the sinus (Fig. 10-10).
85
86
FIGURE 10-10
Peripelvic cyst. A. Longitudinal and (B) transverse views of
left kidney (arrowheads) with a cyst in the renal sinus. The
cyst extends from the hilum and is separated from the
parenchyma by sinus fat. Note the acoustic enhancement
of the distal wall.
Because lymphatics track with the blood vessels, which fan out from the hilum
without branching until they reach the parenchyma, peripelvic cysts are oriented
radially from the hilum without branching. 4 Peripelvic cysts should have thin
walls and no internal echoes.
Hydronephrosis exhibits a branching, calyceal pattern and is usually accompanied
by hydroureter, neither of which occurs with peripelvic cysts. Peripelvic cysts can
coexist with hydronephrosis and accentuate its appearance (see Fig. 13-20). Venous engorgement (see Fig. 23-1) does not appear cystic and the renal vein is dilated. Aneurysms (see Fig. 22-11) and varices (see Fig. 23-7) often extend outside
the renal sinus but can be indistinguishable from peripelvic cysts when limited to
the renal sinus. Differentiation in these cases requires Doppler sonography.
SPORADIC CYSTS
BENIGN COMPLEX CYSTS
omplicated cysts do not meet all the criteria for simple cysts and correspond to class II and class III in the Bosniak classification.' The distinction
between class II (not neoplastic) and class III (possibly neoplastic) is somewhat subjective and usually requires additional imaging. Although complex cysts
have a much higher probability of malignancy than do simple cysts, the vast
majority are benign. Cystic malignant lesions (Bosniak class IV) are discussed in
Chapters 17 and 20.
Interpretation
Sonographic characteristics that render a cyst complex are luminal echogenicity,
thickening or irregularity of the wall, septations, calcification, and a multicystic
appearance. The principal causes of lumen echogenicity are hemorrhage (Figs.
10-11, Fig. 10-12) and infection (Fig. 10-13). Infection and hemorrhage are
FIGURE 1 0 1 1
Hemorrhagic cyst. Longitudinal images of right kidney
from a patient with end-stage renal disease and acute flank
pain. A. The lumen of one cyst (arrowhead) exhibits
homogeneously increased echogenicity (compare to other
simple cyst indicated by the arrow). A computed
tomography scan was consistent with hemorrhage. B. On
repeat study 4 months later, the cyst was anechoic.
87
88
FIGURE 10 1 2
Hemorrhagic cyst. Large cyst that became acutely painful
and tender in a patient with autosomal-dominant
polycystic disease. Highly echogenic material is present
along the distal wall (arrows), representing clotted blood.
There is a homogeneous increase in echogenicity
throughout the remainder of the lumen, indicative of
partially clotted blood.
FIGURE 10-13
Infected cyst. This polycystic kidney had a large cyst with a
heterogeneously echogenic lumen (arrow). The patient had
fever and tenderness over this cyst that were refractory to
antibiotics but that promptly resolved after percutaneous
drainage.
FIGURE 1 0 1 4
Chronic hemorrhagic a cyst. Longitudinal image of right
kidney in a patient with end-stage renal disease
undergoing hemodialysis. There is a heterogeneously
echogenic mass (arrows) in the upper pole that was
avascular on computed tomography scan. Note the thin
hypoechoic rim around the mass. Subsequent studies
showed a gradual decrease in cyst size over several years.
SPORADIC CYSTS
indistinguishable by sonography and present as a homogeneous or heterogeneous

increase in echogenicity, 8 sometimes with wall thickening in the case of infection.8
Hemorrhage may resolve (Fig. 10-11B) or become chronically organized (Fig.
10-14). In the absence of suggestive clinical features, sonography cannot distinguish hemorrhagic or infected cysts from neoplasms, and additional imaging is
required. A rare cause of luminal echogenicity is milk of calcium, a suspension of
microcrystalline calcium 9 that presents as highly echogenic material layering dependently in the lumen (Fig. 10-15). The cysts in this case may be calyceal in origin. Focal irregularity (Fig. 10-16) or thickening (Fig. 10-17) of a cyst wall are
FIGURE 1 0 1 5
Milk of calcium in a cyst. A small cyst (white arrowhead) is
present that contains highly echogenic material layering
out in a dependent fashion (black arrow). (From Yeh H-C,
Mitty HA, Halton K, et al: Milk of calcium in renal cysts:
New sonographic features. J Ultrasound Med 1992;11:195,
with permission.)
FIGURE 1 0 1 6
Complex cyst. Transverse view of right kidney containing
a cyst with an irregular wall and focal areas of thickening
(arrows). This was a benign cyst in a patient with early
polycystic kidney disease.
FIGURE 1 0 1 7
Complex cyst. Longitudinal view of left kidney through the
pelvis. There is an exophytic cyst adjacent to the renal
pelvis with focal thickening of the distal wall (arrows). This
is the same kidney shown in Figure 10-6, with mild hydronephrosis due to partial obstruction of the pelvis by the
cyst. The appearance of this cyst on sonography and
computed tomography has been stable for several years.
89
90
important criteria that warant further imaging studies. Septations are occasionally
encountered (Fig. 10-18) and are very unlikely to indicate malignancy, provided
they are thin, extend completely across the cyst, are not numerous, and lack focal
thickening, either in the septum or at the sites of attachment to the cyst wall.'"
Calcification can occur in otherwise simple cysts (Fig. 10-19) but still warrants a
CT scan.' It is often present in small amounts not detectable by sonography.
Reverberation of sound between the proximal cyst wall and the probe can place
echoes within the fluid. This reverberation artifact is commonly seen in large cysts
close to the skin (Fig. 10-20). Besides infection of preexisting cysts, other infectious
causes of complex cysts include abscesses (see Figs. 9-4, 9-5) and hydatid cysts (see
Fig. 9-16). These diagnoses should be considered in the appropriate clinical setting, particularly when multiple lesions are present. Arteriovenous malformations or
aneurysms with thrombus (see Figs. 22-9B, 22-12) can mimic complex cysts, but the
distinction can be made by Doppler sonography.
FIGURE 10-18
A
Septated cysts. A. Cyst in a polycystic kidney containing a

thin, linear septation (arrow). Because the septum is thin
without focal thickening and the cyst otherwise appears
simple, no further imaging is required. B. Cyst with two
septa (arrows). There is irregular thickening of the septa,
particularly along the wall of the cyst, that warrants further
imaging.
SPORADIC CYSTS
FIGURE 10-1 9
Calcification in cyst wall. Longitudinal image of left kidney
with upper pole cyst exhibiting focal thickening and
increased echogenicity (arrow) with shadowing (arrowheads)
indicating calcification. The kidney is small, echogenic, and
lobulated, indicative of chronic renal failure.
FIGURE 10-20
Reverberation artifact within a cyst. Transverse view of a
polycystic kidney (white outline) with an anterior cyst that
contains multiple echogenic lines (arrows).
REFERENCES
1. Bosniak MA: The current radiological approach to renal cysts. Radiology 1986;158:1.
2. Ravine D, Gibson RN, Donlan J, et al: An ultrasound renal cyst prevalence survey: Specificity data
for inherited renal cystic diseases. Am J Kidney Dis 1993;22:803.
3. Yamagishi F, Kitahara N, Mogi W, et al: Age-related occurrence of simple renal cysts studied by ultrasonography. Klin Wochenschr 1988;66:385.
4. Patel U, Huntley L, Kellett MI: Sonographic features of renal obstruction mimicked by peripelvic
cysts. Clin Radiol 1994;49:481.
5. Amis ES, Cronan JJ: The renal sinus: An imaging review and proposed nomenclature for sinus
cysts. J Urol 1988;139:1151.
6. Baltarowich OH, Kurtz AB: Sonographic evaluation of renal masses. Urol Radiol 1987;9:79.
7. Cronan JJ, Yoder IC, Amis Jr. ES, et al: The myth of anechoic renal sinus fat. Radiology 1982;144:149.
8. Frishman E, Orron DE, Heiman Z, et al: Infected renal cysts: Sonographic diagnosis and management. J Ultrasound Med 1994;13:7.
9. Yeh H-C, Mitty HA, Halton K, et al: Milk of calcium in renal cysts: New sonographic features. J Ultrasound Med 1992;11:195.
10. Rosenberg ER, Korobkin M, Foster W, et al: The significance of septations in a renal cyst. AIR
1985;144:593.
91
CHAPTER
AutosomalDominant Polycystic
Kidney Disease
SONOGRAPHY
utosomal-dominant polycystic kidney disease (ADPKD) is the most common genetic cystic disorder of the kidney and is an important cause of endstage renal disease. Although the disease often begins in childhood, the
clinical manifestations rarely begin before adulthood, except for a rare infantile
form of the disease that presents in neonates.' Sonography is the test of choice in
this disorder and is sufficient for the diagnosis. 2 The principal indications for initial sonography are genetic risk, renal failure, pain, or urinary tract infection. Recurrent complications such as pain, infection, hematuria, and stones are common
indications for subsequent studies. Examination for these complications is difficult because the kidney usually extends beyond the range of the probe, has obliterated architecture, and can be tender. All portions of the kidney must be
examined for stones and for echogenic material within cysts, and areas of tenderness should be noted and correlated with the appearance of the underlying cyst.
Artifacts from reverberation and acoustic enhancement are common causes of luminal echoes. Because urinary obstruction is difficult to recognize, careful examination of the renal pelvis is mandatory. Length is difficult to determine in large
kidneys and is not clinically important. Hepatic cysts are common and should be
noted. Lastly, when sonography is used to screen family members of a patient
known to have ADPKD, it is important to scan the entire kidney for cysts because
the presence of only a single small cyst in a young individual at risk is sufficient
for the diagnosis.
INTERPRETATION
he appearance of the kidneys varies with the stage of the disease and the absence of cysts does not rule out the diagnosis in young subjects. In early disease, only a few cysts may be visible and they may be quite small, and other
subtle findings are frequently presentspecifically, cortical enlargement and poor
delineation of the corticomedullary junction 3 (Fig. 11-1). The cortical enlargement is
not necessarily due to cysts and initially may be manifested only as expansion into
the sinus fat with little increase in length. As the disease progresses, the cysts become more numerous and larger, and the noncystic cortex becomes echogenic (Fig.
11-2). The cause of the increased echogenicity is unknown but could be the result of
microscopic cysts. Both kidneys are involved although there may be significant
94
FIGURE 1 1 - 2
Autosomal-dominant polycystic disease. Longitudinal view
of right kidney showing multiple cysts. The echogenicity of
the noncystic cortex is increased compared to that of the
liver (L).
FIGURE
11-1
Early changes in autosomal-dominant polycystic kidney
disease (ADPKD). Longitudinal images of right kidney
of (A) a child with ADPKD and (B) an unaffected sibling.
Several small cysts are present (arrows) and there is a
reduction in sinus fat due to expansion of the cortex.
AUTOSOMAL-DOMINANT POLYCYSTIC KIDNEY DISEASE
95
FIGURE 1 I -3
Advanced autosomal-dominant polycystic kidney disease.
Longitudinal view of right midkidney, with the poles
extending well beyond the image. Innumerable cysts of
varying size and shape are present with very little
intervening parenchyma.
FIGURE 1 1 - 4
Autosomal-dominant polycystic kidney disease with
hepatic cysts. Longitudinal view of the lower pole of the
right kidney showing numerous renal cysts and two cysts
in the liver (arrows). The border between the liver and
kidney is indicated by the arrowheads. Note the increased
echogenicity of the noncystic renal cortex.
FIGURE
1 1 -5
Nephrolithiasis in autosomal-dominant polycystic kidney
disease. Longitudinal image of right kidney showing
multiple cysts and a stone (arrow) with an acoustical
shadow (arrowheads).
asymmetry in the early stage. When the disease is advanced, the kidneys are essentially huge collections of cysts with little intervening cortex (Fig. 11-3). Hepatic
cysts (Fig. 11-4) are not uncommon and are diagnostic of ADPKD. 4 It is not uncommon for cysts to contain echogenic material, the result of either hemorrhage (see Fig.
10-12) or infection (see Fig. 10-13). There is an increased incidence of nephrolithiasis 4 (Fig. 11-5), a condition that may be difficult to detect because of the echogenic
96
FIGURE 1 1 6
Hydronephrosis in autosomal-dominant polycystic kidney disease. A. Longitudinal view of right kidney ( arrowheads)
showing multiple cysts. The dilated collecting system (arrows) is easily mistaken for cysts. B. In another longitudinal plane,
the calyceal branching (arrows) and dilated pelvis (arrowhead) are more apparent.
cortex and the accoustic enhancement from the multitude of cysts. Stones can lead
to urinary obstruction, recognition of which requires careful scanning to distinguish dilated calyces from cysts (Fig. 11-6).
Diagnosis in individuals at risk is based on detection of cysts, with the
criteria depending on age. 5 In young members of families with ADPKD, identification of only a single cyst is highly suggestive of the disease, and the diagnosis
can be made with certainty when two or more cysts are present. The number of
cysts required for diagnosis increases with age (Table 11-1). Although most affected individuals will manifest cysts by age 20 years, the absence of cysts does
not exclude the diagnosis until after age 30.
TABLE 11-1
Criteria
No. of Cysts,
Kidney
?1
2, L or R
1, L; 1, R
2, L; 2, R
4, L; 4, R
Cut-off for:
Diagnosis
Exclusion
POSITIVE PREDICTIVE VALUES (LEFT COLUMN) AND NEGATIVE PREDICTIVE VALUES (RIGHT COLUMN) IN
PERCENTAGES FOR THE DIAGNOSIS OR EXCLUSION OF AUTOSOMAL-DOMINANT POLYCYSTIC
KIDNEY DISEASE TYPE 1 BY SONOGRAPHY IN INDIVIDUALS AT RISK
Age (y)
20
+
100
97
100
100
100
100
1, L or R
30
+
98 100
99
99
100
100
40
+
97 100
99
99
100
100
50
+
77 100
96
98
100
100
2, L or R
<1
2, L; 2, R
<1
2, L; 2, R
<1
60
+
74 100
95
98
100
100
70
+
46 100
61
85
91
97
2, L; 2, R . 4, L; 4, R
<1
<1
L, Left; R, right. (Adapted from Ravine D, Gibson RN, Walker RG, et al: Evaluation of ultrasonographic diagnostic criteria for autosomal
dominant polycystic kidney disease 1. Lancet 1994;343:824, with permission.)
AUTOSOMAL-DOMINANT POLYCYSTIC KIDNEY DISEASE
ultiple, bilateral simple cysts are not infrequent in chronic renal failure, but
renal size is reduced. Furthermore, when renal failure develops in
ADPKD, the cystic disease is advanced. Localized cystic disease is a nongenetic, nonprogressive disorder that presents with multiple cysts localized to one
segment of an otherwise normal kidney. 6 Acquired cystic disease (see Figs. 12-1,
12-2) occurs in end-stage disease and the cysts are usually smaller. There is a significant amount of intervening parenchyma and rarely is there gross enlargement
and distortion of the kidney. Cystic involvement in von HippelLindau disease (see
Fig. 12-9) can occasionally be extensive and mimic ADPKD. 4 Renal cysts can also
occur in tuberous sclerosis (see Fig. 12-5) but are usually less numerous and smaller
than in ADPKD. 4 ' 7 Most patients with tuberous sclerosis and cysts have renal angiomyolipomas as well. In medullary cystic disease (see Fig. 12-8), the cysts are
small and located in the medulla or at the corticomedullary junction and renal size
is reduced. In autosomal-recessive polycystic disease (see Figs. 12-6, 12-7), the cysts
are very small and often not visible. Multicystic dysplastic kidney (see Fig. 12-11) is
congenital and unilateral. Xanthogranulomatous pyelonephritis (see Fig. 9-13) can
also mimic a multicystic kidney but only one kidney is involved.
REFERENCES
1. Hayden CK, Swischuk LE: Renal cystic disease. Semin Ultrasound CT MR 1991;12:361.
2. Rosenfield AT, Lipson MH, Wolf B, et al: Ultrasonography and nephrotomography in the presymptomatic diagnosis of dominantly inherited (adult-onset) polycystic kidney disease. Radiology
1980;135:423.
3. Fick GM, Johnson AM, Strain JD, et al: Characteristics of very early onset autosomal dominant
polycystic kidney disease. J Am Soc Nephrol 1993;3:1863.
4. Levine E, Hartman DS, Meilstrup JW, et al: Current concepts and controversies in imaging of renal
cystic diseases. Urol Clin North Am 1997;24:523.
5. Ravine D, Gibson RN, Walker RG, et al: Evaluation of ultrasonographic diagnostic criteria for
autosomal dominant polycystic kidney disease 1. Lancet 1994;343:824.
6. Hartman DS, Davis CJ, Sanders RC, et al: The multiloculated renal mass: Considerations and special features. Radiographics 1987;7:29.
7. Mitnick JS, Bosniak MA, Hilton S, et al: Cystic renal disease in tuberous sclerosis. Radiology
1983;147:85.
97
Other Multicystic
Disorders
SONOGRAPHY
lthough it may provide the initial diagnostic clue, sonography is most often employed as a screening or confirmatory test. Unlike in autosomaldominant polycystic kidney disease (ADPKD), the potential for malignant
transformation exists in other multicystic disordersspecifically, acquired cystic
disease and von Hippel-Lindau disease. Although sonography may not be the
best modality for screening these patients for neoplasms, the index of suspicion
for neoplasm should be high whenever these patients are examined and any questionable findings should be investigated by other imaging modalities.
I NTERPRETATION
Acquired Cystic Kidney Disease
Acquired cystic kidney disease (ACKD) is a frequent finding in patients with
end-stage renal disease, and can be seen prior to initiation of renal replacement
therapy. The clinical significance of this disorder is uncertain except that it is associated with a higher risk of renal carcinoma. Despite this increased incidence of
renal cell carcinoma, the benefit of screening for carcinoma is unclear because of
the reduced life expectancy in end-stage disease, the tendency of the tumors not
to be aggressive or metastatic, and the morbidity of nephrectomy. 1 Because of the
greater cost of other imaging modalities and natural history of these carcinomas,
it may be reasonable to follow many complex cysts in ACKD by sonography
rather than refer all patients with them for additional imaging. The typical appearance of ACKD is multiple, small (often tiny), simple cysts without renal enlargement or distortion, an appearance reminiscent of Swiss cheese (Fig. 12-1).
The kidneys are usually not enlarged because the disorder arises in kidneys with
end-stage disease. However, large cysts can occur and occasionally the kidney is
enlarged (Fig. 12-2). There are no firm diagnostic criteria in terms of the quantity
of cysts, although a range of three to five in each kidney is frequently used.1'2
Rarely ACKD appears to be unilateral, but close examination will usually reveal
small cysts in the "uninvolved" kidney. All the cysts should meet the criteria for
simple cysts, but irregular shapes, wall thickening, and cyst clustering are not uncommon (Fig. 12-3) and hemorrhage is frequent (see Fig. 10-11). This, coupled
with the difficulty of imaging kidneys in end-stage disease by sonography, leads
to a high rate of suspicious cysts. Hydronephrosis can occur in end-stage disease
and mimic ACKD (Fig. 12-4) because the thin cortex can cause calyces to appear
as cortical cysts.
100
FIGURE 1 2 1
Acquired cystic kidney disease. Longitudinal view of right
kidney (arrowheads) of a patient with end-stage renal disease
treated with hemodialysis. There are multiple small cysts
with intervening echogenic cortex. The kidney is small with
minimal distortion.
FIGURE 1 2 2
Acquired cystic kidney disease. Longitudinal view of right
kidney (arrowheads) showing enlargement with numerous
cysts distorting the contour of the kidney. Kidney length is
12.3 cm..
FIGURE 1 2 3
Acquired cystic kidney disease. Longitudinal view of left
kidney (arrowheads) showing a large clustering of irregular
cysts in the upper pole. Tiny cysts are present in the
remainder of the kidney. No evidence for a neoplasm was
found on computed tomography scan. S, spleen.
OTHER MULTICYSTIC DISORDERS
101
FIGURE 1 2 -4
Hydronephrosis in a kidney with end-stage disease
simulating acquired cystic kidney disease. Longitudinal
image of left kidney (arrowheads) filled with multiple fluidfilled regions. Close inspection reveals that these are
interconnected and converge on a dilated renal pelvis (P).
Kidney length is 10.6 cm. The right kidney was 7.4 cm and
contained a single 0.5-cm cyst.
Tuberous Sclerosis
Tuberous sclerosis is an autosomal-dominant disorder with varied manifestations,
including neurologic, cutaneous, and renal lesions. The presence of cysts or angiomyolipomas in the kidneys can be very helpful in the diagnosis. Cysts are present in up to 50% of patients and the combination of cysts and angiomyolipomas
35
34
(Fig. 12-5), which is seen in as many as 30%, is diagnostic. Rarely do the cysts
attain the size and number seen in advanced ADPKD.5
FIGURE 1 2 - 5
Tuberous sclerosis. Longitudinal image of right upper pole demonstrating cysts
(C) and two angiomyolipomas (arrows). (From Narla LD, Slovis TL, Watts FB, et
al: The renal lesions of tuberosclerosis (cysts and angiomyolipoma)screening
with sonography and computerized tomography. Pediatr Radiol 1988; 18:205, with
permission.)
102
Autosomal-Recessive Polycystic
Kidney Disease
Autosomal-recessive polycystic kidney disease is rarer than the autosomal-dominant disease, and despite the similarity in names, these disorders have little in
FIGURE 12-6
Autosomal-recessive polycystic kidney disease.
Longitudinal scan of a 5-year-old showing an enlarged
kidney (arrowheads) with poor corticomedullary
differentiation and minimal sinus fat.
12-7
FIGURE
High-resolution sonography in autosomal-recessive polycystic kidney disease. A. Multiple ectatic tubules are present in the
medulla but the cortex (arrows) is normal. B. Transverse scan of left kidney (arrowheads) demonstrating ectatic collecting
ducts arrayed radially. (From Jain M, LeQuesne GW, Bourne AJ, et al: High-resolution ultrasonography in the differential
diagnosis of cystic diseases of the kidney in infancy and childhood: Preliminary experience. J Ultrasound Med 1997;16:235,
with permission.)
common. The recessive disease has its clinical presentation in early childhood
with manifestations of renal failure and hepatic and pulmonary abnormalities)
The kidneys are diffusely enlarged but much smaller than in autosomal dominant
disease. There is increased echogenicity with poor corticomedullary differentiation (Fig. 12-6), an appearance due to the presence of multiple ectatic collecting
ducts in the medulla' that can be seen with high-resolution sonography (Fig.
12-7). Occasionally, enough dilation occurs to produce scattered medullary cysts
visible by standard sonography.
Medullary Cystic Disease

Medullary cystic disease and the closely related disorder, familial juvenile
nephronophthisis, are autosomal-dominant diseases that occur in childhood and
usually present clinically in teenagers and young adults. In its full form, the disease presents as small echogenic kidneys with poor corticomedullary differentiation and medullary cysts 16 ' 7 (Fig. 12-8). The earliest finding is normal-sized
kidneys with increased echogenicity and poor corticomedullary differentiation.
As the disease progresses, renal size decreases and the cysts may enlarge and become visible, though many cases lack cysts.'''
FIGURE 1 2 - 8
Medullary cystic disease. A. Longitudinal view of right
kidney (arrowheads) of a 2-year-old. The echogencity of
the cortex is increased compared to the liver (L) and there
are several small cysts at the corticomedullary junction.
B. Longitudinal view of right kidney (arrowheads) of a
25-year-old showing diffusely increased echogenicity
compared with liver (L) and absence of corticomedullary
differentiation. No cysts are present.
103
104
EMORY UNIVER
LONG LIVER 'R
FIGURE 1 2 -9
Von Hippel-Lindau disease with multicystic kidneys.
Longitudinal image of right kidney (arrowheads) showing
multiple cortical cysts. Unlike autosomal-dominant polycystic
kidney disease, the renal sinus appears normal, indicating the
lack of cortical expansion. This patient eventually developed
end-stage renal disease.
FIGURE 1 2 - 1 0
Renal cell carcinoma in von Hippel-Lindau disease. Oblique transverse
image of left kidney demonstrates a small echogenic renal cell carcinoma (M)
and two cysts (C). (From Forman HP, Middleton WD, Melson GL, et al:
Hyperechoic renal cell carcinomas: Increase in detection at US. Radiology
Von Hippel-Lindau Disease

This is a rare, autosomal dominant, multiorgan disease that in the kidney manifests as cysts in almost two thirds of patients and carcinomas in almost half (8).
Although sonography is useful in documenting cysts, it is not sensitive for identifying small carcinomas. Its role in the latter is to compliment CT scanning in distinguishing solid masses from cysts. The kidneys exhibit scattered bilateral cysts
(Fig. 12-9) that enlarge over time but also involute, so that in most patients the
cysts are small and disease remains relatively stable. 8 Occasionally, the cystic involvement in von Hippel-Lindau disease can advance to a stage indistinguishable
from ADPKD. Sonographic findings are otherwise normal except for the high incidence of renal carcinoma, and the combination of renal cysts and carcinoma (Fig.
12-10) is very suggestive of von Hippel-Lindau disease.
Multicystic Dysplastic Kidney

