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Tubulointerstitial disease ERF 12/12/06

Quizbank: Kidney #41-53, 63-77, 173-179, 192-204, B) Complex pathophysiology


220-240 1) Ischemia and nephrotoxins directly damage
tubules
I) Disorders of the proximal tubule 2) Systemic hypotension and severe poisoning also
A) Congenital: Inborn errors of transport cause intrarenal vasoconstriction, which
1) Renal glycosuria compounds ischemic damage and lowers GFR
2) Renal transport aminoacidurias 3) Damaged tubules become obstructed by casts
B) Acquired Fanconi syndrome: and crud, which further lowers GFR
1) Poisoning: lead, cadmium, bismuth, oxalate, 4) Direct glomerular damage may occur
outdated tetracycline 5) Tubular backleak contributes to oliguria
2) Systemic disease: Wilson’s, plasma cell 6) In ATN, the renal output is normal or low; the
myeloma urine is iso-osmotic with Na concentration close
II) Acute tubular necrosis- to that in glomerular filtrate

Higher mag
Low magnification: note the dilated convoluted tubules, and
their necrotic epithelial walls that shed into the lumen of the
tubules. Glomeruli are relatively intact.
A) What you call all forms of acute renal failure caused
by damage to tubular epithelial cells
1) Ischemic ATN: caused by ischemia (shock,
hemorrhage, septic shock, etc). Also seen in new
transplants, from contrast media, in low-output
states, NSAIDs & ACE-I’s
2) Nephrotoxic ATN: caused by a wide variety of
renal poisons, including heavy metals (mercury),
organic solvents, or antimicrobial agents
3) Pigment nephropathy-massive hemolysis (red
cell stroma plugs the tubules, ABO mismatch,
falciparum malaria, et al), massive
rhabdomyolisis, crush injury, lightening, Higher magnification view showing a normal glomerlus
cocaine, beatings, etc surrounded by necrotic tubules.
4) Viral hemorrhagic fevers often cause temporary
renal shutdown

The tubular vacuolization and dilation here is a result of


ethylene glycol poisoning. This is representative of acute
tubular necrosis (ATN), which has many causes. ATN ATN
resulting from toxins usually has diffuse tubular involvement,
whereas ATN resulting from ischemia (as in profound
hypotension from cardiac failure) has patchy tubular
nvolvement.
C) Histology reflects the pathophysiology
1) Ischemic ATN: a few necrotic cells or basement
membrane may be present. Look for dilated
tubules and interstitial edema. Proximal tubular
cells show evidence of regeneration at all stages
2) Nephrotoxic ATN: frank necrosis is often seen,
usually limited to proximal tubules, w/o rupture
of basement membranes
D) Clinical picture of iscehemic ATN
1) Onset during medical/surgical catastrophe
2) Oliguric stage- w/ urine production 50-400
mL/24 hours and isotonic
3) Diuretic stage- rapid loss of fluid and potassium;
tubule regeneration during this stage
4) Pt will recover unless : in deep coma, has
cancer, severe hypotension, or needs mechanical
ventilation This is an ascending bacterial infection leading to acute pyelonephritis.
E) Other causes of acute renal shutdown other than Numerous PMN's are seen filling renal tubules across the center
ATN: and right of this picture.
1) Atheroembolization
2) Severe rapidly progressive glomerulonephritis
3) Drug hypersensitivity
4) Vasculopathies
5) Hepatorenal syndrome
6) DIC
7) Acute urate nephropathy
8) Severe rapidly progressive glomerulonephritis
III) Hepatorenal syndrome
A) Kidney failure that develops in patients with liver
failure, without anatomic changes in the kidney. This
often follows enthusiastic administration of high-
powered diuretics to a cirrhotic “to help w/ ascites”
B) The pathophysiology is getting worked out
1) Liver failure from any cause produces
hypotension, and “hepatorenal syndrome” may
have component of “shock kidney”
2) Dilation of small arteries in the splanchnic bed The cut surface of this kidney demonstrates many small yellowish
and inappropriate constriction of small arteries microabscesses.
in the kidney
IV) Pyelonephritis and other upper UTI –extremely common
and serious in clinical medicine
A) Causes: Ascending infection (E. coli & gram
negatives, common), Hematogenous infection (staph
& TB, uncommon)
B) Acute pyelonephritis:
1) Predisposing conditions
(a) Bacterial virulence
(b) Urinary obstruction/stasis
(c) Mechanical factors
(d) Diabetes mellitus
(e) Not being circumcised
(f) Pt’s sex and age (<40 females; >40 males)
(g) Vesicoureteral reflux
At high magnification, many neutrophils are seen in the tubules and
(h) Asymptomatic bacteriuria
interstitium in a case of acute pyelonephritis.
(i) Pre-existing renal dzs, especially kidney
stones
(j) Not urininating when you need to, not
drinking enough water
2) PMN’s infiltrate the interstitium and tubules.
3) Patients have fever, pain at costovertebral angle,
PMN’s and white cell casts in the urine
4) Papillary necrosis is a dreaded complication of
acute pyelonephritis that occurs mostly in
diabetics
Acute pyelonephritis
Chronic pyelonephritis
3) An important cause of morbidity and mortality
in the wheelchair-bound
4) Xanthogranulomatous pyelonephritis is common
C) Chronic pyelonephritis (any chronic renal infection) and usually in those who have had several
1) Look for broad U-shaped scars over distorted episodes of acute PN
calyces. Scarring is most likely to be present at (a) Caused by Proteus and a problem w/
renal poles cGMP & probably begins as a penetrating
ulcer of a calyx
(b) Located mostly around the pelvis, the
process tends to spread and can grow out
around kidney and erode the area around
the kidney and produce fistulas to the groin,
back or gut
(c) Lipid-laden macrophages form yellow
nodules that look like renal cell carcinoma
grossly & microscopically

The large collection of chronic inflammatory cells here is in a


patient with a history of multiple recurrent UTI. This is chronic
pyelonephritis.

