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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
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)
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