Multicystic dysplastic kidney, a nonhereditary disorder, is the most common cystic
disease in childhood and is a common cause of abdominal masses in neonates.1
It represents a maldevelopment of the kidney possibly related to early obstruction
in utero. The sonographic appearance is that of a large multicystic mass that bears
no resemblance to a kidney" (Fig. 12-11). A rare segmental form of multicystic
dysplastic kidney can occur when there is duplication of the ureter.' There is no
communication between the cysts and the renal pelvis and ureters are not visible.
However, an incomplete form of multicystic dysplastic kidney (so-called hydronephrotic form) will exhibit some pelvocalyceal dilation. 9 The disorder is usually
unilateral, although contralateral ureteral abnormalities are not uncommon.' The
cysts resolve over time, leaving a small, echogenic atrophic kidney.1
FIGURE 1 2-11
Multicystic dysplastic kidney. Longitudinal scan of right neonatal kidney
(arrowheads) that is enlarged and contains multiple cysts. The left kidney was
normal. (Photo courtesy of Dr. B. Gay.)
ydronephrosis should not be confused with multicystic kidneys. The dilated
calyces interconnect and drain into a dilated pelvis and ureter and are not
located in the parenchyma. The different multicystic disorders are readily
distinguished by sonography and patient characteristics. Only multicystic dysplastic kidney is unilateral. Xanthogranulomatous pyelonephritis (see Fig. 9-13)
could be confused with multicystic dysplastic kidney but the apparent cysts in the
former are not anechoic and this is a chronic, acquired disorder that would not occur in the neonatal period. Cystic neoplasms (see Figs. 17-14, 17-16) are localized to
a portion of the kidney but could mimic a segmental multicystic dysplastic kidney. Of the multicystic disorders, ADPKD produces the greatest cyst burden and
renal enlargement. The early stage may be indistinguishable from tuberous sclerosis or von HippelLindau disease, but these latter disorders rarely develop the
severe degree of cystic involvement seen in advanced ADPKD. ACKD develops in
severe chronic renal failure, and the cystic involvement is much less than in
ADPKD with renal failure. Autosomal-recessive polycystic kidney disease and
medullary cystic disease present in childhood but cysts are rarely numerous or
large and often not visible. Renal size is increased in the former and decreased in
the latter. In the rare childhood presentation of ADPKD," the kidneys are much
larger and contain numerous macroscopic cysts. Angiomyolipomas are only seen
in tuberous sclerosis and only von HippleLindau disease and ACKD have a significant association with renal cell carcinoma.
REFERENCES
2. Gulanikar AC, Daily PP, Kilambi NK, et al: Prospective pretransplant ultrasound screening in 206
patients for acquired renal cysts and renal cell carcinoma. Transplantation 1998;66:1669.
3. Bernstein J: Renal cystic disease in the tuberous sclerosis complex. Pediatr Nephrol 1993;7:490.
4. Narla LD, Slovis TL, Watts FB, et al: The renal lesions of tuberosclerosis (cysts and angiomyolipoma)screening with sonography and computerized tomography. Pediatr Radio! 1988;18:205.
5. Mitnick JS, Bosniak MA, Hilton S, et al: Cystic renal disease in tuberous sclerosis. Radiology
1983;147:85.
6. Grossman H, Rosenberg ER, Bowie JD, et al: Sonographic diagnosis of renal cystic diseases. AIR
1983;140:81.
7. Chuang Y-F, Tsai T-C: Sonographic findings in familial juvenile nephronophthisismedullary cystic disease complex. J Clin Ultrasound 1998;26:203.
8. Choyke PL, Glenn GM, Walther MM, et al: Von Hippel-Lindau disease: Genetic, clinical, and imaging features. Radiology 1995;194:629.
9. Hayden CK, Swischuk LE: Renal cystic disease. Semin Ultrasound CT MR 1991;12:361.
10. Pedicelli G, Jequier S, Bowen A, et al: Multicystic dysplastic kidneys: Spontaneous regression
demonstrated with US. Radiology 1986;160:23.
11. Jain M, LeQuesne GW, Bourne AJ, et al: High-resolution ultrasonography in the differential diagnosis of cystic diseases of the kidney in infancy and childhood: Preliminary experience. J Ultrasound Med 1997;16:235.
105
THE
COLLECTING
SYSTEM
AND
DISTAL
URINARY
TRACT
Hydronephrosis
SONOGRAPHY
onography is frequently performed to rule out urinary obstruction as a cause

of acute renal failure, particularly in the setting of oliguria. Urinary obstruction can also cause chronic renal failure and is an important cause of renal allograft failure. Sonography is also very useful in documenting the resolution of
hydronephrosis. Any fluid-filled areas in the renal sinus should be examined carefully to determine interconnection and continuity with the pelvis and ureter. The
pelvis and ureter should be well visualized, which is best accomplished in the
transverse plane. The dilated collecting system must be examined carefully for luminal echogenicities such as stones, thrombi, fungus balls, or sloughed papillae,
and the location of stents or catheters should be confirmed. An attempt should be
made to follow a dilated ureter distally to the site of obstruction. Hydronephrosis
always warrants an examination of the bladder, both before and after voiding.
INTERPRETATION
ecause the calyces are normally obscured by sinus fat, visualization indicates
dilation, which can either be focal or diffuse. Focal caliectasis is usually the
result of local injury such as reflux nephropathy and chronic infection (Fig.
13-1), nephrolithiasis, lithotripsy,' or papillary necrosis (see Fig. 8-3B) but can be
the result of focal obstruction (see Fig. 15-8) and is apparent as one or more fluidfilled areas that have a calyceal shape (Fig. 13-2). This may be localized to one minor calyx but can also be segmental, involving a major calyx and its minor calyces
(Fig. 13-3). The term hydronephrosis describes diffuse caliectasis, which appears as
interconnected fluid-filled areas in the renal sinus that often, but not always, have
an identifiable branching, calyceal pattern (Figs. 13-4, 13-5). It is important to recognize that hydronephrosis can occur in the absence of urinary obstruction. Vigorous diuresis in normal individuals can produce mild to moderate calyceal
dilation. 2,3 In diabetes insipidus, particularly the congenital nephrogenic form, severe distension of the calyces and ureters can occur (Fig. 13-6). Enlargement of the
calyces and ureter is a normal event in pregnancy (Fig. 13-7) and resolves several
weeks postpartum. 4' 5 The dilation is usually greater on the right than left. Although ureteral dilation is seen only superior to the pelvic brim, it cannot be explained solely by obstruction because the caliectasis begins early in pregnancy4'5
and also occurs in renal allografts (see Fig. 27-3). Dilation of the collecting system
is also observed with urinary reflux, but the sensitivity and specificity of this finding are too low for it to be useful as a screening test. 6 7 However, changes in the
caliber of the collecting system during scanning may be more predictive.'
110
FIGURE 1 3 - 1
Chronic pyelonephritis. Longitudinal scan of right kidney
(arrowheads) shows caliectasis of the lower pole and loss
of parenchyma with scarring (arrows) of the upper pole.
L, liver. (From O'Neill WC: Sonographic evaluation of renal
failure. AM I Kidney Dis 2000;35:1021, with permission.)
FIGURE 1 3 - 2
Dilated minor calyx in a renal allograft after lithotripsy.
Longitudinal image of allograft shows a dilated minor
calyx (arrowhead) and its infundibulum (arrow) draining into
a slightly dilated major calyx. There is no dilation of other
calyces.
FIGURE 1 3 - 3
Segmental caliectasis. A. Longitudinal and (B) transverse images of a renal allograft with dilation of a major calyx and
several minor calyces in the upper pole (arrows).
HYDRONEPHROSIS
111
FIGURE 1 3 -4
Moderate bilateral hydronephrosis. A. Longitudinal view of left kidney (cursors) showing dilation primarily of the major
calyces with some enlargement of the minor calyces. B. Transverse view through pelvis of right kidney (arrowheads) showing
dilation of the pelvis and proximal ureter (arrow).
FIGURE 1 3 -5
Severe, Acute hydronephrosis. Longitudinal view of left
kidney showing dilation of minor calyces (C), major
calyces (arrows), and the pelvis (arrowhead). The minor
calyces extend to the base of the medullary pyramids, and
the cortical thickness is normal. (From O'Neill WC:
Sonographic evaluation of renal failure. AM J Kidney Dis
FIGURE 1 3-6
Nephrogenic diabetes insipidus. Longitudinal view of right
kidney showing severe dilation of the major and minor calyces
with a thin rim of cortex (arrows). L, liver. (From Stevens S, Brown
BD, McGahan JP: Nephrogenic diabetes insipidus: A cause of
severe nonobstructive urinary tract dilatation. I Ultrasound Med
112
FIGURE 13-7
Pregnancy-induced caliectasis. Longitudinal scan of right
kidney (arrowheads) during second trimester showing a
moderate degree of caliectasis as well as some dilation of
the ureter (arrows). The lower pole of the kidney is
obscured by overlying bowel gas .
FIGURE 13-8
Urinary obstruction with minimal hydronephrosis.
Longitudinal view of left kidney (arrowheads) in a patient
with a 3-day history of left flank pain. Only minimal
dilation of the collecting system is seen, but the proximal
ureter is dilated (arrows) and retrograde pyelography
revealed complete ostruction of the ureter by a uric
acid stone.
Although a system for grading hydronephrosis has been developed, it is often not clinically useful because of the variable appearance of urinary obstruction.
In acute obstruction or in oliguric patients, calyceal dilation may be minimaP (Fig.
13-8). Occasionally, the minor calyces are more dilated than the major calyces,
yielding a cystic appearance (Fig. 13-9). The cortex should be normal in acute obstruction (Fig. 13-5), but chronic obstruction eventually leads to thinning (Fig.
13-10), with the calyces sometimes extending to the renal capsule (Fig. 13-11).
Even in kidneys with end-stage disease that produce very little urine, complete
ureteral obstruction can still produce impressive hydronephrosis (Fig. 13-12). The
proximal ureter is usually dilated in obstructive uropathy (Fig. 13-13) and can occasionally be followed to the site of obstruction, even to the bladder. Marked calyceal dilation without ureteral dilation usually indicates obstruction at the
ureteropelvic junction (see Fig. 13-10). The walls of the collecting system and
ureter should be smooth and thin, although they are generally thicker than cyst
walls. Marked thickening is a nonspecific finding seen in chronic obstruction, reflux, and pyelonephritis (Fig. 13-14) as a result of edema or muscular hypertrophy. 9,1 Sonography may provide clues to the underlying cause of hydronephrosis,
such as the presence of stones (Figs. 13-15, 13-16), blood clot (Fig. 13-17), fungus
HYDRONEPHROSIS
FIGURE 1 3 9
Cystic dilation of minor calyces. A. Transverse view of right
kidney showing dilated minor calyces (C) that appear as
cysts. Two of the calyces can be seen to connect (arrow).
Note the preservation of the cortex. B. Longitudinal view of
right kidney from a different patient showing the minor
calyces (C) draining into the pelvis (P) via the major
calyces. Note that the cortex is thin and echogenic,
indicating chronic obstruction. U, ureter.
113
FIGURE 1 3 1 0
Obstruction at the ureteropelvic junction. Longitudinal
view of right kidney showing dilated calyces (C) and pelvis
(P) without dilation of the proximal ureter. The cortex is
reduced in thickness (arrows). (From O'Neill WC:
Sonographic evaluation of renal failure. AM J Kidney Dis
114
FIGURE
13-11
Chronic hydronephrosis. Longitudinal view of right kidney
(cursors) showing dilated minor calyces that extend to the
renal capsule, indicative of an extremely thin cortex. L,
liver. (From O'Neill WC: Sonographic evaluation of renal
failure. AM I Kidney Dis 2000;35:1021, with permission.)
FIGURE 1 3 - 1 2
Severe hydronephrosis in kidney with end-stage disease.
Longitudinal image of right kidney in a patient who
underwent renal transplantation in which the native ureter
was tied and the distal portion used to connect the allograft
to the bladder. The native kidney appears as a large fluid
collection with no visible parenchyma.
FIGURE 1 3 - 1 3
Dilated proximal ureter. A. Longitudinal scan of left kidney (arrowheads) showing the ureter (U) passing next to the lower
pole as it travels inferiorly. B. Transverse scan of a different kidney (arrowheads) with a very dilated ureter (U).
HYDRONEPHROSIS
115
FIGURE 1 3 1 5
Hydronephrosis secondary to nephrolithiasis. Longitudinal
view of right kidney shows severe calyceal dilation. Two
stones are visible as luminal echogenicities (small arrowheads), with the larger one obstructing the renal pelvis.
Large arrowhead indicates liver.
FIGURE 1 3 1 4
Thickening of the ureteral wall. Longitudinal image of a
renal allograft (arrowheads) with hydronephrosis secondary
to obstruction of a ureteral stent (curved arrow). The wall of
the ureter is thickened (straight arrows).
FIGURE 1 3 1 6
Stone obstructing ureter. Longitudinal view of right kidney
(arrowheads) with a stone (straight arrow) obstructing the proximal
ureter (curved arrow). (Photo courtesy of Dr. D. Baumgarten.)
FIGURE 1 3 1 7
Hydronephrosis secondary to obstruction of a nephrostomy
tube by blood clots. Longitudinal view of right kidney
(arrowheads) showing echogenic clots (arrows) in dilated
calyces.
116
FIGURE 13-18
Resolution of acute hydronephrosis. A. Longitudinal view of left kidney showing mild calyceal dilation (arrows) in a patient
with urinary retention. B. Longitudinal view 24 hours after placement of a Foley catheter showing complete resolution.
ball (see Fig. 9-12B), or sloughed papilla (see Fig. 8-6). Acute hydronephrosis
should resolve rapidly after decompression (Fig. 13-18; also see Figs. 27-2, 27-5),
but caliectasis can persist for several months after correction of chronic obstruction (Fig. 13-19). The continued presence of hydronephrosis after ureteral stenting
or percutaneous nephrostomy, particulary when urine output is not robust or renal function does not improve, usually indicates that the stent or tube is out of position or occluded, or possibly that the hydronephrosis was not obstructive.
n chronic pyelonephritis, the caliectasis is usually asymmetric, and there is often

scarring of the cortex (Fig. 13-1). Papillary necrosis (see Figs. 8-3, 8-4) leads to
enlarged minor calyces, but the remainder of the collecting system should be
normal unless obstructed by a necrosed papilla (see Fig. 8-6). Cysts are usually
rounder than calyces, have thinner walls, are not interconnected, and are located
more peripherally (see Fig. 10-7). However, the distinction is more difficult with
parapelvic cysts (see Fig. 10-8) and peripelvic cysts (see Figs. 10-9, 10-10). Peripelvic
cysts can coexist with hydronephrosis and can cause the hydronephrosis to appear more severe (Fig. 13-20). A dilated renal vein (see Fig. 23-1) branches at the
hilum just outside the renal sinus, resulting in a branching pattern more typical of
a bush than the "pruned-tree" appearance of the collecting system. The dilated renal vein tracks medially to the vena cava in contrast to the inferior course of the
ureter. Because the calyces are regularly spaced, they can have the appearance of
medullary pyramids (Fig. 13-9). However, medullary pyramids do not exhibit the
acoustic enhancement typical of fluid, and they should not interconnect. Hypoechoic central renal masses such as transitional cell carcinoma (see Chapter 18) are
not anechoic and lack other features of fluid. Thickening of the walls of the collecting system, often due to mucosal edema, can cause the collecting system or
ureter to appear dilated (Fig. 13-21). Although hypoechoic, the edema is not anechoic, and there are often thin echogenic lines marking the lumen walls. 9,1 When
the edematous mucosa fills the lumen, there may be only a single line (Fig.
13-21B) where the mucosal surfaces meet."
HYDRONEPHROSIS
117
FIGURE 1 3-1 9
Resolution of chronic hydronephrosis. A. Longitudinal view of left kidney (arrowheads) in a patient with urinary retention,
showing marked enlargement of the calyces (C) and ureter (arrows). B. Six weeks after decompression of the bladder,
caliectasis and hydroureter are still present but substantially reduced.
FIGURE 13-20
Peripelvic cyst in hydronephrotic kidney. A. In the longitudinal view, the cyst (large arrowhead) appears to be part of the
dilated collecting system (small arrowheads), giving the appearance of severe hydronephrosis. B. Oblique view shows the
cyst to be distinct from and actually compressing the calyces, which are only moderately dilated. There was no
communication with the collecting system in multiple views.
118
FIGURE 1 3 2 1
Uroepithelial edema. A. Transverse image of a renal

allograft showing an enlarged pelvis (P) and ureter
(arrowheads) containing a stent (two bright parallel lines).
Although it is hypoechoic, the apparent lumen of the ureter
is not anechoic, indicating that this is edema and not fluid.
The edema is easily seen on each side of the stent.
B. Longitudinal image of a different renal allograft with a
slightly enlarged lower pole calyx (arrow). There is a thin,
echogenic line running longitudinally through the center of
the calyx where the mucosal borders meet.
REFERENCES
1. Baumgartner BR, Steinberg HV, Ambrose SS, et al: Sonographic evaluation of renal stones treated
by extracorporeal shock-wave lithotripsy. AIR 1987;149:131.
2. Morin ME, Baker DA: The influence of hydration and bladder distension on the sonographic diagnosis of hydronephrosis. I Clin Ultrasound 1979;7:192.
3. Mosli HA, Rawas MM, Farsi HM: Mannitol-induced diuretic renal ultrasonography: A new technique. Urology 1991;38:267.
4. Fried AM, Woodring MD, Thompson DJ: Hydronephrosis of pregnancy: A prospective sequential
study of the course of dilatation. J Ultrasound Med 1983;2:255.
5. Peake SL, Roxburgh HB, Langlois SLP: Ultrasonic assessment of hydronephrosis of pregnancy.
Radiology 1983;146:167.
6. Jequier S, Forbes PA, Nogrady MB: The value of ultrasonography as a screening procedure in a
first-documented urinary tract infection in children. I Ultrasound Med 1985;4:393.
7. Weinberg B, Yeung N: Sonographic sign of intermittent dilatation of the renal collecting system in
10 patients with vesicoureteral reflux. I Clin Ultrasound 1997;26:65.
8. Haddad MC, Sharif HS, Shahed MS, et al: Renal colic: Diagnosis and outcome. Radiology
1992;184:83.
9. Babcock DS: Sonography of wall thickening of the renal collecting system: A nonspecific finding.
10. Nicolet V, Carignan L, Dubuc G, et al: Thickening of the renal collecting system: A nonspecific finding at US. Radiology 1988;168:411.
11. Cunningham JJ, Bacani-Faulls M: Sonographic "White Line Sign" for detection of minimal mucosal
thickening in renal transplants. Uroradiology 1990;35:367.
Obstruction of the
Lower Urinary Tract
SONOGRAPHY
he lower urinary tract should be examined in any patient with hydronephrosis. Other indications include hematuria, pain, urinary retention, and
urinary tract infections under certain conditions. The ureters coarse inferiorly from the kidneys through the retroperitoneum, crossing over the iliac vessels
and entering the bladder on each side of its base (Fig. 14-1). The bladder is located
in the midline, posterior to the symphysis pubis, has a smooth wall, and contains
no luminal structures. The urethra is at the base of the bladder in the midline and,
in males, is surrounded by the prostate gland and the seminal vesicles. An additional structure that may be encountered is the reservoir of a penile implant (Fig.
14-2). In females, the vagina and uterus lie inferior and posterior to the bladder
(Fig. 14-3). Because of the overlying pubic bone, visualization of the base of the
bladder requires that the probe be angled inferiorly. With sagittal scanning, the inferior aspect of the bladder is placed on the right-hand side of the image. The
bladder should be examined in both the sagittal and transverse planes, before and
after the patient has voided, with measurements, and the base should be well
visualized. If echogenic material is noted along the bladder wall, the patient
should be reexamined in the lateral decubitus position.
INTERPRETATION
typical adult male bladder containing a small amount of urine is shown in

Fig. 14-4. As the bladder becomes distended (Fig. 14-5), it remains oval in
the transverse plane and becomes more elongated in the sagittal plane.
Bladder volume is calculated using the following formula for an ellipsoid: length
x width x depth x 0.523) Because of variations in shape, the error is as high as
25%, particularly in small bladders, and is substantially improved by using a
three-dimensional approach.' However, the error in calculation of bladder volume
in adults by standard sonography is generally less than the biologic variation in
postvoid residual volume. 2 ' 3 Thus, sonography is sufficiently accurate and should
be the technique of choice for measuring bladder volume. The normal postvoid
bladder is empty and usually not visible but may contain up to 10 mL. 3 Significantly greater postvoid volumes are observed in randomly selected, asymptomatic
35 mL. 2 Volumes > 50 mL are associated
men, with 75% having a volume of
with a three-fold increased risk of subsequent, symptomatic urinary retention.2
A transverse view of the base of the bladder reveals the two ureters in crosssection as they enter the posterior wall (Fig. 14-6), with the seminal vesicles posterior to the ureters. 45 The seminal vesicles can become enlarged and cystic in
120
FIGURE 14-2
Reservoir for penile implant. Transverse scan of bladder (B)
demonstrating the fluid-filled reservoir (R) on the left side
of the bladder.
FIGURE 14-1
Structure and relationships of the ureters and bladder in
males, anterior view.
Uterus
Ureteral
orifice
Bladder
Rectum
Symphysis
pubis
Vagina
Urethra
FIGURE 1 4-3
Structure and relationships of
the urinary bladder in
females, sagittal view.
OBSTRUCTION OF THE LOWER URINARY TRACT
121
FIGURE 14-4
Normal male bladder.
A. Transverse and (B) sagittal views of a bladder (B)
containing approximately 60 mL of urine. The urethral
outlet (arrow) and prostate gland (arrowheads) are visible in
the transverse view.
FIGURE 1 4-5
Severe bladder distension. A. Transverse and (B) sagittal views of a neurogenic bladder in a
patient with severe hydronephrosis.
122
FIGURE 1 4 6
Transverse view of the base of a male bladder. The ureters
are seen in cross-section (arrows) as they pass through the
bladder wall into the bladder lumen (B). The seminal
vesicles (arrowheads) are seen behind the ureters.
FIGURE 1 4-7
Cystic enlargement of the seminal vesicles in autosomaldominant polycystic kidney disease. Transverse view of the
bladder (B) with enlarged seminal vesicles containing
multiple cysts (arrows). (From Weingardt JP, Townsend RR,
Russ PD, et al: Seminal vesicle cysts associated with autosomal dominant polycystic kidney disease detected by
sonography. I Ultrasound Med 1995;14:475, with
permission.)
autosomal dominant polycystic kidney disease (Fig. 14-7). Sagittal views show
the ureter posterior to the bladder and then passing through the wall to the lumen
(Fig. 14-8). Occasional jets of urine can be seen entering the bladder from the
ureteral orifices (Fig. 14-9). These appear as subtle, echogenic whisps on grayscale imaging but are much more obvious with color Doppler. 6 Their frequency
varies considerably but averages about three per minute in normal individuals,
and most patients with high-grade ureteral obstruction exhibit either an absence
of jets or continuous, low-level jets. 6 The normal distal ureter is 1-3 mm in diameter and is not always visible. 5 However, dilated distal ureters are easily seen (Fig.
14-10) and can become very large (Fig. 14-11). The bladder wall is echogenic and
smooth, and its thickness varies inversely with the degree of distension, ranging
from 3 to 6 mm. 4 Edema causes the bladder wall to become thickened and less
echogenic (Fig. 14-12), and can cause obstruction of the distal ureters (Fig. 14-13).
Distal ureters can also be obstructed by carcinoma of the bladder (Fig. 14-14),
which presents as focal irregularities in the luminal wal1, 4 or by stones (Fig. 14-15).
Ureteric obstruction also occurs in association with ureteroceles (Fig. 14-16).
Obstruction of the urethra is usually due to prostatic hypertrophy. As the
prostate gland enlarges, it begins to bulge into the bladder lumen (Fig. 14-17), presenting as a large intraluminal mass at the base of the bladder in severe cases
(Fig. 14-18). The gland is also enlarged in acute prostatitis (Fig. 14-19), with a central hypoechoic area representing edema. Obstruction of the bladder outlet is also
seen with stones (Fig. 14-20) and hematoma (Fig. 14-21A). Occasionally, clotted
blood fills the entire lumen (Fig. 14-21B). Both distal ureteral obstruction and
bladder outlet obstruction are observed in urinary schistosomiasis.'
123
FIGURE 1 4-8
Distal ureter. A. Parasagittal view showing the right ureter (arrows) coursing behind bladder
(B) and then entering it. B. Oblique view showing the ureter (arrows) passing through the bladder wall.
FIGURE 1 4 9
Ureteral jets. A. Transverse scan of bladder showing diagonal, echogenic trails (arrows) rising
from each ureter at the base. B. Transverse Doppler scan in a different subject shows a more distinct jet (arrow).
A
FIGURE 1 4 1 0
Dilated distal ureters. A. Sagittal view showing a dilated ureter (U) posterior to the bladder
(B). B. Transverse view of the bladder (B) showing a dilated left ureter (straight arrow) and slightly dilated right ureter
(curved arrow) in cross-section.
124
FIGURE
1 4-11
Dilated distal ureters. Transverse image of the bladder (B) in
a patient with chronic urinary obstruction secondary to
posterior urethral valves. The distal ureters (arrows) are
markedly dilated and the bladder wall is thickened.
FIGURE 14- 1 2
Hemorrhagic cystitis. Transverse view of bladder (arrows)
showing a hypoechoic, edematous wall and a Foley
catheter (F). The echogenic material in the lumen is clotted
blood.
FIGURE 1 4 - 1 3
Edematous bladder wall obstructing distal ureter.
A. Transverse view of bladder (medium arrowheads) showing
thickened, hypoechoic wall and a Foley catheter (large
arrowhead). The distal right ureter is enlarged (small
arrowheads). B. Sagittal view.
125
FIGURE 1 4 1 4
Ureteral obstruction due to bladder carcinoma. A. Sagittal
view of bladder (cursors) with thickening and irregularity of
the base (arrows) due to carcinoma. The vagina (arrowheads)
is visible posterior to the bladder. B. Transverse scan of the
bladder (large arrowheads) in a different patient showing
marked dilation of the distal ureters (small arrowheads). The
balloon of a Foley catheter lies in the urethra between the
distal ureters. (From O'Neill WC: Renal ultrasonography: a
procedure for nephrologists. Am J Kidney Dis 1997;30:579,
with permission.)
FIGURE 1 4 1 5
Stone obstructing distal ureter. Transverse scan of bladder (B)
showing a stone (arrow) lodged in the intramural segment of the
right ureter. (From Davidson AJ, Hartman DS, Choyke PL, et al:
Davidson's Radiology of the Kidney and Genitourinary Tract.
Philadelphia, WB Saunders; 1999; p 371, with permission.)
FIGURE 1 4 1 6
Ureterocele. A. Transverse and (B) sagittal scans of
the bladder of a 1-month-old girl with complete
duplication of the left collecting system and
obstruction of the ureter draining the upper pole.
This ureter balloons into a large ureterocele (U) on
entering the bladder (B). The arrows indicate the
wall of the ureterocele. (Photos courtesy of B Gay,
MD.)
126
FIGURE 1 4 - 1 8
Severe prostatic enlargement. Transverse view of bladder
(B) showing a markedly enlarged prostate gland (P)
extending well into the lumen.
FIGURE 1 4 - 1 7
Prostatic enlargement. A. Sagittal and (B) transverse scans
of the bladder (B) showing an enlarged prostate gland (P)
protruding into the lumen.
127
FIGURE 1 4 - 1 9
Urinary retention secondary to acute prostatitis. Transverse
view of bladder (B) showing an enlarged prostate gland
(arrows) protruding into the lumen. The gland is relatively
hypoechoic because of edema.
FIGURE 1 4 - 2 0
Bladder stone. Sagittal scan of the bladder (B) showing
a stone (arrow) at the base with acoustic shadowing
(arrowheads).
FIGURE 1 4 - 2 1
Clotted blood causing bladder outlet obstruction. Transverse images in patients who developed gross hematuria after
percutaneous renal biopsy. A. Distended bladder with echogenic blood clots (C) at the base. B. Echogenic clot fills the entire
lumen (arrowheads) and the distal ureters are slightly dilated (arrows).
128
ilation of the distal ureter without bladder distension suggests obstruction
at the ureteral orifice, by either a stone, bladder carcinoma, or edema. A
distended postvoid bladder should prompt a search for anatomic obstructions such as prostatic enlargement, clots, stones, or foreign bodies, all of which
present as abnormal luminal echoes at the base of the bladder. A distended bladder without an identifiable anatomic obstruction suggests a neurogenic bladder.
The classic finding in neurogenic bladder is a large prevoid and postvoid volume.
However, in sensory neurogenic bladder, the postvoid volume is normal but the
prevoid bladder is distended and not sensed.8
REFERENCES
1. Riccabona M, Nelson TR, Pretorius DH, et al: In vivo three-dimensional sonographic measurement
of organ volume: Validation in the urinary bladder. J Ultrasound Med 1996;15:627.
2. Kolman C, Girman CJ, Jacobsen SJ, et al: Distribution of post-void residual urine volume in randomly selected men. J Urology 1999;161:122.
3. McConnell JD: Epidemiology, etiology, pathophysiology, and diagnosis of benign prostatic hyperplasia. In: Wash PC, Retik AB, Vaughan ED, et al. (eds): Campbell's Urology, vol. 2. 7th ed. Philadelphia, WB Saunders; 1998; pp 1429-1446.
4. Abu-Yousef MM, Narayana AS, Franken EA, et al: Urinary bladder tumors studied by cystonography. Radiology 1984;153:223.
5. Mirk P, Maresca G, Fileni A, et al: Sonography of normal lower ureters. J Clin Ultrasound
1988;16:635.
6. Burge HJ, Middleton WD, McClennan BL, et al: Ureteral jets in healthy subjects and in patients
with unilateral ureteral calculi: comparison with color Doppler US. Radiology 1991;180:437.
7. Dittrich M, Doehring E: Ultrasonographical aspects of urinary schistomsomiasis: Assessment of
morphological lesions in the upper and lower urinary tract. Pediatr Radio! 1986;16:225.
8. Koch MO: Disorders of micturition. In: Jacobson HR, Striker GE, Klahr S (eds): The Principles and
Practice of Nephrology, vol. . Philadelphia, BC Decker; 1991; p 452.
CHAPTER
1 5
Nephrolithiasis
SONOGRAPHY
ndications for ultrasonography include pain and hematuria, and a careful

search for calculi should be made in these situations. However, nephrolithiasis
is a common incidental finding. Stones are an important cause of ureteral obstruction, and although the obstructing stone may not be visible in the ureter, the
presence of stones in the kidney is an important clue. Hydronephrosis or acute renal colic should prompt a careful search for stones in the distal ureter. The source
of any acoustic shadow should be pinpointed, examined carefully, and imaged in
another plane. Apparent multiple stones should be imaged in several planes to determine whether they are portions of the same stone (staghorn calculus).
INTERPRETATION
he classic sonographic appearance of a renal stone is a brightly echogenic

