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A case of acute kidney injury due to complex,

partial, multifocal ureteral strictures
Alan Segal

S U M M A RY
Background An 89-year-old man with a history of prostate cancer

who had undergone radical prostatectomy 15years ago presented with

hyperkalemia (serum potassium level 6.9mmol/l) and kidney failure
(serum creatinine level 937mol/l [10.6mg/dl]). Ultrasound scan of his
kidneys showed mild bilateral hydronephrosis. Although placement of a
bladder catheter led to an initial increase in glomerular filtration rate, the
improvement was delayed and incomplete. Subsequently, the patients
glomerular filtration rate decreased acutely. This unusual biphasic course
of kidney injury begged explanation.
Investigations Physical examination, measurements of serum creatinine
level and electrolytes, imaging of the urinary tract (ultrasound and CT
scans), and nephrostograms.
Diagnosis Acute kidney injury due to upper (multiple ureteral strictures
bilaterally) and lower (urethral) urinary tract obstruction.
Management Placement of bladder catheter and percutaneous
nephrostomy tubes followed by bilateral internal ureteral stents.
keywords acute kidney injury, hydroureteronephrosis, nephrostogram,
ureteral stent, ureteral stricture

cme

A Segal is an Associate Professor in the Division of Nephrology and Program

Director of the Nephrology Training Program at the University of Vermont,
Colchester, and Fletcher Allen Health Care, Burlington, VT, USA.
Correspondence
Division of Nephrology, Departments of Medicine, Molecular Physiology & Biophysics and
Pharmacology, University of Vermont, 208 South Park Drive, Suite 2, Colchester, VT 05446, USA
alan.segal@uvm.edu
Received 11 July 2007 Accepted 16 October 2007
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doi:10.1038/ncpneph0698

102 nature clinical practice NEPHROLOGY

Vanderbilt Continuing Medical Education online

This article offers the opportunity to earn one Category 1
credit toward the AMA Physicians Recognition Award.
Competing interests
The author declared no competing interests.

THE CASE

An 89-year-old man with a history of hyper

tension, hypercholesterolemia, and stageD2
prostate cancer presented to an outside emergency department with complaints of diarrhea
and mild lower abdominal discomfort for
1week. Blood tests in the emergency department
showed a serum creatinine level of 937mol/l
(10.6mg/dl) and a serum potassium concen
tration of 6.9mmol/l. The patient was treated
for hyperkalemia with sodium polystyrene sulfonate, insulin and glucose. A renal ultrasound
revealed that the patients kidneys were 11.3cm
in length, and that mild bilateral hydronephrosis
was present. A Foley bladder catheter was placed
and the patient was admitted to the outside
hospital. Despite receiving 1liter of 0.9% sodium
chloride solution, the patients serum creatinine
level had increased to 955mol/l (10.8mg/dl)
the following morning, so he was transferred to
another institution for further management and
possible dialysis.
The patient had no history of kidney disease.
He related that he had undergone radical
prostatectomy for prostate cancer 15years before
admission to the second institution. Adjuvant
treatment at that time had included a course
of anti-androgens and some radiation therapy.
About 23years before the current admission,
the patients doctors had discovered lesions
in his spine that were thought to represent
metastatic disease. The patient had increasing
urinary urgency, increasing urinary frequency
and nocturnal enuresis that had all started
1week before the current admission. Other
than increasing weakness and fatigue over the
past month, the review of systems was negative.
At admission, the patient was on losartan 25mg
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per day and fluvastatin 30mg per day. He did not
use tobacco or alcohol.
On physical examination, the patient appeared
younger than his stated age. He was weak but
in no acute distress. His vital signs were as
follows: blood pressure 148/70mmHg; heart rate
72beats per minute; respiratory rate 18breaths
per minute; and temperature 37.2C. Oxygen
saturation of the blood was 97% on room air.
The patients skin was remarkable for multiple
actinic keratoses, but no acute rash was present.
The patients head and neck were normal and
without adenopathy. His lung fields were clear
and his heart sounds were normal. The patients
abdomen was soft, nontender and without
palpable masses. A bladder catheter draining
blood-tinged urine was in place. Rectal examina
tion revealed a firm pelvic mass in the prostatic
base that extended to the bladder base. The
patients extremities were without edema. His
neurological examination was within normal
limits and there was no asterixis.
Upon admission, blood tests showed the
following: sodium level 137mmol/l; potassium
level 6.1mmol/l; chloride level 106mmol/l; total
carbon dioxide concentration 19mmol/l; and
creatinine level 955mol/l (10.8mg/dl). The
patients white blood cell count was 10.97109/l
and his hematocrit was 31.6%. Urinalysis
revealed grossly bloody urine containing
numerous red blood cells and white blood cells.
Urine culture was negative.
CT scan of the patients abdomen showed
mild bilateral hydronephrosis with ureteral
distention to the level of the bladder. Diffuse
wall thickening of the bladder was also revealed.
Mildly enlarged retroperitoneal and iliac chain
lymph nodes were noted, as was a 2cm sclerotic
lesion at the T12 level, suspicious for metastatic
prostate cancer.
The patients hyperkalemia resolved after the
second hospital day and his serum potassium
level remained under control for the remainder
of the hospitalization.
The time course of kidney function during the
hospitalization is shown in Figure 1. The patients
serum creatinine level peaked at 955mol/l
(10.8 mg/dl) on the second hospital day and
remained above 884mol/l (10mg/dl) for
72hours, despite a bladder catheter being in
place. Dramatic improvement in the patients
kidney function occurred on the fourth hospital
day, and his serum creatinine level reached a
nadir of 207mol/l (2.34mg/dl) on the fifth day.