In this specimen the renal pelvis (P) and the calyces (C) are
dilated.
D) Other causes include lupus and other “autoimmune”
problems that generate anti-TBM antibody
E) The BK polyomavirus causes a nephritis in the
Both lymphocytes and plasma cells are seen at high immunosuppressed
magnification in this case of chronic pyelonephritis. It is not
uncommon to see lymphocytes accompany just about any
chronic renal disease: glomerulonephritis, nephrosclerosis,
pyelonephritis. However, the plasma cells are most
characteristic for chronic pyelonephritis.
2) Microscopically it is a patchy process with
periglomerular fibrosis and interstitial scarring
(“thyroidization”)
F) TB of the kidney is relatively common b/c of high (b) Sulfa drugs, rifampin, cyclosporine et al are
oxygen tensions. If there are WBC in urine & no important causes
bacteria, get a TB culture 2) If biopsied, edema is present & interstitial
mononuclear cell infiltration, EOS and NEUTS
may be found too
NOTE: The other important cause of
eosinophiliuria is atheroembolization
B) Analgesic nephritis
1) Chronic renal failure used to be common in
those who took phenacetin-containing
combinations for pain
2) Asprin, fenprovin, naproxen, phenylbutazone,
indomethacin, and ibuprofen have all produced
similar lesions
3) Chronic interstitial inflammation is
characteristic and many patients develop
papillary necrosis
C) Classic non-steroidal anti-inflammatory agents
1) May be today’s most common cause of renal
shutdown in outpatients
2) The prevalence reverses on removal of the
offending drug, is just now being recognized
D) Lithium nephropathy- mostly nephrogenic diabetes
insipidus, supposedly due to fibrosis around the
collecting duct
E) Cyclosporine nephropathy- interstitial fibrosis seems
to result from direct toxicity to tubular epithelial cells
1) Look for:
(a) Hydropic change in proximal tubular cells
(b) Giant mitochondria in tubular cells
TB of kidney
(c) Myxoid change in intima of small vessels
V) Chronic interstitial nephritis- scarring of the kidney from a
(d) Tubular microcalcifications
process that is primarily interstitial
(e) Necrosis of the smooth muscle cells of
blood vessels
(f) Tubular atrophy and interstitial fibrosis
2) Other poisons: cadmium, lead, and bismuth
VII) Hypercalcemic nephropathy- when serum potassium is
very low, the kidney cannot concentrate urine
VIII) Plasma cell meyloma kidney
A) Precipitation of Bence-Jones proteins causes renal
shutdown. Patients experience acute or insidious
onset of renal failure
1) Amorphous pink casts, often surrounded by a
foreign-body reaction w/ multinucleated giant
cells
B) Patients often get amyloidosis B
IX) Oxalate nephropathy- Antifreeze drinkers, inborn errors,
and extreme ascorbic acid abusers; Oxalic acid crystals
interstitial nephritis ruin the kidney
A) Used to be called “chronic pyelonephritis” (which is X) Radiation nephritis- following therapeutic radiation,
an important cause) interlobular arteries narrow. This eventually causes HTN
B) Lupus and Sjogren’s often include an acute or and renal failure
chronic interstitial nephritis, a minor problem XI) Nephrogenic diabetes insipidus- collecting duct is unable
C) “Granulomatous CIN” is due to drugs or sarcoid, the to respond to ADH; could be inborn errors of metabolism
latter is less severe or lack of ADH receptor; gross and widespread damage to
D) Anti-tubular basement membrane antibody is a the medullar occurs and late effects of lithium therapy for
research tool, but no one knows its importance mania
VI) Tubulointerstitial nephritis caused by drugs and poison
A) Acute drug-induced (hypersensitivity) nephritis
1) W/in a month after drug exposure, victim
develops fever, skin rash, eosinophilia,
hematuria, proteinuria, sterile pyuria, and/or
eosinophiliuria. Withdrawal of drugs makes
things better
(a) Methicillin is best known offending drug
XII) Gout PP 10-12 (happy reading)

This is gout. Gouty arthritis results from deposition of sodium urate


crystals in joints. The joint most often affected is the first MP
joint (big toe) as seen here. Acute attacks are characterized by
severe pain, swelling, and erythema of the joint.

If synovial fluid is aspirated from a patient with gout, the fluid can
be examined for the presence of sodium urate crystals, which
are seen here to be needle shaped. If they are observed under
polarized light with a red compensator, they appear yellow
(negatively birefringent) in the main ("slow") axis of the
compensator and blue in the opposite perpendicular direction.

Gout tophus

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