structure within the calyceal system that casts a radially oriented acoustic
shadow (Fig.15-1). The stone often appears linear or crescent shaped because the sound is reflected off the surface or absorbed, preventing imaging of the
interior. However, different acoustic properties can result in the entire stone being
imaged (Fig. 15-2). In some cases, only the shadow is visible (Fig. 15-3) because
of obscuration of the stone by sinus fat and absorption rather than reflection of
sound by the stone. The distinctness and darkness of the shadows vary considerably and are related to the size and surface properties of the stones 1 ' 2 and to the
degree of reverberation artifact.' Shadows may not be visible in some planes but
can usually be elicited with careful scanning in other planes. In rare cases, there
may be no shadows (Fig. 15-4). Stones composed primarily of matrix protein (matrix calculi) are not brightly echogenic 3 and do not cast shadows (Fig. 15-5).
Nephrolithiasis may present as multiple tiny stones that may be visible as such
(see Fig. 15-2) or may appear only as diffuse shadowing (Fig. 15-6). Staghorn calculi may be visible as lengthy stones filling the collecting system (Fig. 15-7A) but
more often appear as multiple distinct stones in individual planes (Fig. 15-7B).
Large stones can become lodged in a major calyx or the renal pelvis where they
can produce obstruction (Fig. 15-8). A unusual cause of nephrolithiasis is poorly
soluble medications such as sulfonamides (Fig. 15-9), acyclovir, indinavir, and
methotrexate.4
130
FIGURE 1 5 1
Nephrolithiasis. Longitudinal image of left kidney showing
a stone in the lower pole (large arrowhead) casting an
acoustic shadow (small arrowheads). The stone appears
linear because only the surface is imaged. Note that the
shadow extends to the bottom of the image.
FIGURE 1 5 2
Nephrolithiasis. Longitudinal image of right kidney
demonstrating a stone in the lower pole (arrow) that casts
a faint shadow (arrowheads) that nevertheless extends to the
bottom of the image. Because less sound is reflected and
absorbed, the entire stone is seen. Several tiny stones are
present in the upper pole (curved arrow).
FIGURE 1 5 3
Nephrolithiasis. Longitudinal image of left kidney with
acoustic shadows emanating from the midkidney and
lower pole (arrowheads). The stone in the midkidney is
visible as an echogenic line (arrow), whereas the stone in the
lower pole is not.
NEPHROLITHIASIS
131
FIGURE 1 5 -4
Nephrolithiasis without acoustic shadowing. Longitudinal
image of right kidney with multiple stones (arrows) in the
upper pole, confirmed by computed tomography scanning.
No acoustic shadow is visible.
FIGURE 1 5 - 5
Matrix calculus. Transverse view of right kidney (arrows)
showing hypoechoic mass with echogenic margins (arrowheads)
filling the renal pelvis. ( From Zwirewich CV, Buckley AR,
Kidney MR, et al: Renal matrix calculus: Sonographic
appearance. J Ultrasound Med 1990;9:61, with permission.)
FIGURE 1 5-6
Nephrolithiasis. Transverse image of left kidney
(arrowheads) with multiple, very small stones producing a
diffuse shadow (arrows). There is also a shadow due to
refraction artifact (curved arrow).
132
B
FIGURE 1 5 7
Staghorn calculi. A. Longitudinal image of right kidney
(cursors) containing a long, curvilinear echogenicity (arrows)
in the renal sinus with a dense acoustic shadow. The upper
pole calyces (C) are dilated. B. Longitudinal image of a
renal allograft (arrowheads) showing several stones in the
collecting system (arrows) that were shown to be portions of
a single stone when visualized in multiple planes.
B
FIGURE 1 5 8
Stone obstructing the collecting system. A. Longitudinal
image of left kidney with a stone (arrows) lodged in the
renal pelvis, producing chronic obstruction of a lower pole
calyx (arrowhead). Note the through-transmission from the
dilated calyx adjacent to the acoustic shadow from the
stone. B. Longitudinal image of left kidney from a different
patient with hydronephrosis due to a stone impacted in the
renal pelvis (arrows). A faint acoustic shadow is visible
(arrowheads).
NEPHROLITHIASIS
FIGURE 1 5 9
Sulfadiazine crystalluria. Longitudinal scan of left kidney showing
crystals layering dependently in a dilated calyx (arrow) and casting an
acoustic shadow (arrowheads). (From Sasson JP, Dratch PL, Shortsleeve
MJ: Renal US findings in sulfadiazine-induced crystalluria. Radiology
ot all acoustic shadows are indicative of stones; some are artifactual. Refraction of the sound as it strikes an interface at an angle reduces distal
sound intensity and casts a shadow suggestive of a stone or calcification
(Fig. 15-10). This refraction artifact commonly emanates from the extreme edge of
the kidney where stones would not occur, but it can also be seen at the edges of
cysts. Acoustic shadows can emanate from fat tissue in the renal sinus but are usually not as distinct ("dirty shadows") and usually do not extend to the bottom of
the image. Brightly echogenic foci with shadows can also be produced by gas, either from emphysematous pyelonephritis (see Figs. 9-8, 9-9) or from instrumentation
of the urinary tract s (Fig. 15-11). Angiomyolipomas (see Fig. 19-1) are almost always
within the parenchyma and most do not cast shadows. Arcuate arteries (see Fig.
2-4) are small, are located at the corticomedullary junction, and do not cast shadows. They can be mistaken for calculi when the pyramid is mistaken for a calyx.
Calcification of intrarenal arteries (see Fig. 22-2) is easily mistaken for calculi, 6 with
the only clues being the shape of the calcification if visible and echogenicity and
shadowing in the extrarenal portion of the renal artery. Ureteral stents (see Fig.
16-6) and nephrostomy catheters (see Fig. 16-8) can cast shadows and mimic stones
when they are not well visualized. Milk of calcium, a microcrystalline suspension
FIGURE 1 5 1 0
Refraction artifact. Transverse image of left kidney with an
acoustic shadow (arrowheads) emanating from the lateral
aspect. The shadow results from refraction of the sound
beam as it strikes the kidney at an oblique angle.
133
134
FIGURE 1 5 1 1
Calyceal air mimicking nephrolithiasis. Longitudinal image of
right kidney (arrowheads) after a voiding cystourethrogram in a
patient with vesicoureteral reflux. There are brightly echogenic
foci in the calyces (arrows) with acoustic shadowing, caused by
reflux of air bubbles from the bladder. (From Kriss VM, Strife
JL: Vesicoureteral reflux of air simulating nephrolithiasis on
sonography. J Ultrasound Med 1993;12:549, with permission.)
FIGURE 1 5 - 1 2
Milk of calcium. A.
Longitudinal image of kidney
with stenosis of the
ureteropelvic junction,
demonstrating dilated calyces
containing brightly echogenic
material (arrows) suggestive of
stones or a staghorn calculus.
Note the dependent layering
in each calyx. B. On repeat
study with the patient upright,
the material shifts to the
dependent position (arrows).
(From Patriquin H, Lafortune
M, Filiatrault D: Urinary milk
of calcium in children and
adults: Use of gravitydependent sonography. AIR
A
that develops in fluid within obstructed calyces, pyelogenic cysts, and calyceal diverticula, 7 '8 can mimic a large stone (Fig. 15-12A). Reexamination of the patient in
the upright position should demonstrate the layering of the crystals (Fig. 15-12B).
REFERENCES
1. King W III, Kimme-Smith C, Winter J: Renal stone shadowing: An investigation of contributing
factors. Radiology 1985;154:191.
2. Rubin JM, Adler RS, Bude RO, et al: Clean and dirty shadowing at US: A reappraisal. Radiology
1991;181:231.
3. Zwirewich CV, Buckley AR, Kidney MR, et al: Renal matrix calculus: Sonographic appearance.
4. Perazella MA: Crystal-induced acute renal failure. Am J Med 1999;106:459.
5. Kriss VM, Strife JL: Vesicoureteral reflux of air simulating nephrolithiasis on sonography. I Ultrasound Med 1993;12:549.
6. Kane RA, Manco LG: Renal arterial calcification simulating nephrolithiasis on sonography. AIR
1983;140:101.
7. Patriquin H, Lafortune M, Filiatrault D: Urinary milk of calcium in children and adults: Use of
gravity-dependent sonography. AIR 1985;144:407.
8. Yeh H-C, Mitty HA, Halton K, et al: Milk of calcium in renal cysts: New sonographic features.
Catheters and Stents
SONOGRAPHY
nstrumentation of the urinary tract is frequent and sonography is useful in assessing the location and function of indwelling catheters and stents. Stents are
also encountered incidentally, occasionally having been forgotten. A history of
stenting should be obtained at sonography and catheters or stents known to be
present should be visualized. If an indwelling bladder catheter is not visible, it can
usually be located by deflating the balloon and then observing the enhanced
echogenicity during refilling (Fig. 16-1). If a catheter is present but the bladder is
not empty, the catheter should be irrigated and sonography should be repeated.
I NTERPRETATION
Foley catheter is easily recognized in transverse scans of the bladder as

a fluid-filled balloon that surrounds the central catheter (Fig. 16-2). On
sagittal views, the catheter can be seen coursing through the balloon (see
Fig. 14-13B). The bladder should be empty; residual urine usually indicates obstruction of the catheter (Fig. 16-3). Occasionally catheters are not properly
placed, usually being in the urethra instead of the bladder (Figs. 16-1,16-4). When
the catheter perforates the urethra, it is seen posterior to the bladder in the sagittal plane (Fig. 16-5). Filling of the catheter balloon during sonography renders it
echogenic, allowing the catheter to be located (see Fig. 16-1). Because of their
small size, ureteral stents may not be seen unless carefully sought out. They appear as thin, parallel, echogenic lines that often cast a shadow (Fig. 16-6). They are
almost always visualized in renal allografts but can be difficult to see in native
kidneys. Stents should be visible entering the bladder (Fig. 16-7), provided there
is sufficient urine in the bladder. Hydronephrosis with a nondistended bladder
indicates that the stent is obstructed (see Fig. 13-14). Nephrostomy tubes have a
similar appearance but enter the calyces through the renal parenchyma, and blood
clots around the tube are not infrequent (Fig. 16-8).
tones(see Chapter 15) usually cast more distinctive shadows, but the appearance of vascular calcification (see Fig. 22-2) is very similar to that of stents.
Echogenic lines can be seen in calyces with mucosal edema (see Fig. 13-21)
and are easily mistaken for stents except that there are no acoustic shadows.
136
FIGURE 1 6 2
Foley catheter in empty bladder. Transverse image
demonstrating the inflated balloon with echogenic walls
(arrowhead) surrounding the central, echogenic catheter.
FIGURE 1 6 1
Real-time localization of a Foley catheter terminating in the
urethra. A. Sagittal image demonstrating that the catheter is
not in the bladder (B). The catheter balloon appears as a
hypoechoic area inferior and posterior to the bladder
(arrows) that shrank when the catheter balloon was
deflated. B. During refilling, the balloon becomes brightly
echogenic.
CATHETERS AND STENTS
137
FIGURE 1 6 - 3
Obstruction of a Foley catheter by blood clot. Transverse
view of a distended bladder (B) with an echogenic blood
clot (C) surrounding a Foley catheter (arrow).
FIGURE 1 6 - 4
Foley catheter terminating in the urethra. Transverse view
of bladder (B) with balloon of Foley catheter lying
underneath (arrows).
FIGURE 1 6 - 5
Perforation of the urethra by a Foley catheter. Sagittal view
of distended bladder (B) showing Foley catheter (arrows)
lying posteriorly. The end of the catheter lies underneath
the superior edge of the bladder (arrowhead).
138
FIGURE 1 6 - 6
Ureteral stent. Longitudinal image of left kidney with a
stent in the collecting system (arrows). The stent appears as
parallel echogenic lines and casts an acoustic shadow
(arrowheads).
FIGURE 1 6 - 7
Ureteral stent in the bladder. Transverse view of distended
bladder in a patient with a transplanted kidney showing a
ureteral stent entering the bladder (arrowhead) and
suspended in the lumen (arrow).
FIGURE 1 6 - 8
Nephrostomy tube in a renal allograft. Longitudinal scan
demonstrating the tube (arrow) entering a dilated calyx (C)
through the parenchyma. Echogenic blood clots surround
the end of the tube.
NEOPLASTIC
DISEASE
CHAPTER
1 7
Renal Epithelial Tumors
SONOGRAPHY
ndications for sonography include pain or hematuria, although tumors may be

incidental discoveries and others may be noted during screening of premalignant conditions such as von HippelLindau disease or acquired cystic kidney
disease (ACKD). 1 The detection of neoplastic lesions depends on their size. 2-5 Although sonography detects almost 100% of tumors that are 3 cm, it identifies
less than 50% that are < 2 cm in diameter. Therefore, sonography should be used
cautiously as a screening test in premalignant conditions. There are no sonographic features that can reliably differentiate the various renal epithelial neoplasms or distinguish benign from malignant tumors. Any focal distortion of the
renal contour should be examined carefully to delineate underlying architecture.
Hypoechoic masses should be examined carefully for enhancement of the posterior
wall or through-transmission to ensure that they are not cysts. The renal vein and
vena cava should be examined for intraluminal tumor invasion.
SOLID TUMORS
Interpretation
The classic appearance is of a well-demarcated, hypoechoic mass that distorts the
renal contour (Fig. 17-1). However, tumors can also have the same echogenicity as
the cortex (Fig. 17-2), in which case they are poorly demarcated and easily overlooked (Fig. 17-3). Small renal cell carcinomas are often hyperechoic compared
with the normal cortex (Fig. 17-4) and can mimic angiomyolipomas, but this is almost never seen in carcinomas > 3 cm. 6 This echogenicity may result from microscopic, multicystic architecture.' s Demarcation is often aided by a thin hypoechoic
rim around the tumor (Fig. 17-5) that probably represents compressed, normal tissue.' This is not specific, because it is also seen around nonneoplastic masses (see
Fig. 10-14). 9 Renal cell carcinomas not infrequently present as large masses (Fig.
17-6) that can be exophytic (Fig. 17-7). Solid tumors should not exhibit properties
of cysts, such as enhancement of the posterior wall or through-transmission. Multiple renal cell carcinomas can occur, particularly in von HippelLindau diseaseLl
(Fig. 17-8). Oncocytomas are benign tumors that are indistinguishable from renal
cell carcinomas when small. When large, they can exhibit a central stellate scar that
is quite characteristic. 9,11, " The sonographic equivalent of this scar is unclear because it has been described as both hypoechoic" and hyperechoic 9 (Fig. 17-9). This
variable appearance may reflect its possible origin as necrosis or hemorrhage that
then organizes and becomes necrotic. 9 Renal cell carcinomas have a propensity to
invade the renal vein and vena cava 13 ' 14 (Fig. 17-10).
142
FIGURE 1 7 - 1
Renal cell carcinoma. Longitudinal view of the right kidney
showing a hypoechoic mass (M) in the upper pole. Note
absence of any acoustic enhancement posterior to the mass.
The uninvolved cortex is echogenic compared to the liver
(L), indicative of underlying chronic renal disease.
FIGURE 17-2
Small renal cell carcinoma. A. Longitudinal scan of right kidney shows
a small bulge in the parenchyma of the midkidney (arrow) that has the
same echogencity as the normal parenchyma. B. The transverse scan
shows an obvious tumor on the hilar lip (arrow). (Photos courtesy of
Dr. D. Baumgarten.)
RENAL EPITHELIAL TUMORS
FIGURE 17-3
Renal cell carcinoma. A. Longitudinal image of
right kidney shows a subtle distortion of the
extreme upper pole (arrows). B. Repeat study 6
months later reveals obvious mass in upper
pole (arrows).
FIGURE 17-4
Small hyperechoic renal cell carcinoma. Longitudinal view
of left kidney showing an echogenic mass (arrow) that is
similar in appearance to an angiomyolipoma.
143
FIGURE 17-5
Renal cell carcinoma in right kidney. Transverse view
showing a hyperechoic mass (M) with hypoechoic rim
(arrow).
4.
144
FIGURE 1 7 - 6
Renal cell carcinoma in left kidney. Longitudinal view
shows large isoechoic mass in lower pole (arrowheads)
distorting the renal contour and architecture. Arrows
indicate the normal upper pole.
FIGURE 1 7 - 7
Large renal cell carcinoma. Longitudinal view of left kidney
with a very large, heterogeneous mass extending from the
lower pole (arrowheads). There is hydronephrosis due to
obstruction of the ureter by the tumor.
FIGURE 17-8
Multiple renal cell carcinomas in a patient with von
Hippel-Lindau disease. Longitudinal view of right
kidney reveals a hyperechoic tumor (M) with a
hypoechoic rim in the upper pole (arrowheads) and
several other, smaller tumors (*). (From Yamashita Y,
Ueno S, Makita 0: Hyperechoic renal tumors:
Anechoic rim and intratumoral cysts in US
differentiation of renal cell carcinoma from
angiomyolipoma. Radiology 1993;188:179, with
permission.)
FIGURE 17-9
Oncocytoma. Longitudinal image of right kidney (large
arrow) demonstrating a large mass (small arrows) in the
lower pole. An echogenic, central stellate scar (arrowheads)
is present in the mass. (From Goiney RC, Goldenberg L,
Cooperberg PL, et al: Renal oncocytoma: Sonographic
analysis of 14 cases. AIR 1984;143:1001, with permisson.)
FIGURE 1 7- 1 0
Renal cell carcinoma with tumor
thrombus. A. Longitudinal image of
right kidney (K) shows a large tumor
(Tu) in the upper pole. B. Longitudinal
scan of the inferior vena cava (C)
shows thrombus (arrow) in the
superior portion. L, liver; Vp, portal
vein; Ar, renal artery. C. Transverse
view of the kidney (K) showing a
distended upper pole vein (Vr)
containing thrombus (cursors). D.
Transverse scan showing a second
vein (Vr) draining the kidney (K) that
is uninvolved. L, liver; C, vena cava;
W, spine; A, aorta. (From Schwerk WB,
Schwerk WN, and Rodeck G: Venous
renal tumor extension: A prospective
US evaluation. Radiology 1985;156:491,
with permisson.)
145
FIGURE
17-11
Duplication artifact mimicking a renal mass. A. Longitudinal view of left kidney showing a mass (M) adjacent to the upper
pole (arrowhead). Note the overlying spleen tip (S). B. A coronal view obtained to avoid the spleen demonstrates only fat
tissue between the upper pole and the spleen (S). Refraction of the sound toward the kidney as it passes from fat tissue into
the spleen and back out into fat tissue places an additional image of the upper pole under the spleen tip.
146
Duplication artifact can mimic a solid tumor (Fig. 17-11) and should always be considered when masses are observed at the extreme upper pole. This artifact arises
from the refraction of sound as it travels into and out of the edge of the liver or
spleen and is usually seen in the left kidney of obese patients. 15 Metastases and lymphoma (see Chapter 20) are indistinguishable from renal epithelial tumors except
that they are often multiple and bilateral, which is unusual with renal epithelial
neoplasms except in premalignant disorders. A hypertrophied column of Bertin (see
Fig. 3-6) has the same echogenicity as the normal cortex, occurs between two
medullary rays, and does not distort the renal contour. Simple cysts (see Figs. 10-1
through 10-4) are anechoic and exhibit accoustic enhancement. Tissue averaging
can obscure these characteristics and cause a cyst to appear as a mass (see Fig.
10-5A). Hemorrhagic cysts (see Fig. 10-11) or infected cysts (see Fig. 10-13) can exhibit homogeneous echogenicity and be indistinguishable from neoplasms. Renal
infarction (see Fig. 22-5) initially appears as a hypoechoic mass, but it is not well
demarcated, is usually apparent from the clinical situation, and disappears in 1-2
days. Adrenal hypertrophy or tumor (see Fig. 1-5) can mimic an upper pole renal
mass. Acute pyelonephritis can produce focal hypoechoic masses (see Fig. 9-2) but
is usually apparent from the clinical picture. More indolent infections, particularly
opportunistic ones, can also produce hypoechoic masses (see Fig. 9-6) but are often multifocal. Angiomyolipomas (see Chapter 19) are more echogenic than are
most renal epithelial tumors, 16 but additional imaging studies are required to reliably distinguish these tumors. Acoustic shadowing, which is seen with some angiomyolipomas, is not observed in echogenic renal cell carcinomas. 16 Splenosis is
a rare cause of a left renal mass 17 (Fig. 17-12). Nodular compensatory hypertrophy appears as a mass (Fig. 17-13) in kidneys that have undergone focal damage such as
that in reflux nephropathy and chronic pyelonephritis. 18 An atrophic duplication
(nubbin sign) can appear as an echogenic mass (see Fig. 3-5), but its location and
the presence of sinus fat are aids in its recognition.
FIGURE 1 7- 1 2
Splenosis. Longitudinal view of left kidney (arrows) showing slightly
hyperechoic mass extending from upper pole (arrowheads). (From Kiser
JW, Fagien M, Clore FF: Splenosis mimicking a left renal mass. AIR
FIGURE 1 7 - 1 3
Nodular compensatory hypertrophy. Longitudinal scans of
left kidney (cursors) from a patient with reflux nephropathy.
The kidney is small and echogenic except for an enlarged
lower pole (arrows) with normal echogenicity. S, spleen.
147
CYSTIC TUMORS
Interpretation
Neoplasms that are primarily cystic are rare. Multilocular cystic nephroma, which
presents as an encapsulated multicystic mass (Fig. 17-14), has thick cyst walls but
no other solid elements. 19 -22 Approximately 5% of renal cell carcinomas are cystic,
usually multilocular, 7'8 '22'23 with the cysts comprising either a portion (Fig. 17-15)
or the bulk (Fig. 17-16) of the tumor. Cysts can exist in other neoplasms, with the
possible exception of angiomyolipomas.' 6 Carcinoma arising within the wall of a
cyst (Fig. 17-17) is rare. 8 Necrosis (Fig. 17-18) or hemorrhage within a tumor can
also lead to a cystic appearance. 8 Cysts associated with neoplasms have one or
more of the characteristics of complex cysts, such as irregularity or thickening of
the wall, solid elements within the lumen, and an adjacent mass.
FIGURE
1 7 1 zi
Multilocular cystic nephroma. Transverse image of left
kidney with a large multicystic mass (arrowheads) in the
upper pole that contains no solid elements. The lower pole
(cursor) is intact. (From Lonergan GJ, Martinez-Leon MI,
Agrons GA, et al: Nephrogenic rests, nephroblastomatosis,
and associated lesions of the kidney. Radiographics
FIGURE 1 7 1 5
Multilocular cyst within a renal cell carcinoma. Transverse
image of right kidney shows hyperechoic mass (arrowheads)
with a central cystic area. The renal vein (V) is dilated.
(From Yamashita Y, Ueno S, Makita 0, et al: Hyperechoic
renal tumors: Anechoic rim and intratumoral cysts in US
differentiation of renal cell carcinoma from angiomyolipoma. Radiology 1993;188:179, with permission.)
FIGURE 1 7- 1 6
Multiloculated renal cell carcinoma. Longitudinal scan of
left kidney containing a multicystic mass in the upper pole
(arrows) with thickened septa. (Photo courtesy of
Dr. D. Baumgarten.)
148
FIGURE 1 7 1 7
Carcinoma in the wall of a cyst. A mass (arrow) can be seen
along the inner wall of a cyst (arrowheads). (From Davidson
AJ, Hartman DS, Choyke PL, et al: Davidson's Radiology
of the Kidney and Genitourinary Tract. Philadelphia,
WB Saunders; 1999; p. 286, with permision.)
FIGURE 1 7 1 8
Renal cell carcinoma with cystic necrosis. Oblique scan of left
kidney containing a large mass in the lower pole (arrowheads)
with cystic areas of necrosis (arrow). (Photo courtesy of
Dr. D. Baumgarten.)
The distinction between a cystic neoplasm and a benign complex cyst cannot
be made by sonography. Acquired cystic kidney disease (ACKD) can have a focal cystic appearance (see Fig. 12-3) but the cyst walls are thin and cysts are almost always present in the other kidney. Renal cell carcinoma is associated with other
multicystic diseases, specifically ACKD and von Hippel-Lindau disease (see Fig.
12-10), but the neoplasms are not necessarily cystic and are not necessarily associated with the cysts. 13 In segmental multicystic disease and localized renal cystic disease, there is no capsule and the cyst walls are thin. 22 Hydatid cysts (see Fig. 9-16)
often have solid elements and therefore can mimic a cystic neoplasm.
REFERENCES
2. Mindell HJ: Pitfalls in sonography of renal masses. Urol Radio! 1989;11:215.
3. Jamis-Dow CA, Choyke PL, Jennings SB, et al: Small ( 3-cm) renal masses: Detection with CT versus US and pathologic correlation. Radiology 1996;198:785.
4. Bosniak MA, Rofsky NM: Problems in the detection and characterization of small renal masses. Radiology 1996;198:638.
5. Waarshauer DM, McCarthy SM, Street L, et al: Detection of renal masses: Sensitivities and specificities of excretory irography /liner tomography, US, and CT. Radiology 1988;169:363.
6. Forman HP, Middleton WD, Melson GL, et al: Hyperechoic renal cell carcinomas: Increase in detection at US. Radiology 1993;188:431.
7. Yamashita Y, Ueno S, Makita 0, et al: Hyperechoic renal tumors: Anechoic rim and intratumoral
cysts in US differentiation of renal cell carcinoma from angiomyolipoma. Radiology 1993;188:179.
8. Yamashita Y, Watanabe 0, Miyazaki T, et al: Cystic renal cell carcinoma: Imaging findings with
pathologic correlation. Acta Radiol 1994;35:19.
9. Goiney RC, Goldenberg L, Cooperberg PL, et al: Renal oncocytoma: Sonographic analysis of 14
cases. AIR 1984;143:1001.
10. Choyke PL, Glenn GM, Walther MM, et al: von Hippel-Lindau disease: Genetic, clinical, and imaging features. Radiology 1995;194:629.
11. Quinn MJ, Hartman DS, Friedman AC, et al: Renal oncocytoma: New observations. Radiology
1984;153:49.
12. Goldman SM: Benign renal tumors: Diagnosis and treatment. Urol Radiol 1989;11:203.
13. McGahan JP, Blake LC, White RD, et al: Color flow sonographic mapping of intravascular extension of malignant renal tumors. J Ultrasound Med 1993;12:403.
14. Habboub HK, Abu-Yousef MM, Williams RD, et al: Accuracy of color Doppler sonography in assessing venous thrombus extension in renal cell carcinoma. AJR 1997;168:1997.
15. Middleton WD, Melson GL: Renal duplication artifact in US imaging. Radiology 1989;173:427.
16. Siegel CL, Middleton WD, Teefey SA, et al: Angiomyolipoma and renal cell carcinoma: US differentiation. Radiology 1996;198:789.
17. Kiser JW, Fagien M, Clore FF: Splenosis mimicking a left renal mass. AIR 1996;167:1508.
Tract. Philadelphia, WB Saunders; 1999; p 68.
19. Davidson AJ, Hartman DS, Choyke PL, et al: Radiologic assessment of renal masses: Implications
for patient care. Radiology 1997;202:297.
20. Charboneau JW, Hattery RR, Ernst EC III, et al: Spectrum of sonographic findings in 125 renal
masses other than benign simple cyst. AIR 1983;140:87.
21. Baltarowich OH, Kurtz AB: Sonographic evaluation of renal masses. Urol Radiol 1987;9:79.
22. Hartman DS, Davis CJ, Sanders RC, et al: The multiloculated renal mass: Considerations and differential features. Radiographics 1987;7:29.
23. Feldberg MAM, van Waes PFGM: Multilocular cystic renal cell carcinoma. AIR 1982;138:953.
149
Pelvocalyceal Tumors
SONOGRAPHY
umors of the renal pelvis are rare and 90% are transitional cell carcinomas, a
disease seen primarily in older men. 1 -3 Indications include hematuria and
pain, and few of these tumors are incidental findings.' The role of sonography is to demonstrate a mass in the renal sinus or pelvis and to distinguish it from
a stone. Sonography cannot reliably distinguish neoplasms from other benign
pelvocalyceal masses.
I NTERPRETATION
ransitional cell carcinoma most commonly presents as a relatively hypoechoic mass within the renal sinus, with fat tissue separating it from the renal parenchyma (Fig. 18-1). These tumors can grow into the lumen (Fig.
18-2), sometimes filling and obstructing the pelvis (Fig. 18-3). A rarer presentation
is of diffuse infiltration of the sinus and parenchyma with preservation of the reniform shape 3 '4 (Fig. 18-4). Echogenicity is either equal to or less than that of the cortex, 2 but an occasional tumor can exhibit hyperechoic regions with acoustic
shadowing (Fig. 18-5) because of keratinization from squamous metaplasia.1'5
Other pelvocalyceal tumors are exceedingly rare and include fibroepithelial
polyps, squamous cell carcinoma, adenocarcinoma, lymphoma (Fig. 18-6), and
neurofibroma. 3 ' 6-8 There are no sonographic features that can distinguish among
the different pelvocalyceal tumors.
ydronephrosis is usually accompanied by ureteral dilation and is completely anechoic, as are peripelvic cysts (see Figs. 10-9, 10-10) and varices
(see Fig. 23-7). Distal acoustic enhancement should be present. Nonneoplastic pelvocalyceal masses are listed in Table 18-1. Most of these are filling defects
that do not expand into masses and split the sinus fat echoes. Stones usually cast
shadows, except for matrix stones (see Fig. 15-5) which can present as relatively
hypoechoic sinus or pelvic masses.
152
FIGURE
18-1
Transitional cell carcinoma of the renal pelvis. Transverse view
of right kidney (arrowheads) with a relatively hypoechoic mass
(arrow) within the sinus. The mass is bordered by sinus fat.
(From Davidson AJ, Hartman DS, Choyke PL, et al: Davidson's
Radiology of the Kidney and Genitourinary Tract. Philadelphia, WB
Saunders; 1999; p. 389, with permission.)
FIGURE 1 8 - 2
Small transitional cell carcinoma of the renal pelvis.
Coronal scan of right kidney showing a small mass (arrows)
protruding into the renal pelvis. (From Nolan RL, Nickel
JC, Froud PJ: Percutaneous endourologic approach for
transitional cell carcinoma of the renal pelvis. Urol Radiol
FIGURE 1 8 - 3
Transitional cell carcinoma. Longitudinal image of
left kidney showing a mass in the pelvis (straight
arrows) obstructing outflow and producing calyceal
enlargement (curved arrows). Note that the mass is
separated from the renal parenchyma by sinus fat
and that although it simulates dilation of the renal
pelvis, it is not anechoic (compare with minor
calyces). (From Grant DC, Dee GJ, Yoder IC, et al:
Sonography in transitional cell carcinoma of the renal
pelvis. Urol Radiol 1986;8:1, with permission.)
PELVOCALYCEAL TUMORS
FIGURE 1 8 4
Large infiltrating transitional cell carcinoma. A. Longitudinal view of left kidney showing obliteration of the upper
pole sinus. The renal contour is preserved. B. The sinus
mass (arrows) is more easily visualized in another
longitudinal view.
153
FIGURE 1 8 5
Transitional cell carcinoma of the renal pelvis
mimicking nephrolithiasis. Longitudinal image of
right kidney showing calicectasis and a slightly
echogenic mass (arrowheads) within the pelvis. A
portion of the mass is brightly echogenic (arrow) and
casts an acoustic shadow. (From Janetschek G, Putz
A, Feichtinger H: Renal transitional cell carcinoma
mimicking stone echoes. J Ultrasound Med 1988; 7:83,
with permission.)
154
FIGURE 18-6
Lymphoma of renal sinus. Transverse view of right
kidney showing a relatively hypoechoic mass in the
sinus (black arrowheads). The collapsed renal pelvis
appears as a linear echo within the mass (white
arrowhead). V, vena cava; A, aorta; S, spine; P, psoas
muscle. (From Ruchman RB, Yeh H-C, Mitty HA, et al:
Ultrasonographic and computed tomographic features
of sinus lymphoma. J Clin Ultrasound 1988;16:35, with
permission.)
TABLE 18-1
NONNEOPLASTIC PELVOCALCEAL MASSES