Serum creatinine (mg/dl; x 88.4 to convert to mol/l)

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12

Foley catheter

11
10
9
8
7
PCNTs

Stents

5
4
3
2
1
0
0

10

11

12 13

14

15

Hospital day

Figure 1 Kidney function throughout the course of hospitalization. Note that

despite the presence of a Foley catheter, there was a delay of approximately
48hours before the initial improvement in kidney function, and a worsening of
kidney function after day5. Bilateral PCNTs were placed on day9 and were
removed on day13, when bilateral internal ureteral stents were placed. The
dashed line indicates the baseline serum creatinine level of 70mol/l (0.8mg/dl).
Abbreviation: PCNTs, percutaneous nephrostomy tubes.

The patients kidney function deteriorated again

over the next 4days, however, with his serum
creatinine level rising to 466mol/l (5.27mg/dl)
on the ninth hospital day. Bilateral percutaneous
nephrostomy tubes (PCNTs) were placed on the
ninth hospital day. The patients kidney function
improved dramatically again following placement of the PCNTs, with his serum creatinine
level decreasing to 167mol/l (1.89mg/dl) the
next day and returning to an apparent baseline
of ~70mol/l (~0.8mg/dl) over the next few
days. On the thirteenth hospital day, the bladder
catheter was removed and the bilateral PCNTs
were replaced with internal ureteral stents. The
patient was discharged in fair condition on
the fourteenth hospital day. Follow-up laboratory tests performed 1month later showed a
serum creatinine level of 79.5mol/l (0.9mg/dl).
Unfortunately, the patient died of his metastatic
disease the following month.
DISCUSSION OF DIAGNOSIS

The unusual case presented here is that of an

89year-old man who presented with marked
acute renal failure due to complex, partial,
multifocal, bilateral ureteral strictures. Despite

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Figure 2 Nephrostograms. (A) Left nephrostogram demonstrating a very

high grade distal ureteral stricture (arrow) extending to the left UVJ. (B) Right
nephrostogram demonstrating a high grade distal ureteral stricture at the right UVJ
(arrow). (C) Nephroureterocystogram from just after placement of bilateral internal
ureteral stents on hospital day 13. Abbreviation: UVJ, ureterovesical junction.

the chronicity of the structural abnormalities, the

renal failure was acute (as evidenced by
the normal appearance of the kidneys), and
kidney function normalized completely following
placement of bilateral ureteral stents. The differential diagnosis and pathogenesis of obstructive
uropathy has been the subject of a number of
review articles.14

secondly, no episode of hypotension or exposure to a potential nephrotoxin had occurred

that might have caused ATN; and thirdly, no
new medication that could have caused AIN had
been administered.
Given that lower urinary tract obstruction
would be expected to resolve upon placement
of a bladder catheter, the possibility of upper
urinary tract obstruction had to be considered.
It should be noted that such upper urinary
tract obstruction would have to be bilateral
and involve both ureters and/or ureterovesical
junctions (UVJs). To explore this possibility,
placement of bilateral PCNTs and nephrostograms were performed on the ninth hospital
day. The nephrostograms showed bilateral hydro
ureteronephrosis with multifocal stenoses (i.e.
strictures) in both ureters. The left nephrostogram demonstrated a stricture in the mid-ureter
and a very high grade stricture in the distal
ureter extending to the left UVJ (Figure 2A).
The right nephrostogram revealed a stricture
in the proximal ureter at the level of the iliac
crest and a high grade stricture in the distal
ureter at the right UVJ (Figure 2B). These
ureteral strictures were most likely complications of the previous radiation treatment.57
Definitive treatment was provided by the placement of bilateral internal ureteral stents. A
nephroureterocystogram performed just after
placement of the stents is shown in Figure 2C.