Blood clot (see Fig. 13-17)
Nephrolithiasis (see Figs. 15-5, 15-8)
Pyonephrosis (see Fig. 9-11)
Fungus ball (see Fig. 9-12)
Sloughed papilla (see Fig. 8-6)
Extramedullary hematopoiesis9
Malacoplakial
REFERENCES
1. Leder RA, Dunnick NR: Transitional cell carcinoma of the pelvicalices and ureter. AIR 1990;
155:713.
2. Grant DC, Dee GJ, Yoder IC, et al: Sonography in transitional cell carcinoma of the renal pelvis.
Urol Radiol 1986;8:1.
3. Bree RL, Schultz SR, Hayes R: Large infiltrating renal transitional cell carcinomas: CT and ultrasound features. J Cornput Assist Tomogr 1990;14:381.
4. Igarashi T, Muakami S, Shichijo Y, et al: Clinical and radiological aspects of infiltrating transitional
cell carcinoma of the kidney. Urol Int 1994;52:181.
5. Janetschek G, Putz A, Feichtinger H: Renal transitional cell carcinoma mimicking stone echoes.
6. Mariscal A, Mate JL, Guasch I, et al: Cystic transformation of a fibroepithelial polyp of the renal
pelvis: Radiologic and pathologic findings. AIR 1995;164:1445.
7. Cheong LL, Khan AN, Bisset RAL: Sonoraphic features of a renal pelvic neurofibroma. J Clin Ultrasound 1990;18:129.
8. Ruchman RB, Yeh H-C, Mitty HA, et al: Ultrasonographic and computed tomographic features
of sinus lymphoma. I Clin Ultrasound 1988;16:35.
9. Tuite MJ, Weiss SL: Ultrasound and computed tomographic appearance of extramedullary
hematopoiesis encasing the renal pelvis. J Clin Ultrasound 1991;19:238.
10. Amis ES, Hartman DS: Renal ultrasonography 1984: A practical overview. Radiol Clin North Am
1984;22:315.
Angiomyolipomas
SONOGRAPHY
ngiomyolipomas are the most common tumors encountered in kidneys,

with an autopsy incidence of 11%. 1 Multiple, bilateral angiomyolipomas
are found in tuberous sclerosis, whereas sporadic tumors are usually unilateral and are found primarily in middle-aged women. L2 Angiomyolipomas are
benign and usually small and clinically unimportant, but they can become large
and have a propensity for hemorrhage. They are usually discovered incidentally,
but sonography may be performed to confirm the diagnosis of tuberous sclerosis.
Occasionally, these tumors will present as intrarenal or perirenal hemorrhage.-
I NTERPRETATION
ngiomyolipomas appear as very echogenic masses, owing to their high fat

content," and therefore can be detected when they are very small 3 (Fig.
19-1). An acoustic shadow is seen in one third of the tumors 3 (Fig. 19-2).
Occasionally, angiomyolipomas are not echogenic (Fig. 19-3), possibly because
of a low fat content. 4 Angiomyolipomas are usually within the renal parenchyma
but can protrude from the outer cortex (Fig. 19-4) and can occur in the renal sinus
(Fig. 19-5), where they can be difficult to visualize.' These tumors often enlarge
(Fig. 19-6), sometimes dwarfing the kidney and filling the abdomen, and multiple
lesions should raise the suspicion of tuberous sclerosis (see Fig. 19-2). A frequent
complication of angiomyolipomas is hemorrhage (Fig. 19-7), whereas a rare complication is extension into the renal vein and vena cava 6 (Fig. 19-8).
enal cell carcinomas can be echogenic (see Figs. 17-4, 17-8) when small but
usually not to the same degree as angiomyolipomas and never with acoustic
shadowing. 3 Angiomyolipomas lack the hypoechoic rim often seen in renal
cell carcinomas' and are not cystic. 3 7 Stones (see Chapter 15) are not located in the
cortex and almost always cast a distinct shadow. In nephrocalcinosis (see Figs. 8-7
through 8-9), the echogenicity is localized to the medullary pyramids, usually
156
with dense shadows. Echogenic medullae and papillae (see Figs. 8-3, 8-4) and arcuate
arteries (see Fig. 2-4) can mimic angiomyolipomas but are limited to the medulla
or the corticomodullary junction. Junctional parenchymal defects (see Figs. 3-7, 3-8)
are usually contiguous with the sinus fat and are not round. Fat tissue used as a
packing after partial nephrectomy 8 (Fig. 19-9) and adrenal myelolipomas (Fig.
19-10) can be mistaken for renal angiomyolipomas.9
FIGURE 1 9 - 1
Angiomyolipoma. Oblique longitudinal view of right
kidney shows a small, brightly echogenic mass in the cortex
(arrow). The lesion is more echogenic than is the sinus fat
but it does not generate an acoustic shadow. The shadow
that is present is a refraction artifact generated by the edge
of the kidney.
FIGURE 1 9 - 2
Multiple angiomyolipomas in a patient with tuberous
sclerosis. Longitudinal view of enlarged right kidney
(arrowheads) shows multiple echogenic masses, with an
accoustic shadow distal to one (arrows).
FIGURE 1 9 - 3
Isoechoic angiomyolipoma. Longitudinal view of left kidney
(arrowheads) showing an isoechoic mass (arrows) protruding from
the upper pole. (From Jinzaki M, Tanimoto A, Narimatsu Y, et al:
Angiomyolipoma: Imaging findings in lesions with minimal fat.
Radiology 1997;205:497, with permission.)
ANGIOMYOLIPOMAS 157
FIGURE 1 9-4
Angiomyolipoma. Longitudinal view of left kidney with a
highly echogenic mass (arrow) protruding from midkidney.
The renal vein (V) is dilated because of congestive heart
failure.
FIGURE 19-5
Angiomyolipoma in renal sinus. Longitudinal
image of left kidney showing a brightly echogenic
mass (arrowheads) extending from the renal sinus.
The renal hilum and the hilar lips of the
parenchyma are obscured. (From Zagoria RJ, Dyer
RB, McCullough DL: Angiomyolipoma arising in
the renal sinus: A difficult radiologic diagnosis.
Urol Radiol 1989;11:139, with permission.)
FIGURE 1 9-6
Angiomyolipoma. Longitudinal view of left kidney (large
arrowheads) shows an echogenic mass (small arrowheads)
occupying much of the lower pole. The mass is not quite as
echogenic as the sinus fat and has a finer echo pattern.
158
FIGURE 1 9 - 7
Hemorrhage in an angiomyolipoma. Longitudinal view of
right kidney demonstrates a large angiomyolipoma (arrows)
with hemorrhage (H) both within the tumor and in the
perirenal space adjacent to the liver. (From Charboneau JW,
Hattery RR, Ernst EC III, et al: Spectrum of sonographic
findings in 125 renal masses other than benign simple cyst.
AJR 1983;140:87, with permission.)
FIGURE 1 9 - 8
Venous extension of renal angiomyolipoma. Oblique sagittal view
shows an echogenic mass (arrows) in the vena cava (IVC). (From
Arenson AM, Graham RT, Shaw P, et al: Angiomyolipoma of the
kidney extending into the inferior vena cava: Sonographic and CT
findings. AIR 1988;151:1159, with permission.)
FIGURE 1 9 - 9
Surgical defect packed with fat tissue, simulating an
angiomyolipoma. Longitudinal image of right kidney
(arrowheads) after a partial nephrectomy. There is a defect
in the lower pole that is filled with echogenic fat tissue
(arrows).
ANGIOMYOLIPOMAS 159
FIGURE 1 9-1 0
Myelolipoma of adrenal gland. Longitudinal view of right
kidney (arrowheads) showing a large echogenic mass
(arrow) adjacent to upper pole. (Photo courtesy of
Dr. D. Baumgarten.)
REFERENCES
1. Raghavendra BN, Bosniak ML, Megibow AJ: Small angiomyolipoma of the kidney: sonographicCT evaluation. AIR 1983;141:575.
2. Goldman SM: Benign renal tumors: Diagnosis and treatment. Urol Radiol 1989;11:203.
3. Siegel CL, Middleton WD, Teefey SA, et al: Angiomyolipoma and renal cell carcinoma: US differentiation. Radiology 1996;198:789.
4. Jinzaki M, Tanimoto A, Narimatsu Y, et al: Angiomyolipoma: Imaging findings in lesions with minimal fat. Radiology 1997;205:497.
5. Zagoria RJ, Dyer RB, McCullough DL: Angiomyolipoma arising in the renal sinus: A difficult radiologic diagnosis. Urol Radiol 1989;11:139.
6. Arenson AM, Graham RT, Shaw P, et al: Angiomyolipoma of the kidney extending into the inferior
vena cava: Sonogaphic and CT findings. AIR 1988;151:1159.
7. Yamashita Y, Ueno S, Makita 0, et al: Hyperechoic renal tumors: Anechoic rim and intratumoral
cysts in US differentiation of renal cell carcinoma from angiomyolipoma. Radiology 1993;188:179.
8. Papanicolaou N, Harbury OL, Pfister RC: Fat-filled postoperative renal cortical defects: Sonographic and CT appearance. AIR 1988;151:503.
9. Cyran KM, Kenney PJ, Memel DS, et al.: Adrenal myelolipoma. AIR 1996;166:395.
Metastases and
Hematologic
Malignancies
SONOGRAPHY
enal involvement usually occurs with advanced disease, so incidental discovery is rare. Sonography may be performed for renal failure in patients
with known disease, which can occur from infiltrative disease or from
ureteral obstruction, although drug toxicity, volume depletion, and sepsis are far
more common causes of renal failure in these diseases.
INTERPRETATION
ther than their tendency to be multiple, metastases appear identical to

other renal neoplasms' and can be either hypoechoic or hyperechoic (Fig.
20-1). Direct renal involvement by lymphoma should be distinguished
from paraneoplastic glomerular disorders. Renal parenchymal invasion is not rare
in lymphoma, with incidences of 5%-20% shown by computed tomography 2'3 and
up to 50% in autopsy studies. The incidence is lower over the whole spectrum of
disease, 4' 5 although there may be a higher incidence in certain types of lymphoma
such as Burkitt's lymphoma. 6 Renal failure is rare, arising either from diffuse infiltration 7' 8 or urinary obstruction. Several patterns of involvement by lymphoma
9
have been described. The most common finding is multiple masses 4 ' that are al3
3,9
most always hypoechoic (Fig. 20-2) and rarely hyperechoic. '" The masses are
homogeneous unless necrosis ensues after therapy, but the borders are usually indistinct. 3 Diffuse infiltration produces enlarged kidneys with echogenicity ranging from hypoechoic (Fig. 20-3) to hyperechoic (Fig. 20-4). Another pattern is
involvement of the perirenal space, producing a hypoechoic "halo" around the
kidney3,430,11 (Fig. 20-5). Although bilateral disease would be expected with lymphoma, the sonographic changes are unilateral in the majority of patients.3
Leukemic infiltration produces swollen, echogenic kidneys (Fig. 20-6).
162
B
FIGURE 2 0- 1
Metastatic disease. Longitudinal views of right kidney
show (A) two hypoechoic foci (arrowheads) of metastatic
adenocarcinoma of the lung and (B) two hyperechoic foci
(arrowheads) of anaplastic carcinoma of the lung. (From
Dershaw DD, Bernstein AL: Sonography of lung carcinoma
metastatic to the kidney. Urol Radiol 1985;7:146, with
permission.)
B
FIGURE 2 0- 2
Lymphoma. A. Longitudinal view of right kidney with two
hypoechoic masses (M). B. The masses disappeared after
therapy. (From Strauss S, Libson E, Schwartz E, et al: Renal
sonography in American Burkitt lymphoma. AIR
METASTASES AND HEMATOLOGIC MALIGNANCIES
FIGURE 2 0 3
Diffuse lymphoma. A. Longitudinal view shows a
massively enlarged left kidney with enlarged,
hypoechoic parenchyma. There is also some expansion
of the sinus with hypoechoic masses. B. There was
marked improvement after therapy. (From Obrador GT,
Price B, O'Meara Y, et al: Acute renal failure due to
lymphomatous infiltration of the kidneys. J Am Soc
Nephrol 1997;8:1348, with permission.)
FIGURE 2 0 4
Diffuse lymphoma. Longitudinal views of right kidney show (A) diffuse enlargement with a
rounded contour and increased echogenicity that (B) resolved after therapy. (From Strauss S,
Libson E, Schwartz E, et al: Renal sonography in American Burkitt lymphoma. AIR 1986;146:549,
with permission.)
163
164
FIGURE 2 0 - 5
Perirenal lymphoma. Longitudinal image of right kidney
(arrows) that is surrounded by hypoechoic lymphoma
(arrowheads). The kidney is diffusely echogenic. (From
Lorigan JG, David CL, Shirkoda A, et al: Macroglobulinaemic
lymphoma presenting with perirenal masses. Br I Radiol
FIGURE 2 0 - 6
Leukemic infiltration of the kidney. Longitudinal image of
right kidney (cursors) that is diffusely echogenic and
swollen. Note the rounded contour and loss of reniform
shape.
ifferential diagnosis consists of other causes of multifocal masses. Infections
can present as multiple hypoechoic masses (see Figs. 9-2, 9-6, 9-14a), but
frank abscesses (see Figs. 9-4, 9-5) are usually heterogeneous with both liquid and solid components. Primary renal neoplasms are rarely multifocal, and
metastases or lymphoma are rarely as echogenic as angiomyolipomas (see Chapter
19). Diffuse infiltration by lymphoma or leukemia can produce a picture that is
similar to acute glomerulonephritis (see Fig. 6-3), acute interstitial nephritis (see Fig.
8-1), diffuse pyelonephritis (see Fig. 9-1), acute allograft rejection (see Figs. 26-2,
26-3), or amyloidosis (see Fig. 6-9).
REFERENCES
1. Choyke PL, White EM, Zeman RK, et al: Renal metastases: Clinicopathologic and radiologic correlation. Radiology 1987;162:359.
2. Weinberger E, Rosenbaum DM, Pendergrass TW: Renal involvement in children with lymphoma:
Comparison of CT with sonography. AIR 1990;155:347.
4. Sheeran SR, Sussman SK: Renal lymphoma: Spectrum of CT findings and potential mimics. AJR
1998;171:1067.
6. Strauss S, Libson E, Schwartz E, et al: Renal sonography in American Burkitt lymphoma. AIR
1986;146:549.
7. Obrador GT, Price B, O'Meara Y, et al: Acute renal failure due to lymphomatous infiltration of the
kidneys. J Am Soc Nephrol 1997;8:1348.
8. Glicklich D, Sung MW, Frey M: Renal failure due to lymphomatous infiltration of the kidneys: Report of three new cases and review of the literature. Cancer 1986;58:748.
9. Heiken JP, Gold RP, Schnur MJ, et al: Computed tomoraphy of renal lymphoma with ultrasound
correlation. J Comput Assist Tomogr 1983;7:245.
10. Villalon FC, Fernandez JE, Garcia TR: The hypoechoic halo: A finding in renal lymphoma. J Clin
Ultrasound 1995;23:379.
11. Lorigan JG, David CL, Shirkoda A, et al: Macroglobulinaemic lymphoma presenting with perirenal masses. Br J Radiol 1988;61:1077.
VASCULAR
DISORDERS
CHAPTER
Anatomy of the
Renal Vessels
SONOGRAPHY
he anatomy of the renal vessels is depicted in Fig. 21-1. The renal arteries
(sometimes multiple) branch laterally off each side of the aorta and then
branch into segmental arteries at the renal hilum prior to entering the renal
sinus. The segmental renal veins converge at the hilum and then course medially
to the inferior vena cava. The right renal artery passes underneath the vena cava,
whereas the left renal vein passes over the aorta just under the superior mesenteric artery. Longitudinal images of the renal vessels are obtained with transverse
scanning. The segmental renal arteries and veins traverse the sinus before branching, which is distinctly different from the collecting system, which branches
within the sinus. This difference is important in distinguishing dilated vessels
from hydronephrosis. Arterial and venous pulsations are often visible and can be
used to identify vessels, but care should be exercised because the pulsations can
be transmitted from the artery to the adjacent vein. Doppler sonography is useful
in determining whether anechoic structures are vascular,' and color Doppler is
useful in delineating luminal masses and narrowing. 2 However, the diagnostic
utility of spectral analysis in native renal vessels remains controversial.
INTERPRETATION
he relationship between the kidneys and the aorta and vena cava can be seen
in coronal scans (Fig. 21-2), but the renal vessels are best seen in transverse
scans. The right renal vein is short and usually easily identified as it
branches off the vena cava (Fig. 21-3). The left renal vein crosses over the aorta
and under the superior mesenteric artery (Fig. 21-4). The appearance of the renal
veins depends on blood flow and central venous pressure, and they may not always be visible. The renal arteries can be seen branching off each side of the aorta
(Fig. 21-5) and then entering the kidney (Fig. 21-6) but can be difficult to visualize at the latter location. Intrarenal vessels are very rarely observed in normal kidneys because of their size and obscuration by sinus fat. An exception is the arcuate
arteries, which, when imaged on cross-section, produce small echogenic dots at
the corticomedullary junctions 3 (see Fig. 2-4).
168
Intralobular
arteries
R renal
vein
Superior
mesenteric
artery
L renal
artery
Interlobular
artery
Arcuate
artery
FIGURE 21-1
Diagram of the renal vasculature, anterior view. L,
left; R, right.
Segmental
artery
Inferior
R uteter vena cava
Aorta
L. renal
vein
FIGURE 2 1 - 2
Aorta and inferior vena cava. Coronal scans of (A) right
and (B) left kidneys (K) adjacent to the inferior vena cava
(V) and aorta (A). The renal vein is visible in the hilum
(arrows). P, psoas muscle.
ANATOMY OF THE RENAL VESSELS
169
A
B
FIGURE 2 1 3
Right renal vein. A. Transverse scan of the right kidney
(arrowheads) showing the renal vein (arrow) draining into
the vena cava (IVC). B. Oblique longitudinal scan showing
renal vein entering the inferior vena cava (IVC). The renal
vein branches at the hilum (arrowhead), outside the renal
pelvis, into segmental veins, one of which is visible (arrow)
entering the sinus.
Liver
SMA
SMV
IVC
LRV
Aorta
B
FIGURE 2 1 4
A. Midline transverse scan. B. Diagram identifying
structures. SMA, superior mesenteric artery; SMV, superior
mesenteric vein; LRV, left renal vein; IVC, inferior vena cava.
170
FIGURE 2 1 5
Origin of the renal arteries. A. Midline transverse scan.
B. Diagram identifying structures. SMA, superior
mesenteric artery; LRV, left renal vein; LRA, left renal
artery; RRA, right renal artery; IVC, inferior vena cava.
FIGURE 2 1 6
Renal artery and vein. Transverse view of left kidney
(arrowheads) showing renal artery (curved arrow) and renal
vein (straight arrow) at the renal hilum.
REFERENCES
1. Platt JF: Doppler ultrasound of the kidney. Semin Ultrasound CT MR 1997;18:22.
2. Helenon 0, Melki P, Correas J-M, et al: Renovascular disease: Doppler ultrasound. Semin Ultrasound CT MR 1997;18:136.
3. Cook JH, Rosenfield AT, Taylor KJW: Ultrasonic demonstration of intrarenal anatomy. Am J
Roentgenol 1977;129:831.
CHAPTER
2 2
Arterial Disorders
SONOGRAPHY
enovascular disease is an uncommon but potentially reversible cause of hypertension and an important cause of renal failure in the elderly and in patients with peripheral vascular disease. Acute infarction is a rare cause of
pain and hematuria. Thus, indications for sonography include chronic renal failure, hypertension, and pain. Evidence for arterial disease comes more from
changes produced in the renal parenchyma rather than from the appearance of the
renal arteries. Thus, when renovascular disease is being considered, discrepancies
in renal size and cortical thickness, as well as irregularities in the renal contour
due to infarcts, should be noted. Doppler and color Doppler sonography can aid
in visualizing the renal artery' and measuring flow, 2 ' 3 but even for experts, these
can be difficult studies.
RENAL ARTERY STENOSIS AND ISCHEMIC

NEPHROPATHY
enal artery stenosis can cause hypertension and, when bilateral, can produce renal failure. It should be considered in any older adult with recent
onset of hypertension.
Interpretation
The classic finding in renovascular disease is discrepancy in size of the two
kidneys (Fig. 22-1). In normal kidneys, the volume of the smaller kidney
should not be less than 37% of the combined renal volume. 4 Assuming that all
dimensions are affected equally, this translates into the smaller kidney having
a length not less than 84% of that of the larger kidney. For a normal renal
length of 10-12 cm, this would be a difference of 1.6-1.9 cm. Thus, a threshold of 2.0 cm is reasonable for diagnosing pathologic size discrepancy. Often,
the difference is larger owing to compensatory hypertrophy of the contralateral kidney. This is apparent in Fig. 22-1, which was obtained from a small
adult in whom a right kidney length of 12.1 is large. There should be other
signs of cortical atrophy such as cortical thinning and irregularity, and the absence of these should raise some doubt about the diagnosis of renovascular
disease. Significant unilateral stenosis can exist without size discrepancy, and
172
B
FIGURE 2 2 1
Renal artery stenosis. Longitudinal scans of (A) right and
(B) left kidneys in a patient with stenosis of the left renal
artery. In addition to being small, the left kidney has a
thin and slightly irregular cortex. (From O'Neill WC:
B
FIGURE 2 2 2
Calcification of the renal arteries. A. Longitudinal image of
left kidney shows the echogenic wall of an intrarenal artery
(arrows) and numerous faint, acoustic shadows emanating
from the renal sinus (arrowheads). B. Transverse image. The
wall of the renal artery is echogenic (arrow) and casts an
acoustic shadow (arrowheads).
ARTERIAL DISORDERS
173
FIGURE 2 2 3
Atherosclerotic aorta. Coronal scan of left kidney (arrowheads)
demonstrating an irregular aorta (A) with an infrarenal
aneurysm (arrow).
FIGURE 2 2 - 4
Fibromuscular dysplasia of the right renal artery. Transverse scan
showing beading of the renal artery (arrows). Star indicates aorta.
(From Helenon 0, Melki P, Correas J-M, et al: Renovascular
disease: Doppler ultrasound. Semin Ultrasound CT MR
renovascular disease is frequently bilateral, so size discrepancy has a low sensitivity for detecting renovascular disease. Occasionally, the appearance of the
vessels can be helpful. Calcification of the renal artery occurs in atherosclerosis and presents as multiple acoustic shadows emanating from the renal sinus
(Fig. 22-2), often with visible echogenic foci. 5 Frequently, there is atherosclerotic
involvement of the aorta as well, apparent as irregularity of the aortic wall,
which, when severe, becomes aneurysmal (Fig. 22-3). Beading of the renal
artery is suggestive of fibromuscular dysplasia (Fig. 22-4). Doppler sonography reveals high velocity and turbulence at the stenotic site. 2 ' 3 When the entire renal artery cannot be investigated, which is common, spectral analysis of
intrarenal tracings can provide information. Although excellent sensitivities and
specificities have been reported," the use of duplex scanning to screen for renal artery stenosis is controversial and probably feasible only in select centers
with specific expertise in this area.2
Advanced renal disease of many causes can produce cortical thinning but should
not be unilateral. Cortical thinning and scarring are also seen with reflux
nephropathy (see Fig. 13-1), but the caliectasis often observed is not seen in ischemic nephropathy.
174
I NFARCTION
egmental infarction is usually the result of emboli, either from the heart or
aorta, whereas global infarction can occur with aortic dissection or severe
shock (bilateral cortical necrosis). An unusual form of ischemia associated
with renal failure and pain occurs after strenuous exercise.6
Interpretation
Acute infarction presents as localized, hypoechoic swelling due to edema (Fig.
22-5). This resolves over several days, eventually becoming echogenic 7-9 (Fig.
22-6). The involved cortex may eventually involute, producing focal thinning
(Fig. 22-7). Multiple wedge-shaped hypoechoic lesions have been reported in
cases of acute renal failure after prolonged, strenuous exercise 6 and presumably
represent edema from ischemic injury. Bilateral cortical necrosis presents initially
FIGURE 2 2 - 5
Acute renal infarction. A. Longitudinal and (B) transverse
scans of the right kidney in a patient who developed acute
flank pain after percutaneous transluminal angioplasty of
the right renal artery. There is a hypoechoic mass in the
upper pole (arrowheads) that (C) was not apparent the
following day. (From O'Neill WC: Sonographic evaluation
of renal failure. Am J Kidney Dis 2000;35:1021, with
permission.)
ARTERIAL DISORDERS
FIGURE 22- 6
Renal infarct. Longitudinal image of left kidney showing a
portion of the lower pole cortex replaced with hyperechoic scar
(arrow). (From Erwin B, Carroll BA, Walter JF, et al: Renal
infarction appearing as an echogenic mass. AJR 1982;138:759,
with permission.)
FIGURE 2 2 - 7
Old infarct. Longitudinal scan of a renal allograft with
previous infarction of the lower pole due to arterial
thrombosis. There is focal thinning of the cortex (arrows) of
much of the lower pole. A stone, which was present at the
time of transplantation, is also present in the lower pole
(arrowhead). (From O'Neill WC: Sonographic evaluation of
renal failure. Am J Kidney Dis 2000;35:1021, with
permission.)
FIGURE 2 2 - 8
Cortical necrosis. Longitudinal image of left kidney in
patient with bilateral cortical necrosis secondary to septic
shock. There is a peripheral hypoechoic band of cortex
corresponding to infarcted tissue (arrows). (From O'Neill
WC: Sonographic evaluation of renal failure. Am J Kidney
Dis 2000;35:1021, with permission.)
with cortical swelling due to a circumferential, hypoechoic band just underneath

the cortex (Fig. 22-8), corresponding to the band of cortical infarction w- 12 and presumably representing edema. Calcification along the infarction boundary may be
observed within 1 week.11
Differentiation of other hypoechoic regions or lesions in the kidney from acute infarction is based on location and the fact that the edema from infarcts is transient.
Medullary pyramids do not extend to the cortex or distort the renal contour. Hypoechoic neoplasms can have the same appearance as acute infarctions and
echogenic scars can mimic hyperechoic neoplasms (see Chapter 17). The hypoechoic regions observed in acute pyelonephritis (see Fig. 9-2) can be transient and
truly mimic infarction but should be apparent from the clinical picture. The focal
cortical thinning in chronic pyelonephritis is usually associated with caliectasis (see
Fig. 13-1). An atrophic duplication can appear as a chronic infarct with focal loss
of parenchyma (see Fig. 3-5).
175
176
MALFORMATIONS
he category of malformations includes arteriovenous fistulas and
aneurysms. Fistulas are either acquired (traumatic) or congenital (arteriovenous malformation). 13 Traumatic fistulas are usually the result of percutaneous renal biopsy.
Interpretation
Fistulas are categorized as either cirsoid, which contain multiple arteriovenous
connections, or aneurysmal, which consist of a single dilated channe1. 13 The former appear as a large anechoic area, representing the collection of enlarged fistulous vessels, and attached tubular, anechoic structures that represent dilated
feeding and draining vessels (Figs. 22-9, 22-10). Fistulas and pseudoaneurysms
are occasionally observed after percutaneous biopsy and appear as cystic structures that
may be pulsatile and demonstrate high-velocity flow on Doppler sonog14,15
raphy.
Examples are presented in Chapter 29. Thrombus is often present in
fistulas (Fig. 22-9B). Aneurysms of the renal artery appear as cystic masses at the
renal hilum that can extend into the renal sinus 13,16 (Figs. 22-11, 22-12). They may
be pulsatile and contain a thrombus 13 (Fig. 22-12).
Arteriovenous malformations can mimic hydronephrosis, 17 with the malformation
appearing as a dilated pelvis, the feeding vessels appearing as enlarged major
calyces, and the renal vein being mistaken for the ureter. In hydronephrosis, however, the minor calyces should be dilated and the ureter tracks inferiorly. Aneurysms
FIGURE 2 2 9
Congenital arteriovenous malformation, cirsoid type. A. Longitudinal and (B) transverse images of right kidney containing
a large anechoic region (M) that represents a collection of enlarged, fistulous vessels. The enlarged arteries and veins that
feed and drain the malformation appear as anechoic tubular structures (arrows). Curved arrow in Figure B indicates
echogenic thrombus in the dilated renal vein. L, liver; c, dilated calyx; I, inferior vena cava; A, aorta. (From Subramanyam
BR, Lefleur RS, Bosniak MA: Renal arteriovenous fistulas and aneurysm: Sonographic findings. Radiology 1983;149:261,
with permission.)
ARTERIAL DISORDERS
177
and aneurysmal fistulas may be indistinguishable from peripelvic cysts (see Figs.
10-9, 10-10), but the latter usually do not extend outside the renal sinus and are
not pulsatile. An extrarenal pelvis (see Fig. 3-14) also has an appearance similar to
that of a renal artery aneurysm. Differentiation of cortical cysts from fistulas requires Doppler sonography to demonstrate flow.
FIGURE 2 2 - 1 0
Arteriovenous fistula. Longitudinal scan of right kidney
showing an anechoic cyst (C) with dilated feeding and
draining vessels (arrows), confirmed as a fistula on
angiography. There was no history of trauma. (From Ha SK, Park C-H, Kim K-W: Use of pulsed Doppler ultrasound
in detecting renal arteriovenous fistula. Nephrol Dial
Transplant 1995;10:2150, with permission.)
FIGURE 2 2 - 1 1
Renal artery aneurysm. Longitudinal scan of left kidney
(LK) demonstrating a large cystic mass (arrows) at the renal
hilum. (From Kwon HS, Shin JS, Yun SN, et al: Renal artery
aneurysm manifested as parapelvic cyst on abdominal
sonography. Nephron 1996;74:229, with permission.)
FIGURE 2 2 - 1 2
Renal artery aneurysm with thrombus. Transverse image
of right kidney (arrowheads) through the hilum showing a
large cystic mass (arrows) consisting of lumen (L) and mural
thrombus (T). (From Subramanyam BR, Lefleur RS, Bosniak
MA: Renal arteriovenous fistulas and aneurysm:
Sonographic findings. Radiology 1983;149:261, with
permission.)
178
REFERENCES
1. Helenon 0, Melki P, Correas J-M, et al: Renovascular disease: Doppler ultrasound. Semin Ultrasound CT MR 1997;18:136.
2. Platt JF: Doppler ultrasound of the kidney. Semin Ultrasound CT MR 1997;18:22.
3. Hansen KJ, Tribble RW, Reavis SW, et al: Renal duplex sonography: evaluation of clinical utility.
J Vasc Surg 1990;12:227.
4. Rasmussen SN, Haase L, Kjeldsen H, et al: Determination of renal volume by ultrasound scanning.
5. Kane RA, Manco LG: Renal arterial calcification simulating nephrolithiasis on sonography. AIR
1983;140:101.
6. Sakemi T, Ikeda Y, Matsuo Y, et al: Renal wedge-shaped lesions on computed tomography and
ultrasonography in two patients who developed acute renal failure with severe loin pain after
exercise. Nephron 1996;73:679.
7. Spies JB, Hricak H, Slemmer TM, et al: Sonographic evaluation of experimental acute renal arterial
occlusion in dogs. AIR 1984;142:341.
8. Becker JA, Butt K, Lipkowitz G: Segmental infarction of the renal allograft: Ultrasound /MRI observations. Urol Radiol 1989;11:109.
9. Erwin B, Carroll BA, Walter JF, et al: Renal infarction appearing as an echogenic mass. AIR
1982;138:759.
10. Voss DM, Bailey RR, Gardner J, et al: Diagnosis of cortical infarction in a renal transplant using
ultrasonography. Nephron 1994;68:378.
11. Smith LE, Adelman RD: Early detection of renal cortical calcification in acute renal cortical necrosis in a child. Nephron 1981;29:155.
12. Sefczek RJ, Beckman I, Lupetin AR, et al: Sonography of acute renal cortical necrosis. AIR
1984;142:553.
13. Subramanyam BR, Lefleur RS, Bosniak MA: Renal arteriovenous fistulas and aneurysm: Sonographic findings. Radiology 1983;149:261.
14. Hubsch PJS, Mostbeck G, Barton PB, et al: Evaluation of arteriovenous fistulas and pseudoaneurysms in renal allografts following percutaneous needle biopsy: Color-coded Doppler sonography versus duplex Doppler sonography. J Ultrasound Med 1990;9:95.
15. Weissman J, Giyanani VL, Landreneau MD, et al: Postbiopsy arterial pseudoaneurysm in a renal
allograft: Detection by duplex sonography. J Ultrasound Med 1988;7:515.
16. Kwon HS, Shin JS, Yun SN, et al: Renal artery aneurysm manifested as parapelvic cyst on abdominal sonography. Nephron 1996;74:229.
17. Kember PG, Peck RJ: Renal arteriovenous malformation mimicking hydronephrosis. J Clin Ultrasound 1998;26:95.
CHAPTER
2 3
Venous Disorders
SONOGRAPHY
enous disorders are usually incidental findings unrelated to the indication

for sonography. However, sonography may be performed for worsening
renal function in patients at risk for thrombosis or in patients with pain
and hematuria. The renal vein and occasionally its branches can be seen in normal people, particularly children and young adults, but are rarely prominent. To
distinguish them from ureters or calyces, follow them to their confluence with the
vena cava and examine them for venous pulsations and for dilation during
Valsalva's maneuver. Dilated veins and the vena cava should be examined carefully for luminal echogenicity that could represent thrombus or tumor.
VENOUS ENGORGEMENT
ncreased venous pressure is transmitted to the renal veins and is seen in such
conditions as congestive heart failure, pulmonary hypertension, nephrotic syndrome, and cirrhosis. Dilation of the renal veins is also common in nephritis,
presumably reflecting increased blood flow. The importance in recognizing venous congestion of the kidneys is to avoid mistaking it for hydronephrosis and to
gain some insight into the status of the patient's intravascular volume.
Interpretation
Dilated renal veins exhibit branching at the renal hilum and then extend directly
to the parenchyma with little if any branching in the sinus (Fig. 23-1). Venous
walls should be thin. The renal vein should follow a medial course toward the
vena cava, which is usually dilated as well (Fig. 23-2).
Venous engorgement and hydronephrosis are often confused, but careful scanning
can easily differentiate between them. The collecting system branches within the
renal sinus and has the appearance of a pruned tree (see Figs. 13-4, 13-15). The renal vein branches outside the sinus and the branches extend to the parenchyma,
with few branches in the sinus, a branching pattern more reminiscent of a bush.
Furthermore, the ureter tracks inferiorly (see Fig. 13-13) as opposed to the medial
path of the renal vein. Renal arteries have a smaller caliber (unless aneurysmal) and
thicker walls. In renal vein thrombosis (Fig. 23-3), the veins are usually quite large
and contain thrombi.
180
FIGURE 23-1
Dilated renal veins. Longitudinal view of a renal allograft
showing a dilated renal vein (V) that branches at the hilum
into multiple segmental veins (arrows). The segmental veins
extend directly to the parenchyma without branching.
FIGURE 23-2
Dilated renal vein. Oblique transverse scan of right kidney
showing dilated renal vein (arrow) draining into the vena
cava (IVC). A, aorta; L, liver.
THROMBOSIS
enal vein thrombosis is a rare but important and reversible cause of renal
failure, occurring with increased frequency in patients with nephrotic syndrome, antiphospholipid antibody syndrome, deficiencies of protein C or
protein S, and other thrombotic diatheses. This diagnosis should be seriously considered in the sonographic evaluation of any such patient with unexplained worsening of renal function or onset of pain and hematuria. Sonography is an excellent
diagnostic test, with an accuracy over 90%)
Interpretation
The classic findings are a large, echogenic kidney with a dilated renal vein containing echogenic thrombi 1 - 3 (Fig. 23-3). A progression of sonographic findings
has been described in this syndrome in neonates. 4 Initially, there is thrombosis of
intrarenal vessels that may be visible, particularly in neonates, as echogenic
streaks representing thrombosed interlobar veins (Fig. 23-4A). This is then followed by swelling and prominence of the medullary pyramids (Fig. 23-4B), eventually resulting in enlarged, echogenic kidneys with poor corticomedullary
VENOUS DISORDERS
181
FIGURE 2 3 - 3 ( left)
Renal vein thrombosis. A. Longitudinal image of a swollen
and echogenic right kidney with a markedly dilated renal
vein (V) containing echogenic clot (arrows). The striated
structure (arrowhead) is the psoas muscle. B. Transverse
image showing dilated vein (V) with thrombus (arrow).
C. Five months later, the kidney is no longer swollen and
the renal vein is not dilated. (From O'Neill WC:
FIGURE 2 3 -4 (above)
Neonatal renal vein thrombosis. A. Longitudinal scan of
right kidney with swelling of the upper pole and echogenic
intermedullary lines (arrows) representing thrombosed
interlobar veins. B. Longitudinal scan showing prominent
and swollen medullary pyramids (arrows). (From Hibbert J,
Howlett DC, Greenwood KL, et al: The ultrasound
appearances of neonatal renal vein thrombosis. Br J Radiol
182
FIGURE 2 3 5
Renal vein thrombosis with thrombus in vena cava.
Longitudinal scan of inferior vena cava (V) containing
an echogenic clot (arrow). (Photo courtesy of Dr. D.
Baumgarten.)
differentiation. Because patients with nephrotic syndrome may have dilated renal
veins on the basis of intravascular volume expansion, and because the kidneys
may be swollen and echogenic owing to the underlying glomerulonephritis, the
diagnosis requires the demonstration of thrombus within the lumen. Often, the
thrombus extends into the vena cava (Fig. 23-5). Because other causes of enlarged,
echogenic kidneys are bilateral, unilateral findings are very suggestive of renal
vein thrombosis.
Swollen, echogenic kidneys with dilated renal veins also occur in glomerulonephritis (see Fig. 6-5) and interstitial nephritis (see Fig. 8-1) but the venous dilation is
usually less and the lumen of the veins should be free of echoes. Acute tubular
necrosis can also produce enlarged echogenic kidneys (see Fig. 7-2) but the kidneys do not usually appear swollen and the veins are not dilated unless volume
overload is present. Renal involvement is symmetric in both these disorders,
which is not necessarily the case in renal vein thrombosis. Tumor thrombus (see Fig.
17-10) is usually associated with a renal mass.
RENAL VEIN ENTRAPMENT
his syndrome has been described in children and young adults with unexplained left flank pain and hematuria, 5 and it also appears to cause orthostatic proteinuria. 6 ' 7 The symptoms and findings are thought to result from
increased venous pressure due to compression of the left renal vein as it passes
between the aorta and the superior mesenteric artery. Renal vein entrapment is
also seen with the rare anomaly of retroaortic renal vein. 8 This diagnosis should
be considered in any child with unexplained episodes of hematuria.
Interpretation
Sonography reveals dilation of the left renal vein with an otherwise normal left
kidney, and normal findings on the right. The dilated vein tapers abruptly where
it crosses over the aorta and under the superior mesenteric artery (Fig. 23-6).
Compression of the vein by the superior mesenteric artery can be relieved by placing the patient in the decubitus or prone position. 5 Because dilation of the left
VENOUS DISORDERS
FIGURE 2 3 - 6
Renal vein entrapment. Transverse midline scan. The
proximal left renal vein (straight arrow) is dilated because of
compression by the aorta and superior mesenteric artery
(arrowheads). The distal vein (curved arrow) is of normal
caliber.
FIGURE 2 3 - 7
Intrarenal varices. Coronal view of right kidney in a patient
with portal hypertension showing two large cystic areas
(arrows) in the renal sinus, one of which is elongated. (From
Erden A, Ozcan H, Aytac S, et al: Intrarenal varices in
portal hypertension: demonstration by color Doppler
imaging. Abdominal Imaging 1996;21:549, with permission.)
renal vein upstream of the aorta is common in children, 5 strict criteria should be
employed for this diagnosis. 9 Three parameters can be used: the ratio of the diameters of the dilated and narrowed portions of the left renal vein (>3.7), the ratio of the diameters of the dilated vein and the aorta (>0.75), and the difference in
maximum diameters of the left and right renal veins (>1.7 mm). In a large series
of children, two or more of these criteria were present in over 90% of children with
idiopathic macroscopic hematuria and in none of the normal children.'
A dilated ureter should track inferiorly rather than medially (see Fig. 13-13A) and
an extrarenal pelvis (see Fig. 3-14) should not extend to the aorta. In renal vein
thrombosis (Fig. 23-3), thrombi are visible in the lumen, and the kidney is enlarged
and echogenic.
VARICES
183
ntrarenal varices are dilated branches of the renal vein within the kidney. They
are associated with portal hypertension or renal vein obstruction but can be
idiopathic and discovered during investigation of hematuria.'
Interpretation
Varices usually occur on the left and appear as fluid-filled, anechoic structures
(Fig. 23-7), occuring anywhere in the venous drainage from the renal parenchyma
to the extrarenal portion of the vein.'- 13 Doppler studies reveal a venous flow
pattern.12,13
184
Dilated calyces and parapelvic cysts (see Figs. 10-9, 10-10) usually do not extend beyond the renal pelvis but otherwise cannot be distinguished from varices without
the benefit of Doppler sonography or angiography. Renal artery aneurysms (see Fig.
22-11) have an appearance identical to that of extrarenal varices and distinction
requires Doppler sonography.
REFERENCES
1. Ricci MA, Lloyd DA: Renal venous thrombosis in infants and children. Arch Surg 1990;125:1195.
2. Braun B, Weilemann LS, Weigand W: Ultrasonographic demonstration of renal vein thrombosis.
Radiology 1981;138:157.
3. Barre P, Bishinsky J, Roy D, et al: Successful treatment with streptokinase of renal vein thrombosis
associated with oral contraceptive use. Am I Nephrol 1986;6:316.
4. Hibbert J, Howlett DC, Greenwood KL, et al: The ultrasound appearances of neonatal renal vein
thrombosis. Br J Radiol 1997;70:1191.
5. Wolfish NM, McLaine PN, Martin D: Renal vein entrapment syndrome: Frequency and diagnosis.
A lesson in conservatism. Clin Nephrol 1986;26:96.
6. Lee SJ, You ES, Lee JE, et al: Left renal vein entrapment syndrome in two girls with orthostatic proteinuria. Pediatr Nephrol 1997;11:218.
7. Shintaku N, Takahashi Y, Akaishi K, et al: Entrapment of left renal vein in children with orthostatic
proteinuria. Pediatr Nephrol 1990;4:324.
8. Reed MD, Friedman AC, Nealey P: Anomalies of the left renal vein: Analysis of 433 CT scans.
I Contput Assist Tomogr 1982;6:1124.
9. Okada M, Tsuzuki K, Ito S: Diagnosis of the nutcracker phenomenon using two-dimensional ultrasonography. Clin Nephrol 1998;49:35.
10. Beckmann CF: Idiopathic renal vein varices: Incidence and significance. Radiology 1982;143:649.
11. Spira R, Kwan E, Gerzof SG, et al: Left renal vein varix simulating a pancreatic pseudocyst by
sonography. AIR 1982;138:149.
12. Takahashi M, Ohishi H, Hirai T, et al: Intrarenal varices: Demonstration by color Doppler sonography. I Ultrasound Med 1998;17:517.
13. Erden A, Ozcan H, Aytac S, et al: Intrarenal varices in portal hypertension: demonstration by color
Doppler imaging. Abdom Imaging 1996;21:549.
RENAL
TRAUMA
CHAPTER
2 4
Renal Trauma
W. Charles O'Neill, John P. McGahan, and John R. Richards
SONOGRAPHY
njury to a kidney can arise from blunt abdominal trauma and from procedures
such as percutaneous biopsy. Spontaneous hemorrhage can occur in cases of
carcinoma, angiomyolipoma, vascular disease, and infection. 1 '2 Indications for
sonography include pain, hematuria, or a history of trauma. Sonography is useful
in evaluating patients with blunt renal trauma, with abnormalities detected in one
third to one half of patients with hematuria, and essentially for all patients with
major injuries. 3-5 Thus, sonography is a useful screening test in renal trauma.3,4'6
The abnormalities are primarily the presence of retroperitoneal or intraperitoneal
fluid, which is easily diagnosed by sonography. Renal parenchymal abnormalities
such as lacerations or hematomas are more difficult to detect,' but severe
parenchymal injury is usually recognized by sonography. 5 ' 7 Bilateral, traumatic
renal injury is rare. 3A Sonography is extremely useful in diagnosing or excluding
significant hemorrhage following renal biopsy.
HEMATOMA
etroperitoneal hemorrhage is common after blunt trauma. 3' 6 Small retroperitoneal and subcapsular hematomas are common after percutaneous biopsy8
but are rarely large or clinically significant. 9 Hematomas can be subcapsular, perirenal, or outside the perirenal space either in the retroperitoneum or the
surrounding muscles.
Interpretation
The appearance depends on the age and location of the hematoma. Acute
hematomas are usually well marginated and either hypoechoic (Figs. 24-1, 24-2)
or of heterogeneous echogenicity owing to the presence of clot (Figs. 24-3, 24-4).
Subcapsular hematomas displace and compress the renal parenchyma (Fig. 24-1).
Subcapsular and parenchymal hemorrhage can arise from rupture of a cyst in
which case the cyst is visible with echogenic clot within (see Fig. 24-1). Perirenal
hematomas are immediately adjacent to the kidney and can dissect all the way
around to the renal pedicle (see Fig. 24-2). Sizable hematomas may also occur in
the musculature and appear as heterogeneous masses containing both clotted and
unclotted blood, posterior to the kidney (see Fig. 4-4).
188
FIGURE 2 4 - 2
Perirenal hematoma. Longitudinal image of the left kidney
after a sonographically guided biopsy demonstrating a
hypoechoic hematoma (arrows) dissecting along the
perimeter of the kidney.
FIGURE 2 4 - 1
Subcapsular hematoma. A. Longitudinal and (B) transverse
images of the left kidney obtained after a computed
tomograph-guided renal biopsy showing a large
hypoechoic hematoma (H) compressing the parenchyma
(K). A cyst (arrow) noted to be simple on scanning prior to
biopsy now contains echogenic material, suggesting that
the hematoma arose from rupture of the cyst.
RENAL TRAUMA
189
FIGURE 2 4 3
Retroperitoneal hematoma. Longitudinal scan showing a
large hematoma (arrows) in the posterior pararenal space
behind the kidney (K) in this patient involved in a motor
vehicle accident. Gerota's fascia is visible as an echogenic
line separating the hematoma from the kidney. (From
McGahan JP, Richards JR, Jones CD, et al: Use of
ultrasonography in the patient with acute renal trauma.
J Ultrasound Med 1999;18:207, with permission.)
FIGURE 2 4-4
Large pararenal hematoma. Longitudinal scan showing a
large heterogeneous mass in the anterior pararenal space
(arrows) displacing the kidney (K) in a 9-year-old hit by an
automobile. Gerota's fascia can be seen separating the
hematoma from the kidney. At surgery, there was complete
avulsion of the renal pedicle, requiring nephrectomy.
Urinomas also appear as perirenal fluid collections and occur with trauma but are
usually homogeneous with little if any echogenicity. Perinephric fat (see Fig. 1-11)
can occasionally be hypoechoic and mimic a fluid collection. A perirenal abscess (see
Fig. 9-7) may also be confused with a perirenal hematoma. An abscess will usually appear less echogenic than a retroperitoneal hematoma. However, some abscesses may have mixed echogenicity or appear echogenic, owing to debris. Renal
cell carcinoma (see Chapter 17) should be considered in the differential diagnosis of
any renal or perirenal mass. The history of trauma is important in distinguishing
between these masses. Additionally, renal cell carcinoma usually appears as a
mass within the kidney, although some renal cell carcinomas may be exophytic.
Other peritoneal neoplasms, such as Wilms' tumor, neuroblastoma, sarcoma, and lymphoma, may be considered in the differential diagnosis. Again, patient age and lack
of recent major trauma are important differential points. However, some patients
with tumors may give a medical history of minor trauma as a reason for seeking
medical attention, and tumors can produce spontaneous hemorrhage.12
CALYCEAL HEMORRHAGE
ross hematuria is usually a sign of clinically important renal injury and can
result in significant blood loss. Additionally, blood clots can lead to urinary
obstruction.
190
FIGURE 24-5
Calyceal hemorrhage. A. Longitudinal scan of a renal
allograft after biopsy of the lower pole. The calyces are
dilated and there is echogenicity in a major calyx draining
the lower pole (arrows,) consistent with clotted blood.
B. Transverse scan showing a dilated plevis distended
with echogenic blood clot (arrow).
Interpretation
The sonogram shows a dilated pelvocalyceal system, often with echogenic clots
(Fig. 24-5). Blood may also be visible in the bladder (see Fig. 14-21).
Pyonephrosis (see Figs. 9-10, 9-11) also presents with calyceal dilation with luminal echogenicity but should not produce hematuria. Stones can also produce hydronephrosis and/or hematuria with luminal echogenicity (see Fig. 15-8) but
usually cast acoustic shadows. Transitional cell carcinoma (see Chapter 18) should
always be considered in the differential diagnosis of dilated calyces with an infraluminal mass.
RENAL TRAUMA
RENAL CONTUSION
ontusion is the most common finding in renal trauma, 1 presenting as

hematuria without significant parenchymal injury.
Interpretation
Sonography should show an intact renal capsule with no perirenal or retroperitoneal hematoma. 6 Abnormalities are limited to intrarenal hematomas and subcapsular hematomas, 4 ' 6 and sonographic findings are frequently normal.4
Parenchymal hematomas initially present as focal hypoechoic regions (Fig. 24-6)
with or without distortion of the renal contour.
Infarction (see Fig. 22-5) has the same appearance as an intrarenal hematoma and
can occur with trauma. Other causes of hypoechoic lesions (carcinoma, lymphoma,
or abscess) are not usually diagnostic considerations in the setting of trauma, but
patients with these lesions may seek medical attention because of minor trauma.
Renal cell carcinomas are often incidental findings.
FIGURE 2 4 - 6
Intraparenchymal hematoma. Longitudinal view of left
kidney showing a hypoechoic mass in the upper pole
(arrows and cursors). (From Furtschegger A, Egender G,
Jakse G: The value of sonography in the diagnosis and
follow-up of patients with blunt renal trauma. Br J Urol
191
192
RENAL LACERATION AND AVULSION