Differential diagnosis of acute kidney injury

As judged from his history, the patient initially

appeared to have acute kidney injury (AKI)
that was due to lower urinary tract obstruction,
resulting in urinary retention with overflow
incontinence. Only ~350ml of urine drained
when a bladder catheter was placed, however,
indicating a modestly increased post-void
residual urine volume consistent with a component of bladder outlet obstruction, but one that
was too small to cause overflow incontinence.
Furthermore, if the AKI was due to urinary retention secondary to urethral obstruction, prompt
improvement would have been expected upon
placement of a bladder catheter. The biphasic
course of AKI was puzzling, and the differential
diagnosis during the waning phase included
renal hypoperfusion (perhaps associated with
postobstructive diuresis), and AKI due to acute
tubular necrosis (ATN) or acute interstitial
nephritis (AIN). Evidence against these diagnostic possibilities included the following: firstly,
there were no clinical signs of hypovolemia;

DISCUSSION OF PATHOPHYSIOLOGY
AND MANAGEMENT

The unusual features of this case can be summar

ized by the following questions. Firstly, why did
it take more than 48hours after bladder catheter placement to see the initial improvement
in kidney function? Secondly, why did all the
imaging procedures show only mild bilateral
hydronephrosis, which remained unchanged
despite placement of the bladder catheter? And
thirdly, what are the underlying mechanisms
that would explain the relapse after the fifth
hospital day?
One could propose that the answers to these
questions relate to multiple partial obstructions
in both the lower and upper urinary tract. The
mass palpated at the prostatic base, presumably a result of local recurrence of the prostate
cancer, most likely caused partial obstruction of
the lower tract at the level of the membranous
urethra.4 The nephrostograms showed that each
ureter had developed strictures, possibly due to

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previous radiation ureteritis,6,7 and high grade

stenoses in each distal ureter at the level of the
UVJ. Perhaps these multiple partial obstructions led to the decrease in glomerular filtration
rate (GFR) and the loss of ureteral peristalsis,
both of which might have contributed to the
delay between placement of the bladder catheter and initial improvement. Once this level of
functional obstruction improved, the GFR
of the patients well-preserved kidneys was
re-established, only to wane again when decompression of the bladder and ureters permitted
the ureteral strictures to narrow and become the
rate-limiting factor. The appearance of this
second functional obstruction led to a worsening
of GFR, which only improved after the PCNTs
were placed. Throughout all of these events, the
nephrostogram images continued to show only
mild bilateral hydronephrosis, probably due to
non-dilated obstructive uropathy810 from the
ureteral strictures.
The main determinants of GFR are as follows:
1) the hydrostatic pressure gradient across the
glomerular capillary, P, which is calculated by
PGCPT (where PGC and PT are the hydrostatic
pressures in the glomerular capillary and in
the Bowman space, respectively); 2) the colloid
oncotic pressure across the glomerular capillary,
, given by GCT (where GC and T are the
colloid oncotic pressures in the glomerular capillary and the Bowman space, respectively); and
3) the glomerular ultrafiltration coefficient, Kf,
given by the product of hydraulic permeability
and surface area for filtration. The GFR is given
by KfPUF, where PUF is the net pressure for
ultrafiltration, given by P. Because T is
negligible, GFR=Kf [PGC(PT+GC)].
In animal models, urinary tract obstruction is
associated with a biphasic increase in the hydrostatic pressure of the collecting system that is
transmitted back to the urinary space via the
tubules, resulting in a similar biphasic increase
in PT11 that directly decreases GFR. Interestingly,
obstruction affects GFR not only by changes in
PT, it also leads to complex changes in Kf and
in the autoregulation of renal blood flow, as
discussed in detail by Wright.11
The pressure in the ureter and the renal
tubules increases early in the course of experimental ureteral obstruction. Indeed, despite the
distensibility of the pelvicalyceal system, pressure in the ureter can exceed 50mmHg within
15minutes of obstruction in dogs undergoing
saline diuresis.11 Within 10hours, however, the
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pressure decreases to baseline in the ureter and