e nal lacerations result from direct trauma to the kidney and/or the retroperitoneum. They may be minor or may extend deep into the parenchyma,
Resulting in severe renal injury. Damage to the renal pedicle results from
severe injury to the retroperitoneum.1
Interpretation
Most renal lacerations are not identified by ultrasound 3,7, " because they are small
and are often isoechoic with the rest of the kidney. When visible, they appear as a
bulge in the renal contour, often with a corresponding wedge-shaped defect in the
renal parenchyma (Fig. 24-7) that can range from hypoechoic to hyperechoic. 4 ' 6 A
perirenal hematoma is almost always present. 3 ' 4 ' 6' 7 With severe renal lacerations
(fracture), the kidney is completely disorganized and may appear as a heterogeneous mass (Fig. 24-8). Injury to the renal pedicle, including avulsion, is not visible as such but the sonogram is usually abnormal due to concurrent kidney
fracture with complete loss of the renal contour or because of surrounding
hematoma (Fig. 24-4). Color flow or pulsed Doppler ultrasound has not been routinely utilized to demonstrate lack of normal arterial flow to the kidney in these
injuries.
In the setting of trauma, the differential diagnosis includes intraparenchymal
hematoma (Fig. 24-6), which can produce a mass effect. An infarct can also distort
the renal contour (see Fig. 22-5). However, these lesions should not result in
perirenal hematomas, which are almost always seen with lacerations.
FIGURE 2 4 7
Renal laceration. Longitudinal scan of the left kidney shows a wedge-shaped
hypoechoic defect (arrows) with bulging of the renal contour. (From
Furtschegger A, Egender G, Jakse G: The value of sonography in the
diagnosis and follow-up of patients with blunt renal trauma. Br J Urol
RENAL TRAUMA
193
FIGURE 2 4- 8
Fractured kidney. Longitudinal scan showing completely
disorganized appearance to the kidney (between arrows) in a
patient with a severely fractured kidney.
FIGURE 2 4 - 9
Urinoma. Longitudinal scan from a patient with a
neurogenic bladder shows a large anterior fluid collection
(cursors) compressing the kidney (K). (From Kennelly MJ,
Ritchey ML: Perinephric urinoma secondary to neurogenic
bladder in myelodysplasia. J Llrol 1995;153:458, with
permission.)
URINOMA
erirenal urinomas are uncommon and are the result of leakage from the collecting system or proximal ureter due to obstruction or to direct trauma.12
Interpretation
Urine leaks appear as simple fluid collections (Fig. 24-9) that may completely surround the kidney. 13 In the case of trauma, associated abnormalities such as lacerations may be visible (Fig. 24-10). Inflammation induced by urine can lead to
thickening and irregularity of the wall with echogenic debris within the lumen.12
194
FIGURE 24-10
Laceration with urinoma. A. Longitudinal scan shows a
urine collection separating the two renal fragments
(arrowheads). B. Repeat scan immediately after percutaneous
drainage of the urinoma shows apposition of the two
fragments. (From Wilkinson AG, Haddock G, Carachi R:
Separation of renal fragments by a urinoma after renal
trauma: Percutaneous drainage accelerates healing. Pediatr
Radio' 1999;29:503, with permission.)
Hematomas are usually more heterogeneous with echogenic clot. Ascites (see Fig.
1-12) should be separated from the kidney by fascia and fat tissue.
PERITONEAL FLUID
ignificant renal injury may result in intraperitoneal fluid or blood. Free fluid
can be detected by sonography in the majority of patients with renal traumas
but may also arise from injury to other organs because it is seen in only one
third of patients with isolated renal trauma. 3 In some patients requiring nephrectomy due to significant renal injury, there may be no evidence of hemoperitoneum
on ultrasound examination.'' It is important that the patient's bladder be full to
provide an adequate acoustic window when one is trying to detect peritoneal
fluid in the pelvis.
RENAL TRAUMA 195
FIGURE 2 4 - 1 1
Free peritoneal fluid. Transverse scan through the pelvis
shows free fluid (curved arrow) posterior to the bladder.
Interpretation
Peritoneal fluid and/or blood will usually localize in the hepatorenal fossa
(Morison's pouch) or in the pelvis (Fig. 24-11). Fluid in the pelvis is common, as
the pelvis is the most dependent portion of the peritoneal cavity. The fluid may be
echogenic but is more often anechoic in appearance. The free fluid in the pelvis
can be missed without using the full-bladder technique.
Other fluid collections should be considered. Physiologic free fluid may occur in the
pelvis of ovulating adolescents and women. This is usually a small collection seen
in the cul-de-sac. Ascitic fluid (see Fig. 1-12) is usually of a greater volume and is
often visible in the upper abdomen. Retroperitoneal fluid collections (hematomas
or urinomas) are localized and cannot distribute into dependent areas.
REFERENCES
1. Belville JS, Morgentaler A, Loughlin KR, et al: Spontaneous perinephric and subcapsular renal
hemorrhage: Evaluation with CT, US, and angiography. Radiology 1989;172:733.
2. Bosniak MA: Spontaneous subcapsular and perirenal hematomas. Radiology 1989;172:601.
3. McGahan JP, Richards JR, Jones CD, et al.: Use of ultrasonography in the patient with acute renal
trauma. J Ultrasound Med 1999;18:207.
4. Rosales A, Arango 0, Coronado J, et al: The use of ultrasonography as the initial diagnostic exploration in blunt renal trauma. Urol Int 1992;48:134.
5. McGahan JP, Rose J, Coates TL, et al: Use of ultrasonography in the patient with acute abdominal
trauma. J Ultrasound Med 1997;16:653.
6. Furtschegger A, Egender G, Jakse G: The value of sonography in the diagnosis and follow-up of
patients with blunt renal trauma. Br J Urol 1988;62:110.
7. Jakse G, Furtschegger A, Egender G: Ultrasound in patients with blunt renal trauma managed by
surgery. J Urol 1987;138:21.
8. Kim D, Kim H, Shin G, et al: A randomized, prospective, comparative study of manual and automated renal biopsies. Am J Kidney Dis 1998;32:426.
9. Nass K, O'Neill WC: Bedside renal biopsy: Ultrasound guidance by the nephrologist. Am J Kidney
Dis 1999;34:955.
10. Cass AS, Luxenberg M, Gleich P, et al: Clinical indications for radiographic evaluation of blunt
renal trauma. J Urol 1986;136:370.
11. McGahan JP, Richards JR: Blunt abdominal trauma: The role of emergent sonography and a review
of the literature. AIR 1999;172:897.
Tract. Philadelphia, WB Saunders; 1999; pp 542-545.
13. Tien R, Shirkhoda A, David R: Circumferential perirenal urinoma mimicking nephromegaly on
urography. Urol Radiol 1989;11:92.
14. Shanmuganathan K, Mirvis SE, Sherbourne CD, et al: Hemoperitoneum as the sole indicator of abdominal visceral injuries: A potential limitation of screening abdominal US for trauma. Radiology
1999;212:423.
Sonography
of the
Normal Allograft
SONOGRAPHY
enal allografts are most commonly placed below the peritoneum in the iliac
fossa (Fig. 25-1). The vessels are usually anastomosed to the external iliac
vessels, with the common iliac vessels used in certain cases. In infants, the
allograft is placed behind the cecum, with vascular anastomosis to the aorta and
vena Cava' (Fig. 25-2). Kidneys from very young donors are often transplanted
en bloc with the donor vessels, and the donor aorta and inferior vena cava are
anastomosed to the native vessels 1 ' 2 (Fig. 25-3). Patients should be examined in the
supine position with initial imaging parallel to the incision. The first task is to determine the orientation of the allograft, which usually lies beneath the surgical incision but can have a variable position and orientation because it is restrained only
by its pedicle. Understanding the orientation facilitates obtaining the necessary
images and will indicate when certain images are not obtainable. Any structures
adjacent to the allograft should be defined and identified. Real-time observations
of peristalsis (indicating intestines), pulsations (indicating vessels), or movement
with flexion of the leg at the hip (indicating psoas muscle) are useful in this
regard.
Vena cava
Aorta
Cecum
FIGURE 25-1
corn. iliac a.
corn. iliac v.
int. iliac a., v.
Anatomy of a renal allograft in the right iliac

fossa. a., artery; corn., common; v., vein.
Allograft
ext. iliac a.
Bladder
ext. iliac v.
Ureter
200
Renal Vein- Vena Cava

Anostomosis
Renal Artery-Distal Aorta

Anastomosis
Cec um
FIGURE 2 5 - 2
Anatomy of a renal allograft in an infant.
(From Hanto DW, Simmons RL: Renal
transplantation: Clinical considerations.
Radiol Clin North Am 1987;25:239, with
permisson.)
FIGURE 2 5 - 3
Anatomy of en bloc transplantation of a pair of kidneys
into the right iliac fossa. The proximal ends of the donor
aorta (straight arrow) and vena cava (curved arrow) are
oversewn, and the distal ends are anastomosed to the
external iliac vessels of the recipient. (From Memel DS,
Dodd GD, Shah AN, et al: Imaging of en bloc renal
transplants: Normal and abnormal postoperative findings.
AIR 1992;160:75, with permission.)
INTERPRETATION
here are only slight differences between the sonographic appearance of renal allografts and that of native kidneys. However, the perirenal anatomy
differs substantially and is important in recognizing many of the abnormalities that occur after renal transplantation.
Perirenal Anatomy
The sonographic anatomy of an allograft placed in the right iliac fossa is shown in
Fig. 25-4. The location and orientation can vary tremendously, even to the extent
that the longitudinal axis is perpendicular to the skin (Fig. 25-5). Because of its
proximity to the skin and the lack of overlying bowel, the ureter is often visible
even when not obstructed (Fig. 25-6). It tracks directly to the bladder, which lies
SONOGRAPHY OF THE NORMAL ALLOGRAFT
201
FIGURE 25-4
Perirenal anatomy of a renal allograft in right iliac fossa.
Longitudinal scan of allograft shows the lower (medial)
pole (K), the psoas muscle (P), the external iliac vessels
(arrow), and the bladder (B).
FIGURE 25-5
Perpendicular orientation of a renal allograft. Transverse
view of the right pelvis demonstrating a renal allograft
whose longitudinal axis is oriented anteroposteriorly,
perpendicular to the probe. The renal veins are prominent
(arrows).
medial to the allograft and often in close proximity (Fig. 25-4). The renal vein and
artery can often be visualized in the renal hilum (Fig. 25-5). The artery has a
thicker wall and exhibits arterial pulsations, but these pulsations can be transmitted to the adjacent vein. Distinction between artery and vein is usually not necessary during routine scanning. Care must be taken in distinguishing dilated veins
from hydronephrosis (Fig. 25-6). The vein branches at the hilum, outside the renal sinus (see Chapter 21). The renal vein tracks posteriorly to the external iliac
vein, which is usually directly underneath the lower (medial) pole, as opposed to
the medial path of the ureter to the bladder. With a standard allograft position, the
iliac vessels pass underneath perpendicular to the longitudinal axis of the allograft. With longitudinal imaging of the allograft, they will usually appear in crosssection, whereas transverse imaging of the allograft will visualize the vessels
longitudinally (Fig. 25-7). In kidneys that are transplanted en bloc, the renal vessels track to the donor aorta and vena cava, which lie between the kidneys
(Fig. 25-8).
The peritoneum is often visible as it reflects over a portion of the allograft, appearing as a beaklike projection containing heterogeneous material (liquid, solid,
gas) typical of intestine (Fig. 25-9). Herniated bowel can appear as a complex
mass immediately adjacent to the allograft 3 (Fig. 25-10). Another structure that is
202
B
FIGURE 25-6
Venous engorgement of a renal allograft. A. Longitudinal
view of allograft shows dilated veins branching from the
hilum (arrow). There is no further branching until the veins
reach the cortex, a pattern distinctly different from that of
the collecting system. The ureter (arrowhead) is just under
the lower (medial) pole tracking medially toward the
bladder. B. Transverse image of an allograft (arrowheads)
from a different patient showing a dilated renal vein
(arrows) tracking posteriorly to the external iliac vein.
B
FIGURE 25-7
External iliac vessels. A. Longitudinal scan of the lower
( medial) pole of a renal allograft (K) shows the external
iliac vessels (arrows) in cross-section. The psoas muscle (P)
is also visible in cross-section. B. Transverse image of renal
allograft (K) shows iliac artery (A) and vein (V) passing
underneath. The psoas muscle is also visible (P).
SONOGRAPHY OF THE NORMAL ALLOGRAFT
203
FIGURE 2 5 - 8
Paired kidneys transplanted en bloc. Transverse image of
both kidneys (arrowheads) at the level of the pelvis of the
right donor kidney. The right renal vein (arrows) can be seen
draining into the donor vena cava and the donor aorta
(curved arrow) is adjacent to the left kidney.
FIGURE 2 5 - 9
Peritoneum overlying renal allograft. Longitudinal image
of a renal allograft (K) demonstrating the beaklike
projection of the peritoneum (arrowhead) over the allograft.
Individual bowel loops are visible (arrows).
FIGURE 2 5 - 1 0
Herniated bowel adjacent to renal allograft. Transverse
image of allograft (K) with a large, complex anterior fluid
collection (arrows) containing bowel loops.
204
FIGURE 2 5 - 1 1
Psoas muscle. Transverse scan of allograft (K) provides a
longitudinal image of the psoas muscle (P) and the iliac
vessels (arrows).
FIGURE 2 5 - 1 2
Polycystic native kidney mimicking a peritransplant fluid
collection. Longitudinal view of upper pole of a renal
allograft in a patient with polycystic kidney disease. The
native polycystic kidney (arrowheads) appears as a fluid
collection adjacent to the upper pole.
frequently seen immediately adjacent to the allograft is the psoas muscle. In longitudinal views of the allograft, the psoas muscle is seen in cross-section and appears as an oval mass posterior and medial to the allograft (Fig. 25-7; Fig. 25-11).
It is often immediately adjacent to the allograft and can be mistaken for a
hematoma or other mass. Identification can be made by observing its contraction
when the ipsilateral lower extremity is actively flexed at the hip. In patients with
polycystic kidney disease, the native kidney can abut the allograft and mimic a
fluid collection (Fig. 25-12).
Renal Anatomy
Length can be difficult to measure in allografts because proximity to the skin prevents placement of the entire allograft within the scanning sector. An allograft
undergoes significant enlargement after transplantation (both cadaveric and
living-related), beginning within 2 weeks and stabilizing after 6 months, 4 resulting in a 20%-40% increase in volume. 5-7 However, no increase in cortical thickness
was seen in a study of living-related allografts. 8 The formula that best approximates allograft volume is length X width X depth X 0.612, 9 but this is prone to the
error associated with measuring length. Cross-sectional area at the renal pelvis
can be accurately measured and correlates with changes in allograft volume.10
There is no reference structure against which to judge cortical echogenicity, so that
increased echogenicity is a much more subjective determination than in native
kidneys and is reliable only when echogencity is markedly increased or the
medullary pyramids are prominent. Neither size nor echogenicity are commonly
used in clinical decisions because of the inherent inaccuracy and because biopsy
is a simple and benign procedure. However, allograft volume does correlate with
renal function,} and small, echogenic allografts indicate advanced, irreversible
disease just as they do in native kidneys. Allografts usually contain less sinus fat
and are closer to the probe than are native kidneys, rendering the collecting system and intrarenal blood vessels more visible. Whereas these structures are rarely
seen in a native kidney, they can be prominent in allografts (see Fig. 25-5) and
appear dilated to the untrained eye.
SONOGRAPHY OF THE NORMAL ALLOGRAFT 205
FIGURE 2 5 1 3
Peritoneum intervening in biopsy path. Transverse image of
the left iliac fossa showing peritoneum (arrowheads)
overlying allograft (arrow) and intervening in potential
biopsy path (dotted line).
Percutaneous Biopsy
Because the indication for biopsy is usually an elevated serum creatinine level, it
is important to rule out structural causes of allograft dysfunction such as hydronephrosis and urinoma. Percutaneous biopsies of renal allografts are performed with the patient in the supine position. Once the sonographer has
determined the orientation of the allograft, the biopsy path must be chosen. In
most patients, the abdomen is not flat, so the reference plane for maintaining perpendicularity is the bed. This is difficult in most patients, so it is best to maintain
the probe perpendicular to the abdominal surface. Even though this can be imprecise, the shallowness of the allograft allows for this. Once the angle has been
determined, the probe should be held at that angle for the remainder of the procedure and applied to the skin with minimal pressure to avoid artifactual shortening of the biopsy depth. Any structures anterior to the allograft, particularly the
peritoneum (Fig. 25-13), must be identified and avoided. If possible, blood vessels
posterior to the allograft also should not lie in the biopsy path. Once a suitable
biopsy path has been chosen, it should be confirmed in the other plane after rotating the probe 90. The kidney is then centered in each plane and the distance to
the allograft is noted. Because allografts can be quite mobile, particularly in obese
individuals, and because the transducer indents the skin, the actual biopsy depth
is often greater than the measured depth.
REFERENCES
1. Hanto DW, Simmons RL: Renal transplantation: Clinical considerations. Radiol Clin North Am
1987;25:239.
2. Memel DS, Dodd GD, Shah AN, et al: Imaging of en bloc renal transplants: Normal and abnormal
postoperative findings. AIR 1992;160:75.
3. Burks DD, Fleischer AC, Richie RE: Sonographic diagnosis of a perirenal transplant bowel hernia.
4. Absy M, Metreweli C, Matthews DCR, et al: Changes in transplanted kidney volume measured by
ultrasound. Br J Radiol 1987;60:525.
5. Jurriaans E, Dubbins PA: Renal transplantation: the normal morphological and Doppler ultrasound examination. J Clin Ultrasound 1992;20:495.
6. Lachance SL, Adamson D, Barry JM: Ultrasonically determined kidney transplant hypertrophy.
J Urology 1988;139:497.
7. Raiss GJ, Bree RL, Schwab RE, et al: Further observations in the ultrasound evaluation of renal allograft rejection. J Ultrasound Med 1986;5:439.
8. Raj DSC, Hoisala R, Somiah S, et al: Quantitation of change in the medullary compartment in renal allograft by ultrasound. J Clin Ultrasound 1997;25:265.
9. Solvig J, Ekberg H, Hansen F, et al: Accuracy of noninvasive ultrasonic volume measurements on
human kidney transplants: Presentation of a new formula. Nephron 1998;80:188.
10. Nicholson ML, Williams PM, Bell A, et al: Prospective study of the value of ultrasound measurements in the diagnosis of acute rejection following renal transplantation. Br J Surg 1990;77:656.
Parenchymal Disease
SONOGRAPHY
wo types of parenchymal disease are observed in allografts, that related to

transplantation (rejection, acute tubular necrosis [ATM, and nephrotoxicity)
and that related to recurrent disease. Delayed function of an allograft is usually due to acute tubular necrosis and occasionally due to acute rejection. Later
episodes of acute renal failure are due primarily to acute rejection or to nephrotoxicity produced by cyclosporine or related medications. Progressive renal failure is due to chronic allograft nephropathy (previously termed chronic rejection)
or to recurrent disease, with proteinuria frequently indicating recurrence of the
original renal disease. Sonography has a limited role in diagnosis and is usually
performed to rule out structural causes of renal failure. When these are absent, the
allograft can be marked for percutaneous biopsy, which is required in most cases.
INTERPRETATION
Acute Rejection
In acute rejection, the allograft can range from normal in most mild cases to
slightly swollen and echogenic in moderate cases (Fig. 26-1) and markedly
swollen and echogenic in severe cases (Fig. 26-2). Although not very sensitive, allograft enlargement is fairly specific for acute rejection (Fig. 26-2). Sensitivity is
increased when cross-sectional surface area is used as a measure of allograft size,3
thereby eliminating the common problem of measuring allograft length. A 10%
increase in surface area is about 80% sensitive and specific for acute rejection s - 7 but
requires a baseline sonogram that is often not available. The increase in echogenicity presumably represents cellular infiltration and can be particularly marked
when there is superimposed hemorrhagic infarction (Fig. 26-3). Prominence and
widening of the medullary pyramids has been proposed as a marker of acute rejection, but this is nonspecific and has a poor negative predictive value. 9-11 More
often than not, there is poor corticomedullary differentiation 12 (Fig. 26-4) which is
also not a useful finding because medullary pyramids are not always visible in
allografts with normal function. The experience at this institution indicates that
prominence of the medullary pyramids correlates best with tubular necrosis or interstitial fibrosis (Fig. 26-5) rather than with rejection per se. Resistive indices of
blood flow measured by Doppler are nonspecific and of no use in diagnosing
rejection.11-14
208
FIGURE 2 6 - 1
Acute allograft rejection. Transverse image of renal allograft
with acute rejection. The cortex is echogenic, as judged
from the very prominent medullary pyramids. Cortical
thickness is not markedly increased, but the cortex has
expanded into the sinus.
FIGURE 2 6 - 2
Acute allograft rejection. Longitudinal images of (A) an
allograft with acute rejection superimposed on chronic
allograft nephropathy, and (B) the same allograft 5 months
earlier. The allograft has enlarged and has a rounded
contour, prominent medullary pyramids, and expansion
of the cortex into the sinus.
PARENCHYMAL DISEASE
209
FIGURE 26-3
Severe rejection with hemorrhagic infarction. Longitudinal
. view of allograft that is brightly echogenic with obliteration
of the renal sinus. Two prominent medullary pyramids are
present (arrows).
FIGURE 26-4
Acute allograft rejection. Longitudinal view of allograft in a
patient who stopped her immunosuppressive medications
and presented with acute renal failure and graft tenderness.
The parenchyma is expanded and the medullary pyramids
are not visible. An upper pole calyx is dilated (arrow).
FIGURE 26-5
Prominent medullary pyramids in a renal allograft.
Longitudinal image of an allograft in a patient with
borderline rejection and interstitial fibrosis. The cortex is
thin and the medullary pyramids (arrows) are very
prominent, indicating increased cortical echogenicity.
210
FIGURE 26-6
Acute tubular necrosis. Longitudinal image of a cadaveric
allograft (cursors) with perioperative acute tubular necrosis
and delayed function. The allograft is enlarged (>13 cm in
length) and the medullary pyramids are prominent.
Acute Tubular Necrosis

ATN is seen primarily in the perioperative period. Serial measurements of size
have shown no increase in length, 8 cross-sectional area , 5 or volume' compared with
normally functioning allografts. However, the baseline studies were performed the
day after surgery and any enlargement associated with ATN might have already
occurred. The appearance of the cortex and medulla is reported to be normal in
most cases of ATN, 8 ' 15 but the experience of this author with postoperative ATN is
that the allograft is frequently enlarged with echogenic cortex and prominent
medullary pyramids (Fig. 26-6), similar to the findings in native kidneys.
Nephrotoxicity
Cyclosorine nephrotoxicity is not associated with an increase in allograft SiZe35'7'16
and no consistent qualitative changes have been reported.
Chronic Allograft Nephropathy

Formerly known as chronic rejection, chronic allograft nephropathy is frequently
associated with increased cortical echogenicity (Fig. 26-7), presumably caused by
fibrosis and sclerosis, often with prominence of the medullary pyramids. Unlike
chronic failure in native kidneys, reduced size and cortical thinning are often not
seen until late in the process.
Recurrent Disease
Diseases that affected the native kidneys can recur in allografts, most notably diabetic nephropathy, focal segmental glomerulosclerosis, and immunoglobulin A
nephropathy. The onset is usually heralded by proteinuria, followed by progressive renal failure. The sonographic findings are variable and nonspecific (Fig.
26-8). As in native kidneys, diabetes is associated with a larger allograft volume.4
Almost all parenchymal diseases eventuate in reduced size and parenchymal thinning (Fig. 26-9), as seen in native kidneys.
PARENCHYMAL DISEASE
211
FIGURE 2 6 - 7
Chronic allograft nephropathy. Longitudinal image of an
allograft (arrowheads) that is echogenic to the extent that it
blends with surrounding tissue. The medullary pyramids
are prominent (arrows) and cortical thickness is slightly
increased.
FIGURE 2 6 - 8
Multiple myeloma affecting renal allograft. Longitudinal
view of allograft (arrowheads) from a patient who developed
renal failure after transplantation, owing to myeloma. The
cortex is enlarged and brightly echogenic, with prominent
medullary pyramids. This appearance is indistinguishable
from that of acute rejection.
FIGURE 2 6 - 9
End-stage allograft failure. Longitudinal image of allograft
(arrowheads) showing reduced size and parenchymal
thinning (arrows) in a patient with chronic allograft
nephropathy and recurrent glomerulonephritis.
212
onography has a very limited role in differentiating rejection from other

parenchymal diseases, because the allograft can appear normal in mild or
moderate cases and because the enlargement and increased echogenicity
seen in severe cases is nonspecific. Furthermore, the cause of the renal lesion is
often multifactorial, such as recurrence of disease superimposed on either acute
rejection or chronic allograft nephropathy. The distinction among various parenchymal disorders rests on other clinical parameters and, ultimately, on renal
biopsy.
REFERENCES
1. Raiss GJ, Bree RL, Schwab RE, et al: Further observations in the ultrasound evaluation of renal allograft rejection. J Ultrasound Med 1986;5:439.
2. Townsend RR, Tomlanovich SJ, Goldstein RB, et al: Combined Doppler and morphologic sonographic evaluation of renal transplant rejection. J Ultrasound Med 1990;9:199.
3. Parvin SD, Rees Y, Veitch PS, et al: Objective measurement by ultrasound to distinguish cyclosporin A toxicity from rejection. Br J Surg 1986;73:1009.
4. Absy M, Metreweli C, Matthews DCR, et al: Changes in transplanted kidney volume measured by
ultrasound. Br J Radiol 1987;60:525.
5. Nicholson ML, Williams PM, Bell A, et al: Prospective study of the value of ultrasound measurements in the diagnosis of acute rejection following renal transplantation. Br J Surg 1990;77:656.
6. Slovis TL, Babcock DS, Hricak H, et al: Renal transplant rejection: Sonographic evaluation in children. Radiology 1984;153:659.
7. Nicholson ML, Bell A, Burton PR, et al: Probability of rejection predicted from ultrasonographic
measurement of renal transplant swelling. Br J Surg 1993;80:1059.
8. Swobodnik WL, Spohn BE, Wechsler JG, et al: Real-time ultrasound evaluation of renal transplant
failure during the early postoperative period. Ultrasound Med Biol 1986;12:97.
9. Hoddick W, Filly RA, Backman U, et al: Renal allograft rejection: U.S. evaluation. Radiology
1986;161:469.
10. Linkowski GD, Warvariv V, Filly RA, et al: Sonography in the diagnosis of acute renal allograft
rejection and cyclosporine nephrotoxicity. AJR 1987;148:291.
11. Kelcz F, Pozniak MA, Pirsch JD, et al: Pyramidal appearance and resistive index: Insensitive and
nonspecific sonographic indicators of renal transplant rejection. AIR 1990;155:531.
12. Griffin JF, McNicholoas MMJ: Morphological appearance of renal allografts in transplant failure.
13. Genkins SM, Sanfilippo FP, Carroll BA: Duplex Doppler sonography of renal transplants: Lack of
sensitivity and specificity in establishing pathologic diagnosis. AIR 1989;152:535.
14. Pelling M, Dubbins PA: Doppler and color Doppler imaging in acute transplant failure. J Clin
15. Griffin JF, Short CD, Lawler W, et al: Diagnosis of disease in renal allografts: Correlation between
ultrasound and histology. Clin Radio! 1986;37:59.
16. Pozniak MA, Dodd GD, Kelcz F: Ultrasonographic evaluation of renal transplantation. Radiol Clin
North Am 1992;30:1053.
Urinary Obstruction
in Renal Allografts
SONOGRAPHY
ydronephrosis is a common cause of allograft dysfunction, being encountered in 8% of studies performed for acute allograft failure at Emory University Hospital and is the principal indication for sonography in this
setting. Sonography is an excellent test for detecting urinary obstruction in allografts, with a sensitivity of 90% when the degree of hydronephrosis is moderate
or greater.' When hydronephrosis is noted, it is imperative to identify the proximal ureter and trace it toward the bladder. If there is a significant amount of urine
in the bladder, the study should be repeated after the patient voids.
INTERPRETATION
ydronephrosis has the same appearance in allografts as in native kidneys

(see Chapter 13). Unlike in native kidneys, however, the collecting system
and ureter of allografts are commonly visible and sometimes dilated in the
absence of obstruction 2.3 (Fig. 27-1). Reasons for this probably include proximity
of the allograft to the probe, reduced sinus fat, and backpressure from the bladder.
The minor calyces are usually not be dilated (Fig. 27-1) and their enlargement is
an important clue to the presence of significant hydronephrosis (Fig. 27-2).
Nonobstructive calyceal dilation frequently resolves when the bladder is emptied,
but mild dilation may persist and is usually of no clinical significance. 2 '3 The degree of dilation shown in Figure 27-1 is almost never responsible for acute renal
failure, and other diagnoses should be sought in this situation. Nonobstructive
dilation of the collecting system can occur in pregnancy (Fig. 27-3), as it does in
native kidneys. 4 The causes of ureteral obstruction vary depending on the interval
since transplantation. In the immediate postoperative period, edema, hematomas,
blood clots, and ureteral kinking need to be considered, whereas lymphoceles and
ureteral strictures are the principal causes at later stages 35 Hydronephrosis can
also be caused by bladder retention and urine leaks.
Urinary Retention
Bladder dysfunction is common in allograft recipients and a frequent cause of hydronephrosis. The ureter should be enlarged all the way to the bladder (Fig. 27-4)
and there should be prompt resolution of the hydronephrosis and hydroureter after decompression of the bladder (Fig. 27-5). Even when the ureter cannot be
214
FIGURE 2 7 - 1
Nonobstructive calyceal enlargement. Longitudinal image
of allograft (arrowheads) showing mild dilation of the major
calyces and pelvis. A nondilated minor calyx and its
infundibulum are also visible (curved arrow). Percutaneous
antegrade pyelogram revealed no obstruction.
FIGURE 2 7 - 2
Hydronephrosis secondary to lymphocele. Longitudinal
images of allograft (A) before, (B) immediately after, and
(C) 5 days after percutaneous drainage of a large
lymphocele (arrows). The hydronephrosis resolved
immediately but recurred when the lymphocele
reappeared. Although the calyceal enlargement is not
marked, the minor calyces are dilated. The proximal ureter
is visible just below the lower (medial) pole (arrowheads).
URINARY OBSTRUCTION IN RENAL ALLOGRAFTS
FIGURE 2 7 - 3
Allograft hydronephrosis and hydroureter in pregnancy.
A. Transverse image of allograft shows caliectasis (arrow)
and a dilated ureter (arrowhead). B. Oblique longitudinal
view of lower (medial) pole of allograft (K) showing dilated
ureter (arrowheads). Although the ureter appears to be
obstructed by the gravid uterus (arrows), the ureter distal to
the uterus is also dilated. Percutaneous antegrade
pyelogram showed no obstruction. The fetal head (F) is
visible within the uterus.
215
FIGURE 2 7 - 4
Allograft hydroureter secondary to urinary retention.
Transverse image showing dilated ureter (small arrowheads)
extending to the bladder (large arrowhead) in a patient with
moderate hydronephrosis. The hydronephrosis and
hydroureter resolved after catheterization of the bladder.
216
FIGURE 2 7 - 5
Allograft hydronephrosis secondary to urinary retention.
Longitudinal images of allograft (A) before and (B) 2 hours
after drainage of a distended bladder (B) showing complete
resolution of the hydronephrosis.
FIGURE 2 7 - 6
Hydronephrosis secondary to lymphocele. A. Longitudinal
view of allograft with hydronephrosis. B. Transverse view
shows lymphocele (L) compressing ureter (arrow).
tracked to the bladder, urinary retention should always be the initial diagnosis
when hydronephrosis is associated with a distended bladder.
Lymphocele
Compression of the proximal ureter by a lymphocele is probably the most common cause of hydronephrosis in allografts (Fig. 27-6). The dilated ureter extends
to and tapers at the lymphocele but should be completely separate from it. There
is usually immediate resolution of the hydronephrosis when the lymphocele is
drained percutaneously (Fig. 27-2), but unfortunately, the lymphocele and hydronephrosis almost always recur.
1111
217
Ureteral Stricture
Strictures commonly occur at the ureteropelvic junction (Fig. 27-7), most likely the
result of trauma during harvesting and transplantation.' The dilated calyceal system abruptly tapers at the renal pelvis and the ureter is not visible. Strictures are
also encountered in the distal ureter at or near the anastomosis with the bladder
(Fig. 27-8), probably as a result of poor vascular supply. 5,7 In this case, the dilated
ureter can be followed all the way to the bladder and should remain dilated after
the bladder is emptied.The ureter is capable of substantial dilation (Fig. 27-9).
Strictures can occur in the midureter as well (Fig. 27-9) and tumors are an unusual
cause of ureteral obstruction in this region (Fig. 27-10).
FIGURE 27-7
Stricture at the ureteropelvic junction. Oblique transverse
view of allograft showing marked dilation of the pelvis (P)
that tapers and disappears at the beginning of the ureter
(arrow).
FIGURE 2 7 - 8
Stricture of the distal ureter at the anastomosis with the bladder. A. Longitudinal view of allograft shows a dilated ureter
(arrows) tracking medially. B. Transverse image of bladder shows that the dilated ureter (arrows) extends to the bladder (B).
The caliber of the ureter did not change when the bladder was emptied.
218
FIGURE 2 7 - 9
Stricture of the midsection of an allograft ureter. Transverse
view of allograft (arrowheads) shows a markedly dilated
ureter (U) that tapers abruptly.
FIGURE 2 7 - 1 0
Obstruction of the allograft ureter by lymphoma.
Longitudinal view shows lower (medial) pole of allograft
with a dilated proximal ureter (U) immediately beneath.
The ureter terminates abruptly at the site of a mass (arrows).
he differential diagnosis is similar to that for hydronephrosis in native kidneys. Because the renal veins are more easily seen in allografts, differentiation
from the collecting system is more difficult. In most cases, the distinction can
be made by the branching pattern (see Figs. 23-1, 25-1) and by tracking the vein
to the native vessel (see Fig. 25-6B). The ureter is immediately adjacent to the
lower (medial) pole of the allograft (Figs. 27-2, 27-8A). Calyceal thickening (see
Figs. 13-14, 13-21) due to edema and inflammation is a common finding in the
collecting system of allografts that can mimic mild hydronephrosis. It was originally thought to be an indication of acute rejection but is now known to be a nonspecific finding." The edema is not completely anechoic and there is often an
echogenic line marking the apposition of the mucosal borders. Peripelvic cysts can
mimic hydronephrosis but are rare in allografts.1
REFERENCES
1. Gottlieb RH, Voci SL, Cholewinski SP, et al: Sonography: A useful tool to detect the mechanical
causes of renal transplant dysfunction. J Clin Ultrasound 1999;27:325.
2. Balchunas WR, Hill MC, Isikoff MB, et al: The clinical significance of dilatation of the collecting
system in the transplanted kidney. J Clin Ultrasound 1982;10:221.
North Am 1992;30:1053.
4. Levine D, Filly RA, Graber M: The sonographic appearance of renal transplants during pregnancy.
5. Amante AJ, Kahan BD: Technical complications of renal transplantation. Surg Clin North Am
1994;74:1117.
6. Cullmann H-J, Prosinger M: Necrosis of the allograft ureterevaluation of different methods in
early diagnosis. Urol Int 1990;45:164.
7. Ghasemian SM, Guleria AS, Khawand NY, et al: Diagnosis and management of the urologic complications of renal transplantation. Clin Transplant 1996;10:218.
8. Babcock DS: Sonography of wall thickening of the renal collecting system: A nonspecific finding.
9. Nicolet V, Carignan L, Dubuc G, et al: Thickening of the renal collecting system: A nonspecific finding at US. Radiology 1988;168:411.
10. Ehrman KO, Kopecky KK, Wass JL, et al: Parapelvic lymph cyst in a renal allograft mimicking
hydronephrosis: CT diagnosis. I Comput Assist Tomogr 1987;11:714.
219
Perinephric Fluid
Collections
,ONOGRAPHY
luid collections are a common complication of transplantation and an important cause of allograft failure, and virtually all clinically important collections are detected by sonography. 1 They are usually discovered during
evaluation of renal failure and may be related to the allograft dysfunction or may
be an incidental finding. Other indications for sonography include pain or
swelling around the allograft, wound drainage, occult blood loss, and swelling of
the ipsilateral lower extremity. The boundaries of any fluid collection should be
clearly defined, particularly in relationship to the ureter and bladder, and ascites
should be ruled out. Care must be taken to ensure that any fluid collection is separate from the bladder, which lies in close proximity (Fig. 28-1). Voiding of the
bladder is helpful in ambiguous cases.
FIGURE 28-1
Lymphocele adjacent to bladder. A. Longitudinal view of allograft shows extreme lower (medial) pole of allograft (KID)
and the bladder. Between the two is a questionable fluid collection that appears to be part of the bladder. B. A transverse
view through the bladder reveals the fluid collection (L) to be separate from the bladder. A septation is present in the
lymphocele (arrow).
222
INTERPRETATION
haracteristics of fluid (enhancement of the posterior wall and throughtransmission) should be present in all fluid collections. Because body fluids
all have similar sonographic properties, further differentiation is based on
other parameters, such as the shape and location of the collection, the presence of
internal echoes, and the interval since transplantation.
FIGURE 28-2
Allograft lymphocele. A. Transverse view through lower pole shows triangular fluid collection. B. Longitudinal view
shows minimal hydronephrosis and a slightly dilated ureter (arrow) adjacent to the lymphocele (cursors). Two weeks later,
(C) transverse and (D) longitudinal scans demonstrate enlargement of the lymphocele with significant hydroureter (arrow)
and hydronephrosis.
PERINEPHRIC FLUID COLLECTIONS
223
Lymphoceles
Lymphoceles are the most frequent fluid collections encountered, occurring in as
many as 20% of patients, z3 and are a common cause of hydronephrosis. They can
appear between 1 week and 4 years after surgery, with one half occurring within
the first 10 months after transplantation. 3 Their size ranges from very small to immense and they are usually asymptomatic unless they compress the ureter or the
iliac vein. Most asymptomatic collections resolve spontaneously. 3 Although the
exact origin of lymphoceles (donor versus recipient lymphatics) is still unclear,
two patterns consistent with different origins are encountered. 2-4 Some arise adjacent to the allograft (presumably originating from donor lymphatics) and are usually posterior and medial to the allograft and immediately adjacent to the renal
pelvis. When not too large, they have a characteristic wedge-shaped appearance
and, because of their location, have a propensity to obstruct the ureter (Fig. 28-2,
see also Fig. 27-6). When large, lymphoceles can attain any size and location (Fig.
28-3), sometimes surrounding the allograft (Fig. 28-4; see also Fig. 27-2). Lymphoceles may also be more distant from the allograft, usually located posteriorly
in proximity to the native vessels (Fig. 28-5). These may arise from native lymphatics disrupted during vascular anastomosis and have a propensity to cause
edema of the ipsilateral lower extremity, presumably by obstructing venous
drainage 4' 5 (Fig. 28-6). Occasionally, septations are present (Fig. 28-7), but otherwise, there should be no internal echoes. Internal echoes can be seen in the rare
cases of hemorrhage (Fig. 28-8) or infection (Fig. 28-9), or when a percutaneous
catheter has been inserted or a sclerosing agent has been instilled (Fig. 28-10).
FIGURE 2 8 3
Large lymphocele obstructing the ureter. Longitudinal
image of allograft shows very large lymphocele (L) adjacent
to the renal pelvis . The calyces (C) and pelvis (P) are
markedly dilated.
FIGURE 28-4
Large lymphocele surrounding allograft. Longitudinal view
shows lymphocele extending around upper (lateral) pole
and over anterior surface (arrowheads). Mild hydronephrosis
is present.
224
FIGURE 2 8 - 5
Native lymphocele. Longitudinal view of the lower
(medial) pole of the allograft (arrow) shows a posterior and
medial fluid collection (cursors) separated from the
allograft.
FIGURE 2 8 - 6
Lymphocele obstructing the external iliac vein.
Longitudinal view of the external iliac vein (arrowheads)
shows compression by a lymphocele (arrows). (From
Pozniak MA, Kelcz F, Dodd GD: Renal transplant
ultrasound: Imaging and Doppler. Semin Ultrasound CT
MR 1991;12:319, with permission.)
FIGURE 2 8 -7
Septated lymphocele. Transverse image through lower pole
of allograft (K) adjacent to a large septated fluid collection.
The allograft is artifactually echogenic because of acoustic
enhancement from the overlying fluid.
225
FIGURE 2 8 8
Hemorrhage into a lymphocele. Longitudinal view of
allograft shows lower (medial) pole (K) and an adjacent
lymphocele (L) containing an echogenic thrombus (arrow).
The bladder (B) is visible medial to the collection.
FIGURE 2 8 9
Infected lymphocele. A. Transverse image shows a lymphocele (L)
adjacent to the bladder (B). B. Same view 3 weeks later, after the
lymphocele became infected with Staphylococcus aureus. Note the
echogenic debris and the fluid layer (arrow). (From Ridge JA, MancoJohnson ML, Weil R: Ultrasonographic diagnosis of infected
lymphocele after kidney transplantation. Eur Urol 1987;13:31, with
permission.)
FIGURE 2 8 1 0
Sclerosed lymphocele. Longitudinal view of lower (medial)
pole of allograft (arrowheads) after instillation of a sclerosing
agent into a lymphocele (cursors). The echogenic
lymphocele is immediately adjacent to the renal pelvis
with a typical triangular appearance.
226
Hematomas
Postoperative hematomas are frequent 2.4 and appear as variably shaped collections ranging from primarily fluid filled (anechoic) to solid, usually with a combination of both (Fig. 28-11). They can occur in any location and can be quite large
(Fig. 28-12). Bleeding anterior to the allograft in the subcutaneous tissue of the abdominal wall is an infrequent complication of percutaneous biopsy (Fig. 28-13).
Subcapsular hematomas may also occur in allografts (Fig. 28-14). Hematomas
become organized over time, appearing as echogenic masses (Fig. 28-15). In the appropriate location these can be confused with the psoas muscle (see Figs. 25-4, 25-7B)
but do not contract with hip flexion.
FIGURE 28-11
Perinephric hematoma. Longitudinal view shows a
hematoma (arrowheads) containing both unclotted
(anechoic) and clotted (echogenic) blood, anterior to upper
(lateral) pole of allograft (K).
FIGURE 2 8 - 1 2
Large postoperative hematoma. Transverse view of
allograft (K) with large hematoma (arrowheads) along the
lateral aspect of the allograft. There is a significant amount
of echogenic material in the lumen consistent with clot
(arrow).
227
FIGURE 2 8 1 3
Hemorrhage into abdominal wall following percutaneous allograft biopsy. Longitudinal images of renal allograft (A) before
and (B) after percutaneous biopsy. After biopsy, a large hematoma (arrows) displaces the allograft (K) posteriorly.
FIGURE 2 8 1 4
Subcapsular hematoma in a renal allograft. A. Longitudinal and (B) transverse scans after a percutaneous
renal biopsy. The hematoma is contained within the
renal capsule (arrows) and compresses the kidney.
FIGURE 2 8 1 5
Organized perinephric hematoma. Longitudinal view of
allograft (K) shows echogenic hematoma (H) adjacent to
lower (medial) pole. The renal pelvis is slightly dilated
(arrow).
228
Urinomas
Urinomas result from ureteral leaks, which occur in up to 3% of transplants, 6 usually within several weeks of transplantation. 2 They are thought to arise from
ureteral damage during dissection of the renal hilum and from ureteral necrosis
due to compromised blood flow or rejection. Failure of the ureterovesicular anastomosis is a rare cause. Symptoms include pain and tenderness in one half of patients and fever in one quarter. 6 Urinomas can range from very small (Fig. 28-16)
to huge (Fig. 28-17) and are usually in close proximity to the ureter. The borders
can be irregular and indistinct, probably representing dissection through tissue
planes and inflammatory reaction. There is often dilation of the proximal ureter
and collecting system (Fig. 28-18), presumably due to tissue pressure and partial
obstruction by inflammatory reaction around the leak. 5 ' 6 If there is a clinical suspicion, the fluid should be aspirated for measurement of creatinine concentration.
FIGURE 2 8 -
1 6
Urine leak. A. Transverse image of allograft demonstrates

an anterior fluid collection (small arrowheads) and a small
collection around the ureter at the renal pelvis (large
arrowhead). A stent is present in the ureter. B. A more medial
image shows fluid tracking along the ureter on each side of
the stent.
229
FIGURE 2 8 1 7
Large urinoma. Longitudinal view of allograft (large
arrowheads) in a patient with anuria after transplantation. A
large fluid collection surrounds the allograft. There is mild
hydronephrosis and a dilated ureter (small arrowheads) that
terminates in an echogenic area within the fluid collection
(arrow), representing the site of the leak with inflammatory
reaction. The echogenicity of the allograft is artifactually
increased because of enhancement by the overlying fluid.
(From O'Neill WC: Renal ultrasonography: a procedure for
nephrologists. Am I Kidney Dis 1997;30:579, with
permission.)
FIGURE 2 8 - 1 8
Urinoma with hydronephrosis. Longitudinal image of
allograft with moderate hydronephrosis. A portion of a
very large urinoma (arrows) is visible medial to the
allograft. Note the irregularity of the wall of the urinoma.
Seromas
Serosanguinous fluid collections are commonly observed in the immediate postoperative period, resolve spontaneously, and are usually of no clinical significance. The importance in recognizing these is not to confuse them with other
types of fluid collections. Seromas usually occur anterior to the allograft and are
often linear, tracking along tissue planes (Fig. 28-19). There is usually some tissue
between the fluid and the allograft and septations are common.
230
FIGURE 2 8 - 1 9
Seroma. Transverse view of allograft (arrowheads) showing
a large anterior fluid collection with septations (arrows).
There is tissue between the fluid collection and the
allograft. Percutaneous drainage revealed serosanguinous
fluid.
FIGURE 2 8 - 2 0
Ascites. Transverse image of allograft (arrows) through the
renal pelvis demonstrating large fluid collections (A) on
either side. Note the echogenic tissue intervening between
the ascites and the allograft.
Ascites
Ascitic fluid collections are frequently large and extend superiorly, with tissue
intervening between the fluid and the allograft (Fig. 28-20). They are most commonly seen in patients who underwent peritoneal dialysis prior to transplantation. Ascites is of no significance in terms of the renal allograft except for possible
confusion with other types of fluid collections.
ther causes of perinephric fluid collections near an allograft are polycystic
kidneys (see Fig. 25-12), bladder diverticula, and ovarian cysts.' Because
sonography cannot differentiate fluid types, diagnosis depends on other
parameters such as location, shape, internal echoes, and clinical presentation.
Location
Lymphoceles emanate from the hilum and urinomas are associated with the
ureter, but either can extend to any location when large. They can be immediately
adjacent to the allograft with no intervening tissue. Seromas occur anterior to the
allograft, and although this is also a common location for hematomas, hematomas
can occur anywhere. Ascites is seen medial and lateral (and occasionally anterior)
to the allograft and extends superiorly. There is usually intervening tissue between the allograft and seromas or ascitic collections.
Shape
Allograft lymphoceles are triangular or wedge-shaped when small but can have
any shape when large. Seromas are usually elongated and follow tissue planes
and rarely obtain a large size. Lymphoceles have a thin, distinct, and smooth wall.
This can be true for urinomas, but often, the wall is indistinct and irregular. The
bladder has a thicker wall and empties with voiding.
Internal Echoes
Uncomplicated lymphoceles have no internal echoes except for septations. Urinomas are predominantly anechoic but can exhibit some echogenicity along the
edges. Bowel loops may be present in ascitic fluid, but there should be no septations. Seromas are frequently septated. Hematomas are not septated and usually
contain a large amount of echogenic clot.
Clinical Presentation
Hematomas, urinomas, and seromas are usually seen within the first 1 or 2 weeks
after surgery, whereas lymphoceles can present many months after surgery.
Hematomas and urinomas can be painful or tender, whereas uncomplicated lymphoceles and seromas are rarely painful. Hydronephrosis is commonly associated
with lymphoceles and urinomas, although urinomas do not produce severe
hydronephrosis. Lymphoceles can also produce edema of the ipsilateral lower
extremity.
REFERENCES
1. Gottlieb RH, Voci SL, Cholewinski SP, et al: Sonography: A useful tool to detect the mechanical
causes of renal transplant dysfunction. J . Clin Ultrasound 1999;27:325.
2. Amante AL Kahan BD: Technical complications of renal transplantation. Surg Clin North Am
1994;74:1117.
3. Khauli RB, Stoff JS, Lovewell T, et al: Post-transplant lymphoceles: A critical look into the risk factors, pathophysiology, and management. J Urology 1993;150:22.
North Am 1992;30:1053.
5. Pozniak MA, Kelcz F, Dodd GD: Renal transplant ultrasound: Imaging and Doppler. Semin Ultrasound CT MR 1991;12:319.
6. Cullmann H-J, Prosinger M: Necrosis of the allograft ureterevaluation of different methods in
early diagnosis. Urol Int 1990;45:164.
7. Kliewer MA, Woodruff WM, Bowie JD: Mucinous cystadenoma simulating renal transplant lymphocele. J Clin Ultrasound 1989;17:119.
231
Vascular Complications
of Renal Allografts
Deborah A. Baumgarten
SONOGRAPHY
ascular complications are a rare but important cause of allograft dysfunction that often require prompt diagnosis, particularly in the immediate
postoperative period. Because of their location, the vessels of allografts are
far more amenable to examination by Doppler sonography. Conventional grayscale imaging should be performed first to evaluate the collecting system and to
look for signs of vascular complications. Color Doppler sonography should then
be performed, followed by duplex Doppler analysis of both normal vascular
structures and abnormal areas of color flow. Occasionally, the indication for
sonography is to investigate renal artery stenosis in patients with severe hypertension. In contrast to vessels in native kidneys, the vasculature of renal allografts
is very accessible to Doppler evaluation, with high sensitivities and specificities.
A typical study consists of duplex Doppler analysis of the main renal artery and
vein (Fig. 29-1) as well as sampling of the interlobar arteries (Fig. 29-2). A resis-
FIGURE 2 9 - 1
Normal allograft vein. Transverse image of a
renal allograft shows a normal main venous
duplex tracing, with flow below the baseline
(away from the kidney).
EMORY UNIVERSITY,
.24 MAIN VII
IPW . PWR<508
12:19:1P
C3
2.5MHz
,30dB 0/-/D
RENAL
2.5mm/1PW. Dr- 26mm
*TEXT
.24
INVERTED
234
EMORY UNIVERSITY
.16 INTERLOBAR UPPER
PW PWR<500
30dB 0/-/D
2.0mm/1
PW D= 38mm
11:28 39AM
C3
2.514t 20mm
RENAL
FIGURE 2 9 - 2
Normal interlobar artery. Longitudinal
image of a renal allograft shows a normal
upper pole interlobar arterial duplex tracing.
There is a sharp rise to peak velocity in
systole and ample diastolic flow.
tive index can be calculated, but it is very nonspecific and of little clinical utility.1-3
Color Doppler allows an overview of long segments of vessels and facilitates
identification of intrarenal vascular structures. Color Doppler is not able to quantify vascular flow disturbances, necessitating the use of duplex Doppler. Power
Doppler sonography can also be used when color Doppler is inadequate for flow
visualization.
RENAL ARTERY STENOSIS

enal artery stenosis is the most common vascular complication of renal
transplantation, occurring generally within the first 3 years after the procedure. 4 The kidneys are more often from cadavers than live donors. Most patients present with hypertension, often new, progressive, or poorly controlled.
There may be a detectable bruit.
Interpretation
Color Doppler is used to image the main renal artery from its anastamosis with
the external iliac artery to the kidney. Duplex Doppler is used to evaluate areas
of color change indicative of elevated flow velocities or turbulence. Doppler shifts
> 200 cm/s in association with post-stenotic turbulence have been associated with
significant stenoses 5 ' 6 (Fig. 29-3). A limitation of this technique is the necessity to
visualize the renal artery in its entirety. Angiography may be needed when visualization is incomplete or there are accessory renal arteries, and to exclude segmental arterial stenoses.
False positive results can occur with low-grade stenoses that cause subclinical
flow disturbances.
VASCULAR COMPLICATIONS OF RENAL ALLOGRAFTS
11.39
235
35H
C3
2.5MHz .20m
RENAL
L. CA IRE
FIGURE 2 9 - 3
Renal artery stenosis. Doppler interrogation
of the main artery of a renal allograft reveals
an area of increased systolic velocity
(> 200cm/s).
RENAL ARTERY THROMBOSIS

cute thrombosis of the renal artery is an uncommon but very serious complication of transplantation and generally occurs early in the postoperative
period (within the first month). The most frequent causes are hyperacute
and acute rejection. The thrombosis can be of the main artery, which results in
graft loss in the vast majority of patients, or segmental occlusion, which leads to
focal scarring (see Fig. 22-7).
Interpretation
Color and duplex Doppler sonography will show lack of flow in the renal artery
branches beyond the site of occlusion. If the main renal artery is occluded, there
will be absent venous flow as well; if there is segmental occlusion, venous flow
will be seen, but not in the affected segment.
Improperly functioning or calibrated equipment may cause a false positive diagnosis of renal artery thrombosis. Scanning over the iliac or femoral vessels (especially where a pulse can be felt) should help to exclude this possibility. Very
high grade renal artery stenosis can result in very low flow states and care should
be taken to maximize Doppler settings to detect flow. (Power Doppler may be of
use in this setting.) Ultimately, angiography may be necessary to confirm the
diagnosis.
RENAL VEIN THROMBOSIS

enal vein thrombosis is another rare complication of transplantation also occurring in the early postoperative period. Predisposing factors include peritransplant fluid collections (with compression of the vascular structures)
and femoral or iliac vein thrombosis. Early intervention may save the allograft.
236
FIGURE 2 9 4
Renal vein thrombosis. A. Longitudinal
image and (B) spectral analysis of a renal
allograft revealing the typical reversal of
flow during diastole in the main renal artery.
Venous flow was not detected.
Interpretation
Routine gray-scale imaging may show enlargement and decreased echogenicity of
the transplant. With color and duplex Doppler, there is absence of venous flow
and reversal of arterial flow during diastole (Fig. 29-4). Specificity is very high
when both findings are present.4
Reversal of arterial flow in diastole also occurs in high-grade ureteral obstruction
and severe rejection.
ARTERIAL PSEUDOANEURYSM
rterial pseudoaneurysm may occur either at the anastamosis between
the renal and iliac arteries or within the kidney as a sequela of biopsy. The
former is more dangerous because of the risk of rupture and excessive
bleeding.
237
Interpretation
On gray-scale imaging, an extrarenal pseudoaneurysm presents as an anechoic,
rounded perirenal fluid collection that may contain an echogenic thrombus (Fig.
29-5A). Disorganized flow is seen within the anechoic region by color or duplex
Doppler (Fig. 29-5B). Intrarenal pseudoaneurysms appear as simple cysts on
gray-scale imaging (Fig. 29-6A), but color and duplex Doppler studies reveal flow
within the lesion. If the neck of the pseudoaneurysm is small enough, jets of flow
into and out of the pseudoaneurysm can be observed during systole and diastole,
respectively (Fig. 29-6B). Follow-up imaging usually demonstrates rapid resolution of intrarenal pseudoaneurysms (Fig. 29-6C).
FIGURE 2 9 - 5
Extrarenal pseudoaneurysm. A. Transverse
image of the renal allograft reveals a round,
predominantly anechoic collection medial to
the kidney. Areas of peripheral thrombus are
noted (arrows). B. Spectral analysis of the
lesion reveals disordered internal flow.
RENAL -ix TRANS