tubules (~12mmHg) in the case of complete
unilateral ureteral obstruction. In contrast to
ureteral pressure, GFR falls rapidly after obstruction, decreasing by approximately 75% within
6hours, and staying at this level for 24hours
after obstruction.11,12 This finding might in
part explain why it took more than 48hours
for the GFR to begin to improve in the patient
presented here.
The schematic diagrams shown in Figure 3
provide an interpretation of the events occurring in the patient described in this Case Study.
Figure3A is a model of the urinary tract in
health, and depicts the outflow of urine from the
kidney. The final urine exiting the collecting ducts
of the kidney drains into the renal pelvis and
flows through the ureteropelvic junction. From
there, it is transported down the ureters, which
are distensible and collapsible muscular tubes
that undergo peristalsis.1316 The urine then
passes through the UVJwhich acts as a oneway valveinto the bladder.17 The urine is stored
in the bladder until it is voided by the process
of micturition, which involves the opening of
the urethral sphincter in association with
contraction of the bladder, in order to provide
pressure-driven flow through the urethra.
Figure 3B models the probable situation in
the patient over the weeks before his admission
to hospital. He had partial strictures in both
ureters (only one ureter is shown), abnormally
low ureteral compliance due to fibrosis, and
partial bladder outlet obstruction. The ureteral
strictures resulted in restriction of urine flow
(and also abnormal ureteral peristalsis), but the
presence of bladder outlet obstruction produced
enough back pressure to keep the ureters open at
the level of the strictures. That is, the back pressure kept the intraureteral pressure above the
tube pressure,14 so that, despite some ongoing
reflux, the ureters did not collapse.
As this process was progressing over time, the
(probable) radiation-induced ureteral strictures
presented more resistance to reflux than would
have otherwise occurred, leading to further
bladder wall thickening and also limiting the
extent of hydroureteronephrosis. The latter is
not only due to the resistance produced by the
strictures, but also from decreased compliance
of the upper urinary tract. Increased pressurization of the whole system because of decreased
bladder volume and compliance could explain
the symptoms of overflow incontinence at low
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Kidney

Ureteropelvic
junction

Renal pelvis
Ureteral
stricture

Ureter
Normal
ureteral
compliance
Ureterovesical
valve

Ureteral
stricture
Abnormal
ureteral
compliance

Abnormal
ureteral
compliance

Ureterovesical
junction
Bladder
Urethral
sphincter

Impending
bladder outlet
obstruction

Urethral
sphincter

Urethral
sphincter

Ureteral
stent

Ureteral
stricture with
obstruction

Ureteral
stricture

Established
bladder outlet
obstruction

Abnormal
ureteral
compliance

Abnormal
ureteral
compliance

Abnormal
ureteral
compliance

Foley
catheter

Foley
catheter

Foley
catheter

Figure 3 Schematic hydrodynamic models showing an interpretation of the events occurring in the patient.
The models illustrate the outflow of urine from the kidney. The thickness and completeness of the vertical
arrows represent the ease of urine flow. Please see the main text for details of what each panel represents.
(A) Schematic model of the urinary tract in health. (B) Schematic model of the situation in the patient during
the weeks just before his admission to the first hospital. (C) Schematic model of the situation in the patient
upon hospital admission. (D) Schematic model of the situation just after placement of a Foley catheter.
(E) Schematic model of the situation 5days after placement of a Foley catheter. (F) Schematic model of the
situation following the placement of ureteral stents.

bladder volumes, as well as the signs of functional (upper and lower) obstruction despite
only mild hydronephrosis.
Figure 3C illustrates the probable situation when the patient was admitted to the
first hospital. At that point, the bladder outlet
obstruction had become critical; the reflux
and obstruction worsened and the patient
developed severe renal failure, with his serum

creatinine level peaking at 970mol/l (11mg/dl).

The presence of chronic fibrosis along the
urinary tract prevented the development of more
than mild hydroureteronephrosis,810 despite a
marked decrease in GFR. As in Figure 3B, the
increased back pressure caused by the bladder
outlet obstruction kept the intraureteral pressure above the tube pressure, thereby preventing
collapse at the level of the strictures.