PW P R500
35dB 13/-/D
5.0mm/1
PW D= 73mm
6HZ
C3
MN* 140mm
/V
RENA
238
FIGURE 2 9 6
Intrarenal pseudoaneurysm.
A. Transverse image of the midrenal
allograft reveals an anechoic round lesion
(arrow); with color Doppler sonography,
flow was seen within the lesion.
B. Spectral analysis of the pseudoaneurysm neck demonstrates the typical
jet of flow during systole and reversal of
flow in diastole. C. Four days later, the
pseudoaneurysm has decreased in size.
C
239
FIGURE 2 9 7
Arteriovenous fistula (AVF). Spectral analysis of an AVF shows the usual (A) high-velocity, low-resistance
diastolic flow (arrow) within the feeding artery and (B) arterialization (pulsatile flow) of the venous
outflow. (From Dodd GD, Mitchell ME, Shah A, et al: Imaging of vascular complications associated with
renal transplants. AIR 1991;157:449, with permission.)
Gray-scale sonography cannot distinguish between extrarenal pseudoaneurysms
and other perirenalfluid collections (see Chapter 28). Findings that should raise the
suspicion of pseudoaneurysm are pulsatility and proximity to the anastomosis of
the renal artery to the external iliac artery. Intrarenal pseudoaneurysms mimic
simple cysts without the benefit of Doppler sonography.
ARTERIOVENOUS FISTULAS
rteriovenous fistulas (AVFs) are almost always the result of percutaneous
biopsy, are not generally of clinical significance, and usually spontaneously
resolve. In rare cases, the AVF may cause decreased renal perfusion because
of arteriovenous shunting.
Interpretation
AVFs are not generally detected by gray-scale imaging but can appear as cystic lesions. Color Doppler reveals an area of disorganized color, and decreasing the
Doppler settings will allow visualization of the affected vessels. Duplex scanning
of the feeding artery demonstrates high-velocity, low-impedance flow (Fig. 29-7A),
whereas interrogation of the vein demonstrates arterialization of the waveform'
(Fig. 29-7B).
Pseudoaneurysms may also produce disorganized flow but are more apparent on
gray-scale imaging.
240
FIGURE 2 9 8
Torsion. A. Baseline longitudinal image of the
renal allograft demonstrates normal orientation of
the renal hilum (arrow). B. A longitudinal image 6
months later reveals interval change in the
orientation of the renal hilum that is now pointed
anteriorly (arrow). The cortex of the upper pole is
thin and hypoechoic (arrowheads), suggestive of
ischemia. (From Wong-You-Cheong JJ, Grumbach
K, Krebs TL, et al: Torsion of intraperitoneal renal
transplants: imaging appearances. AIR
TORSION
orsion is an extremely rare complication of transplantation, occurring

when the transplants are placed intraperitoneally." The kidney rotates about
its vascular pedicle, leading to acute vascular occlusion and resultant parenchymal necrosis.
Interpretation
There may be a change in the orientation of the kidney, with the renal hilum
pointed anteriorly instead of posteriorly' (Fig. 29-8). Hydronephrosis is a variable
finding. The findings with color and duplex Doppler are also variable, consisting
of one of the following patterns: normal flow; absence of renal vein flow only; normal vein flow with reversal of arterial flow in diastole; or absence of both venous
and arterial flow.'
Isolated renal vein thrombosis can present with similar findings, but the orientation
of the kidney should remain normal.
REFERENCES
1. Genkins SM, Sanfilippo FP, Carroll BA: Duplex Doppler sonography of renal transplants: Lack of
sensitivity and specificity in establishing pathologic diagnosis. AIR 1989;152:535.
2. Felling M, Dubbins PA: Doppler and color Doppler imaging in acute transplant failure. I Clin
3. Renowden SA, Griffiths DF, Nair S, et al: Renal transplant sonography: Correlation of Doppler and
biopsy results in cellular rejection. Clin Radio! 1992;46:265.
4. Dodd GD, Tublin ME, Shah A, et al: Imaging of vascular complications associated with renal transplants. Am I Radio! 1991;157:449.
5. Taylor KJW, Morse SS, Rigsby CM, et al: Vascular complications in renal allografts: Detection with
duplex Doppler US. Radiology 1987;162:31.
6. Snider JF, Hunter DW, Moradian GP, et al: Transplant renal artery stenosis: Evaluation with duplex
sonography. Radiology 1989;172:1027.
7. Wong-You-Cheong JJ, Grumbach K, Krebs TL, et al: Torsion of intraperitoneal renal transplants:
Imaging appearances. AIR 1998;171:1355.
241
INDEX
Note: Page numbers in italics refer to illustrations; page numbers followed by t refer to tables.
A
Abscess, 68-69, 68, 69
vs. cyst, 68, 90
vs. hematoma, 69, 189
vs. hydatid disease, 68, 76
vs. tuberculosis, 68, 75
vs. tumor, 68, 164
Acquired cystic kidney disease, 99, 100, 101
vs. autosomal-dominant polycystic kidney disease, 97, 100
vs. cystic neoplasm, 100, 148
Acute tubular necrosis, 53-56, 54, 55
of allograft, 210, 210
vs. acute interstitial nephritis, 57
vs. allograft rejection, 56, 208, 209
vs. glomerulonephritis, 45-46
vs. renal vein thrombosis, 54, 182
Adrenal gland, 3, 4, 5
myelolipoma of, 156, 159
Age, kidney length and, 15, 16
Air, calyceal, 133, 134
Allograft, acute tubular necrosis of, 210, 210
anatomy of, 199, 199, 200, 204
arterial pseudoaneurysm and, 236-238, 237, 238
arteriovenous fistula and, 239, 239
ascites and, 230, 230
biopsy of, 205, 205, 227
calyceal dilation in, 109, 110
calyceal enlargement and, 213, 214
calyceal thickening in, 218
chronic nephropathy of, 210, 211
cyclosporine effect on, 210
donor vessels and, 201, 203
end-stage failure of, 210, 211
enlargement of, 204
external iliac vessels and, 201, 202
hematoma and, 226, 226, 227, 231
herniated bowel and, 201, 203
hydronephrosis in, 213-218, 214-218, 222
in infant, 199, 200
in pregnancy, 213, 215
in right iliac fossa, 199, 200-201, 200, 201
lymphocele in, 213, 214, 216, 216, 222-224, 231
lymphoma-related ureteral obstruction and, 217, 218
multiple myeloma of, 210, 211
normal artery in, 233, 234
normal vein in, 233, 233
peritoneum and, 201, 203, 205, 205
perpendicular orientation of, 201
polycystic kidney and, 204, 204
psoas muscle and, 204, 204
Allograft (Continued)
recurrent disease in, 210, 211
rejection of, 207-209, 208, 209
vs. acute tubular necrosis, 56, 208, 209
vs. lymphoma, 108, 109, 164
renal artery stenosis and, 233, 235
renal artery thrombosis and, 235
renal vein thrombosis and, 235-236, 236
seroma and, 229, 230, 231
torsion and, 239-240, 240
ureteral stricture and, 217-218, 217, 218
urinoma and, 228-229, 228, 229, 231
venous engorgement and, 201, 202
volume of, 204
Amyloidosis, 49-50, 49
vs. diabetic nephropathy, 49, 49
vs. glomerulonephritis, 47
vs. lymphoma, 49, 164
Analgesic nephropathy, 58, 59, 61
Anatomy, developmental variants of of, 21-33. See also specific
variants.
normal, 11-19
coronal section for, 12
dimensions of, 15, 15-17
longitudinal views of, 12-14
neonatal, 14
oblique views of, 13
of cortex, 15, 17-18
of medulla, 18-19
sagittal section for, 12
transverse view of, 14
perirenal, 3-9
coronal section for, 4
tissue compartments of, 7, 7
transverse section for, 4
Aneurysm, 176, 177
vs. cyst, 90, 177
vs. peripelvic cyst, 86, 177
vs. varices, 177 184
Angiomyolipoma, 155-159, 156-158
hemorrhage in, 158
in tuberous sclerosis, 101, 101
venous extension of, 158
vs. acute pyelonephritis, 67
vs. epithelial tumor, 146
vs. junctional fusion defect, 26
vs. lymphoma, 164
vs. nephrolithiasis, 133, 156
vs. opportunistic infection, 75, 156
vs. tuberculosis, 75
243
244
INDEX
Aorta, 3, 167, 168

atherosclerosis of, 173, 173
Arcuate artery, 13, 167, 168
vs. angiomyolipoma, 13, 156
vs. chronic interstitial nephritis, 13, 60
Arteriovenous fistula, 176-177, 177, 239, 239
vs. cortical cyst, 84, 239
Arteriovenous malformation, 176, 176
vs. cyst, 90, 176
Ascites, 7, 8, 18
allograft and, 230, 230, 231
vs. urinoma, 8, 194
Aspergilloma, 69
Autosomal-dominant polycystic kidney disease, 93-97
diagnosis of, 96, 96t
differential diagnosis of, 97, 105
early changes in, 93, 94
hepatic cysts with, 95, 95
hydronephrosis in, 96, 96
nephrolithiasis in, 95, 95
progression of, 93, 94, 95, 95
seminal vesicle cystic enlargement in, 122
vs. xanthogranulomatous pyelonephritis, 73
Autosomal-recessive polycystic kidney disease, 102-103, 102
B
Bardet-Biedl syndrome, 27
Bertin, column of, 13
hypertrophy of, 24, 24
vs. epithelial tumor, 24, 146
Biopsy, allograft, 205, 205, 227
percutaneous, 35-37, 36, 37
Bladder, carcinoma of, ureteral obstruction with, 122, 125
edema of, 122, 124
Foley catheter in, 135, 136, 137
hematoma of, 127
male, 119, 121, 122
neurogenic, 121, 128
severe distension of, 121
stones of, 127
volume of, 119
vs. lymphocele, 221
Blood clot. See also Hematoma; Hemorrhage.
vs. fungal infection, 73, 115, 190
vs. pyonephrosis, 72, 115, 190
Body height, kidney length and, 15, 15, 16
Bowel, 4, 6
herniation of, renal allograft and, 201, 203
Bowel gas, 4, 70
C
Calcification, in cyst, 90, 91
vs. opportunistic infection, 75, 172
vs. stent, 135, 172
Calcium, milk of, vs. nephrolithiasis, 133-134, 134
Calculi, bladder, 127
renal. See Nephrolithiasis.
ureteral, 115, 122, 125
Caliectasis, 109, 110, 111. See also Hydronephrosis.
Calyx, air in, 133, 134
cyst of, 27
dilation of, 23
vs. varices, 184
Calyx (Continued)
hemorrhage of, 189-190, 190
in allograft, 218
major, 13, 29
minor, 13
Carcinomatosis, gastric, pararenal space in, 9
Catheter, Foley, 135, 136, 137
Column of Bertin, 13
hypertrophy of, 24, 24
Complex cysts, 87-91, 87-91
Contusion, 191, 191
Cortex, 13
atrophy of, vs. fetal lobulation, 27, 42
echogenicity of, 17-18, 18
thickness of, 15, 17
in amyloidosis, 49, 49, 50
in chronic renal failure, 41, 42, 43
in diabetic nephropathy, 47-49, 48
in glomerulonephritis, 45, 46
in hydronephrosis, 112, 113, 114
Cortical scar, vs. junctional fusion defect, 26, 110, 175
Crystal nephropathy, 61, 62
Cyst(s). See also Autosomal-dominant polycystic kidney disease.
acquired, 99, 100, 101
calcification in, 90, 91
calyceal, 27
carcinoma in, 147, 148
complex, 87-91, 87-91
hemorrhagic, 87, 88, 89
hepatic, 95, 95
hydatid, 76-77, 76
in tuberous sclerosis, 97, 101, 101
in von Hippel-Lindau disease, 104, 104
infected, 88
localized, vs. autosomal-dominant polycystic kidney disease, 97
vs. cystic neoplasm, 148
medullary, 103, 103
milk of calcium in, 89, 89
parapelvic, 84, 85
vs. hydronephrosis, 84, 116
vs. varices, 85, 86, 184
peripelvic, 85-86, 85, 86
vs. fistula, 85, 86, 177
vs. hydronephrosis, 85, 86, 116, 117, 218
reverberation artifact in, 90, 92
septated, 90, 90
simple, 81-84, 82-84, 82t
in hydronephrotic kidney, 84
prevalence of, 82t
renal pelvis obstruction with, 83
vs. autosomal-dominant polycystic kidney disease, 97
vs. epithelial tumor, 82, 83, 146
vs. abscess, 68, 89
vs. fistula, 177
Cystitis, hemorrhagic, 122, 124
D
Diabetes mellitus, hydronephrosis in, 109, 111
Diabetic nephropathy, 47-49, 48
INDEX
Diabetic nephropathy (Continued)

vs. amyloidosis, 48, 50
vs. chronic renal failure, 43, 48
Dromedary hump, 28, 29, 48
Duplication, of collecting system, 21-24, 22, 23
Duplication artifact, vs. tumor, 145, 146
E
Echinococcal infection, 76-77, 76
Ectopic kidneys, 30-33, 30-32
Edema, mucosal, vs. hydronephrosis, 116, 118
vs. stent, 118, 135
Emphysematous pyelitis, 69-70, 70
Emphysematous pyelonephritis, 69-70, 70
Ethylene glycol ingestion, acute tubular necrosis with, 55, 55
Extrarenal pelvis, 28, 29
F
Fascia, pararenal, 7, 7
Fat, 7, 8
vs. hematoma, 8, 189
Fetal lobulation, 26-27, 26, 27
Fibromuscular dysplasia, 173, 173
Fistula, arteriovenous, 176-177, 177, 239, 239
Fluid collection. See also Hematoma; Lymphocele.
ascitic, 7, 8, 18, 194, 230, 230, 231
perinephric, 221-231
peritoneal, 194-195, 195
physiologic, 195
serosanguinous, 229, 230, 231
simulation of, 204, 204
urinoma, 193-194, 194, 228-229, 228, 229, 231
vs. pseudoaneurysm, 240
Fluid-debris level, in pyonephrosis, 71
Foley catheter, 135, 136, 137
Fracture, 192, 193
Fungal infection, 69, 72-73, 73
Fused kidneys, 30-33, 30-32
G
Gas, 4, 69-70, 70
Gastric carcinomatosis, pararenal space in, 9
Gerota's fascia, 8
Glomerulonephritis, 45-47, 46, 47
vs. acute pyelonephritis, 46, 67
vs. acute tubular necrosis, 46, 55-56
Goodpasture's syndrome, 46
H
Height, body, kidney length and, 15, 15, 16
Hematoma, intraparenchymal, 191, 191
of bladder, 127
pararenal, 187, 189
perirenal, 187, 188
postoperative, 226, 226, 227, 231
posttraumatic, 187-189, 188, 189
retroperitoneal, 187, 189
subcapsular, 187, 188, 227
vs. abscess, 68, 188, 189
Hematoma (Continued)
vs. laceration, 191, 192
vs. urinoma, 194
Hemolytic uremic syndrome, 50
Hemorrhage, calyceal, 189-190, 190
in angiomyolipoma, 158
into lymphocele, 225
with percutaneous biopsy, 37, 37
Hemorrhagic cyst, 87, 88, 89
Hemorrhagic cystitis, 122, 124
Horseshoe kidney, 31, 32
Human immunodeficiency virus (HIV) nephropathy, 50, 51
Hydatid disease, 76-77, 76
Hydronephrosis, 13, 109-118
bladder distension in, 121
cortical thickness in, 112, 113, 114
grading of, 112
in allograft, 213-218, 214-218, 222
in autosomal-dominant polycystic kidney disease, 96, 96
in diabetes mellitus, 109, 111
in fused ectopic kidney, 32
minimal, 112, 112
moderate, 109, 111
nephrolithiasis and, 115
nephrostomy tube obstruction and, 115
of duplicated collecting system, 23
resolution of, 116, 116, 117
severe, 109, 111, 114
ureteral dilation in, 114
ureteral stones and, 115
ureteral wall thickening in, 115
urinoma and, 229
vs. arteriovenous malformation, 176
vs. calyceal thickening, 118, 218
vs. chronic interstitial nephritis, 60
vs. duplication, 24
vs. mucosal edema, 116, 118
vs. multicystic kidneys, 105
vs. pelvocalyceal tumor, 151
vs. peripelvic cyst, 86, 116, 117, 218
vs. renal veins, 180, 199, 218
vs. tuberculosis, 75, 142, 143
vs. venous engorgement, 111, 115, 179
vs. xanthogranulomatous pyelonephritis, 73, 113, 114
Hyperplasia, adrenal, 5
Hypertensive nephrosclerosis, vs. chronic renal failure, 43
IgA nephropathy, 50
Iliac vein, lymphocele obstruction of, 224
Infarction, 174-175, 174, 175
vs. contusion, 174, 191
vs. laceration, 190, 192
Infection, fungal, 69, 72-73, 73
HIV, 50, 51
of lymphocele, 225
vs. tumor, 66, 69, 74, 146, 164
245
246
I NDEX
Interstitial nephritis, acute, 57, 58

chronic, 58-61, 59-61
vs. acute tubular necrosis, 55-56, 58
vs. glomerulonephritis, 45, 58
Intrarenal artery, calcification of, vs. nephrolithiasis, 133, 172
Intrathoracic kidney, 31
Junctional fusion defect, 25-26, 25

L
Laceration, 192-193, 192, 193

urinoma with, 193, 194
Leukemia, 161, 164
Liver, 3, 4, 5, 7
cyst of, 95, 95
neonatal, 14
Lobulation, fetal, 26-27, 26, 27
Lower urinary tract. See also specific structures.
anatomy of, 119, 120
obstruction of, 119-128, 121-127
Lupus nephritis, 47
Lymphocele, 223-225, 223-225
allograft and, 213, 214, 216, 216, 222-224, 231
hemorrhage into, 225
iliac vein obstruction by, 224
infection of, 225
sclerosing agent treatment of, 225
vs. bladder, 221
Lymphoma, 151, 154, 161, 162-164
allograft and, 217, 218
vs. hematoma, 189
vs. xanthogranulomatous pyelonephritis, 73, 162
M
Medulla, 18-19
Medullary cystic disease, 103, 103
Medullary pyramids, 12, 13, 14
fusion of, 27-28, 27
in acute tubular necrosis, 54
in allograft, 209
in chronic interstitial nephritis, 58, 59, 60
in nephrocalcinosis, 62, 63
vs. cortical cyst, 84
vs. infarction, 175
Medullary sponge kidney, nephrocalcinosis with, 61, 62
Membranoproliferative glomerulonephritis, 45, 46, 47
Membranous nephropathy, 50, 51
Metastasis, 161, 162
Milk of calcium, 133-134, 134
Mucosal edema, vs. hydronephrosis, 116, 118
vs. stent, 118, 135
Multicystic dysplastic kidney, 104, 105
Multilocular cystic nephroma, 147, 147

Multiple myeloma, acute tubular necrosis in, 55
Myelolipoma, adrenal, 156, 159
N
Necrosis, cystic, in renal cell carcinoma, 147, 148

papillary, 60
vs. hydronephrosis, 59, 60, 116
vs. opportunistic infection, 60, 61, 75
tubular. See Acute tubular necrosis.
Nephrectomy, kidney dimensions after, 15
Nephritis, interstitial. See Interstitial nephritis.
Nephrocalcinosis, 61-63, 62, 63
vs. emphysematous pyelonephritis, 62, 63, 70
Nephrolithiasis, 129-138, 130-132
drug-induced, 129, 133
hydronephrosis and, 115
in autosomal-dominant polycystic kidney disease, 95, 95
in lower pole, 130
in midkidney, 130
in renal pelvis, 131, 132
in upper pole, 131
longitudinal image of, 130, 131, 132
staghom, 132, 132
transverse image of, 131
vs. angiomyolipoma, 155
vs. calyceal air, 133, 134
vs. emphysematous pyelitis, 70
vs. junctional fusion defect, 26
vs. milk of calcium, 133-134, 134
vs. nephrocalcinosis, 63
vs. pyonephrosis, 72
vs. refraction artifact, 131, 133, 133
vs. transitional cell carcinoma, 151, 153
Nephroma, cystic, multilocular, 147, 147
Nephropathy, diabetic, 47-49, 48
vs. chronic renal failure, 43
HIV, 50, 51
IgA, 50
membranous, 51
reflux, vs. chronic interstitial nephritis, 60
vs. chronic renal failure, 43
vs. renal artery disease, 173
sickle cell, 59
Nephrosclerosis, hypertensive, vs. chronic renal failure, 43
Nephrostomy tube, 135, 138
obstruction of, hydronephrosis and, 115
Neuroblastoma, vs. hematoma, 189
Nodular compensatory hypertrophy, vs. epithelial tumor, 146, 146
Nubbin sign, 23
O
Obstructive uropathy, vs. chronic renal failure, 43, 113, 114

vs. extrarenal pelvis, 28
Oncocytoma, 141, 144
INDEX
Opportunistic infection, 75, 75

Oxalosis, 63
P
Pancreatitis, pararenal space in, 9
Parapelvic cyst, 84, 85
vs. hydronephrosis, 84, 116
vs. varices, 184
Pararenal spaces, 7, 7, 9
Patient position, for biopsy, 36
Pelvic kidney, 30, 30
Pelvis, extrarenal, 28, 29
vs. renal artery aneurysm, 29, 177
vs. renal vein entrapment, 29, 183
Percutaneous biopsy, 35-37, 36, 37
Peripelvic cyst, 84, 85-86, 85, 86
vs. hydronephrosis, 85, 86, 116, 117, 218
Perirenal spaces, 7, 7
Perirenal vein, anomalous, 8
Peritoneal fluid, 194-195, 195
Peritoneum, allograft and, 201, 203, 205, 205
Pneumocystis carinii infection, 75, 75
POEMS syndrome, vs. amyloidosis, 50
Polycystic kidney disease, 89, 204, 204
autosomal-dominant, 93-97. See also Autosomal-dominant
polycystic kidney disease.
autosomal-recessive, 102-103, 102

reverberation artifact in, 92
Preeclampsia, 50, 51
Pregnancy, allograft in, 213, 215
hydronephrosis in, 109, 112
kidney dimensions during, 15, 17
ureteral enlargement in, 28
Prostate gland, enlargement of, 122, 126
Proteinuria, in interstitial nephritis, 57
Pseudoaneurysm, 236-238, 237, 238
Pseudokidney, 4, 6
Pseudomembranous colitis, 6
Psoas muscle, 3, 4, 7
Pyelitis, emphysematous, 69-70, 70
Pyelonephritis, acute, 65-67, 66, 67
diffuse, 66
focal, 66, 67
hemorrhagic, 67
vs. abscess, 66, 68
chronic, 109, 110, 116
emphysematous, 69-70, 70
vs. infarction, 66, 110, 175
xanthogranulomatous, 73, 73
Pyonephrosis, 70-72, 71
vs. calyceal hemorrhage, 71, 190
vs. fungal infection, 71, 73
vs. xanthogranulomatous pyelonephritis, 71, 73
R
Reflux nephropathy, vs. chronic interstitial nephritis, 60
vs. renal artery disease, 110, 173
Refraction artifact, 131, 133, 133
Renal artery, 167, 168, 170
aneurysm of, 176, 177
vs. varices, 177, 184
calcification of, 172, 173
Renal artery (Continued)

fibromuscular dysplasia of, 173, 173
stenosis of, 171-173, 172, 233, 235
thrombosis of, 177, 235
vs. venous engorgement, 179
Renal cell carcinoma, 141-148, 142-145
cystic necrosis in, 147, 148
in von Hippel-Lindau disease, 144, 148
multilocular cyst within, 147, 147
thrombus with, 145
vs. abscess, 68, 147, 148
vs. acute pyelonephritis, 67
vs. angiomyolipoma, 143, 144, 155
vs. duplication artifact, 145, 146
vs. hematoma, 189
vs. hydatid disease, 76-77, 147, 148
vs. tuberculosis, 75
vs. xanthogranulomatous pyelonephritis, 73, 147, 148
Renal failure, chronic, 41-43, 42, 43
sulfadiazine-induced, 63
Renal papillae, necrosis of, 60
vs. hydronephrosis, 59, 60, 116
sloughed, 61
Renal sinus, angiomyolipoma of, 157
lymphoma of, 151, 154
Renal vein, 167, 168, 170
dilation of, vs. hydronephrosis, 116, 180
engorgement of, 179, 180
entrapment of, 182-183, 183
left, 170
right, 168, 169
thrombosis of, 180-182, 181, 182, 235-236, 236
vs. acute interstitial nephritis, 57, 181
vs. acute tubular necrosis, 55-56, 181
vs. venous engorgement, 179, 181
vs. allograft-related hydronephrosis, 180, 199, 218
Renovascular disease, 171-184. See also Renal artery; Renal vein.
Retroperitoneum, 7, 7
Reverberation artifact, 90, 92
S
Sarcoma, vs. hematoma, 189
Scar, vs. dromedary hump, 28, 110, 175
vs. fetal lobulation, 27, 110, 175
Segmental vein, 13
Seminal vesicles, cystic enlargement of, 122
Septated cyst, 90, 90
Seroma, 229, 230, 231
Shadowing artifact, 18
Sickle cell nephropathy, 59
Simple cysts, 81-84, 82-84, 82t
in hydronephrotic kidney, 84
prevalence of, 82t
renal pelvis obstruction with, 83
vs. autosomal-dominant polycystic kidney disease, 97
Spleen, 3, 4, 5
accessory, 6
Splenosis, vs. epithelial tumor, 146, 146
Staghorn calculi, 132, 132
247
248
I NDEX
Stent, ureteral, 135, 138

Sulfadiazine, toxicity of, 63, 129, 133
Supernumerary kidney, 30, 31
T
Thrombosis, of renal artery, 177, 235
of renal vein, 235-236, 236. See also Renal vein, thrombosis of.
Torsion, 239-240, 240
Transitional cell carcinoma, 151, 152, 153
vs. calyceal hemorrhage, 190
vs. duplication, 24
vs. hydronephrosis, 116
vs. hypertrophied column of Bertin, 24, 24
Tuberculosis, 74-75, 74
Tuberous sclerosis, cyst in, 97, 101, 101
Tumors. See also Renal cell carcinoma; Transitional cell carcinoma.
cystic, 147-148, 147, 148
epithelial, 141-146, 142-146
vs. nodular compensatory hypertrophy, 146, 146
vs. splenosis, 146, 146
metastatic, 161, 162
pelvocalyceal, 151-154, 152-154
vs. duplication artifact, 145, 146
vs. infarction, 175
U
Ureter, 119, 122, 122, 123

bladder carcinoma obstruction of, 122, 125
dilation of, 122, 123, 124, 128
duplication of, 21-24, 22, 23
enlargement of, 28, 29
Ureter (Continued)
stones of, 122, 125
hydronephrosis and, 115
stricture of, allograft and, 217-218, 217, 218
urine jet from, 122, 123
Ureteral stent, 135, 138
Ureterocele, 122, 125
Urethra, catheter perforation of, 135, 137
obstruction of, 122, 126, 127
Uric acid deposition, 61, 62
Urine, ureteral jet of, 122, 123
Urinoma, 193-194, 193, 194
allograft and, 228-229, 228, 229, 231
vs. abscess, 68, 193, 228
vs. hematoma, 189
V
Varices, intrarenal, 183-184, 183
Vena cava, inferior, 168, 170
thrombus in, 182
Venous engorgement, in allograft, 201, 202
Volume, renal, 15
in renovascular disease, 171, 172
Von Hippel-Lindau disease, cyst in, 97, 104, 104
renal cell carcinoma in, 144, 148
Wilms' tumor, vs. hematoma, 189

X
Xanthogranulomatous pyelonephritis, 73, 73
vs. multicystic dysplastic kidney, 73, 105

Atlas of Renal Ultrasonography

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CONTENTS

SECTION I ANATOMY AND SONOGRAPHY OF

RENAL PARENCHYMAL DISEASE

SECTION III CYSTS AND CYSTIC DISEASE

SECTION IV THE COLLECTING SYSTEM AND DISTAL

SECTION V NEOPLASTIC DISEASE

SECTION VI VASCULAR DISORDERS

SECTION VII RENAL TRAUMA

SECTION VIII SONOGRAPHY OF RENAL ALLOGRAFTS

ATLAS OF RENAL ULTRASONOGRAPHY

ATLAS OF RENAL ULTRASONOGRAPHY

The tissue compartments surrounding the kidneys are diagrammed in Figure

ATLAS OF RENAL ULTRASONOGRAPHY

(K) showing a fluid collection (arrows) betweeen the kidney

he kidneys should first be imaged in the longitudinal axis until a maximal

ATLAS OF RENAL ULTRASONOGRAPHY

SONOGRAPHY OF THE NORMAL KIDNEY

ATLAS OF RENAL ULTRASONOGRAPHY

SONOGRAPHY OF THE NORMAL KIDNEY 15

165 170 175

180 185 190 195

ATLAS OF RENAL ULTRASONOGRAPHY

SONOGRAPHY OF THE NORMAL KIDNEY 17

ATLAS OF RENAL ULTRASONOGRAPHY

echogenic than the liver and there is a progressive decrease in echogenicity so

SONOGRAPHY OF THE NORMAL KIDNEY

evelopmental variants are common and usually of no clinical significance

uplication of the collecting system is a common abnormality that arises

ATLAS OF RENAL ULTRASONOGRAPHY

ATLAS OF RENAL ULTRASONOGRAPHY

HYPERTROPHIED COLUMN OF BERTIN

JUNCTIONAL FUSION DEFECT

ATLAS OF RENAL ULTRASONOGRAPHY

FUSED MEDULLARY PYRAMID

ATLAS OF RENAL ULTRASONOGRAPHY

dromedary hump is seen in the left kidney and is of no clinical importance

ATLAS OF RENAL ULTRASONOGRAPHY

ECTOPIAS AND FUSIONS

ATLAS OF RENAL ULTRASONOGRAPHY

junction. Coronal view showing two right kidneys (arrowheads)

onography has revolutionized percutaneous renal biopsy, making it a far

ATLAS OF RENAL ULTRASONOGRAPHY

PERCUTANEOUS RENAL BIOPSY

he most common complication is hemorrhage, which is easily diagnosed by

ATLAS OF RENAL ULTRASONOGRAPHY

he natural history of many renal diseases converges on a final common state

he sonographic appearance of chronic renal failure is easily recognized12

ATLAS OF RENAL ULTRASONOGRAPHY

CHRONIC RENAL FAILURE

ATLAS OF RENAL ULTRASONOGRAPHY

ATLAS OF RENAL ULTRASONOGRAPHY

ATLAS OF RENAL ULTRASONOGRAPHY

OTHER GLOMERULAR DISORDERS

ncreased echogenicity occurs in hemolytic uremic syndrome and may correlate

ATLAS OF RENAL ULTRASONOGRAPHY

Acute Tubular Necrosis

ATLAS OF RENAL ULTRASONOGRAPHY

ACUTE TUBULAR NECROSIS

ATLAS OF RENAL ULTRASONOGRAPHY

be no venous engorgement in ATN unless volume overload or right heart failure

ACUTE INTERSTITIAL NEPHRITIS

ATLAS OF RENAL ULTRASONOGRAPHY

CHRONIC INTERSTITIAL NEPHRITIS