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On admission to the first hospital, a bladder

catheter was placed. Initially, catheterization decompressed the bladder, but had little
effect on the upper urinary tract obstruction.
Figure3D shows the situation early in the course
of hospitalization. Although placement of the
catheter across the urethral sphincter relieved
the bladder outlet obstruction, the patients
GFR did not improve for more than 48hours.
This phenomenon, which in this case might have
been related to abnormal peristalsis, has been
observed in animal models after the release
of complete ureteral obstruction.11,12 At this
point, the partial ureteral strictures remained
patent; once peristalsis resumed, the patients
GFR improved markedly and his serum creatinine level fell from ~970mol/l (11mg/dl) to
207mol/l (2.34mg/dl).
Following this marked improvement, however,
the patients GFR began to fall progressively after
day 5, despite a working Foley bladder catheter.
A hypothetical model to explain this situation is
presented in Figure 3E. At this point, the hypo
thesis is that, following the return of ureteral
peristalsis, relief of the lower tract obstruction
allowed enough decompression of the system to
permit reduction of the back pressure to below
the tube pressure, causing essentially complete
(and bilateral) ureteral obstruction.
The placement of bilateral PCNTs a few days
later immediately improved the situation by
providing low resistance pathways for urine
flow directly out of the renal pelves by means
of completely bypassing the ureters (with their
strictures and lack of peristalsis), thickened
small volume bladder, and any residual bladder
outlet obstruction. As the latter was then of no
consequence, the bladder catheter was removed
when serum creatinine fell to its baseline level
of ~70mol/l (0.8mg/dl). Four days later, the
PCNTs were removed and internal ureteral stents
were placed bilaterally. The placement of internal
ureteral stents (Figure 2C) provided a long-term
solution. This final situation is schematized in
Figure 3F. Definitive treatment with ureteral
stents permitted the normal passage of urine
flow, regardless of the lack of peristalsis and
decreased ureteral compliance.
CONCLUSIONS

The manner in which this patient presented

and the way in which the complex, partial, multifocal upper and lower urinary tract obstructions
unfolded provide insights into the pathogenesis
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of obstructive uropathy. Bilateral partial obstruction in the upper urinary tract was produced by
high grade ureteral strictures that were most
likely caused by radiation ureteritis. Partial
obstruction of the lower urinary tract was probably a result of local recurrence of prostate
cancer. Because the upper urinary tract obstruction was rate-limiting, the initial management
aimed at relieving the partial obstruction of the
lower urinary tract enabled us to make additional
observations as the initial improvement gave
way to a subsequent relapse, and also allowed us
to develop an explanation (summarized in the
schematic diagrams) for each event that occurred
in the patient, reflecting the pathogenesis of the
obstructive uropathy.
Interim management with PCNTs led to a
prompt return of kidney function to baseline,
indicating that renal parenchymal function was
preserved despite the chronicity and complexity
of the partial obstruction; therefore, in contrast
to the poor outcome usually observed in animal
models (i.e. short-term, complete ureteral
obstruction),1,18 humans with postobstructive
uropathy (i.e. longer term, incomplete ureteral
or urethral obstruction) generally exhibit
improved and stable kidney function.19,20
Ultimately, the PCNTs were replaced by
internal ureteral stents. It might be expected
that internal stenting would have caused the
patients GFR to fall slightly in the future,
because the stents require urine to again exit
the ureteropelvic junctions and flow down
tubes that lack optimum peristalsis, enter
a small bladder, and then pass through any
residual bladder outlet obstruction. Indeed, a
slight decrease in GFR was noted 1month after
discharge. At that point, the upper urinary
tract obstructions had been relieved, albeit not
minimized as they were when the PCNTs were
in place, but the lower urinary tract obstruction might have again placed an upper limit on
the GFR.
Finally, it should be mentioned that although
serial measurements of serum creatinine
levels were sufficient for this case, emerging
biomarkers of AKI (e.g. cystatin C, interleukin18 and neutrophil gelatinase-associated
lipocalin) hold the promise of earlier detection,
faster kinetics, and increased sensitivity and/or
specificity for detection of AKI.2123 Such
bioassays might facilitate the modeling of AKI,
especially in cases where the GFR fluctuates in
both directions.
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Acknowledgments
The author is indebted to
Dr Christopher Morris,
Dr Anant Bhave, and their
superb team in the Division
of Interventional Radiology
at Fletcher Allen Health
Care for their valuable
contributions in this case.
The author would also like
to thank Professor Jason
Bates and Professor Burton
Sobel for reviewing the
manuscript and for helpful
discussions regarding the
development of Figure 3.

Competing Interests
The author declared no
competing interests.

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