shosh: renal pathology

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  1. Name the nephrotic syndromes
    • MCD
    • Membranous glomerulonephritis
    • FSGS
    • Membranoproliferative glomerulonephritis
    • Mesangial proliferation
  2. Name the nephritic syndromes
    • IgA nephrophathy (Berger's disease)
    • Poststreptococcal glomerulonephritis
    • TTP-HUS
    • Alport's
    • Membranoproliferative glomerulonephritis
    • Henoch-Schonlein purpura
  3. Glomerular disease with cresents on light microscopy
    • Goodpasture's
    • Immune complex diseases (Henoch-Schonlein, hypersensitivity vasculitis, cryoglobullinemia, SLE)
    • Pauci immune diseases (Wegener's, Churg-Strauss, microscopic polyarteritis, PAN)
  4. Acute poststreptococcal GN
    • Seen in children, following a strep infection with impetigo and periorbital edema
    • Enlarged, hypercellular glomeruli
    • Subepithelial immune complexes on EM
    • Granular immunofluorescence pattern
  5. Rapidly progressive glomerulonephritis
    • Crescents on light microscopy and immunofluorescence
    • Includes Goodpasture's, Wegener's, and microscopic polyarteritis
  6. Renal and lung disease with crescents on light microscopy and linear immunofluorescence
  7. Subendothelial immune complexes with wire loop capillary pattern on light microscopy and granular immunofluorescents
  8. Immune complex deposits in mesangium with symptoms of nephritic syndrome, following acute gastroenteritis or URI
    Berger's disease, IgA nephropathy
  9. Alport's disease
    Caused by a mutation in type IV collagen. Splitting of the basement membrane with ocular disorders and deafness
  10. Membranous glomerulonephritis
    • Mosst common cause of adult nephrotic syndrome
    • Diffuse capillary and GBM thickening on light microscopy
    • Spike and dome appearance with subepithelial deposits on EM
  11. Minimal change disease
    • Nephrotic syndrome that may be triggered by a recent infection and is most common in children
    • No abnormalities on light microscopy
    • Podocyte destruction on EM which causes loss of albumin, due to impaired charge barrier
  12. Diabetic glomerulonephropathy
    • Non-enzymatic glycosylation increases thickness of glomerular BM
    • Non-enzymatic glycosylation of efferent arteriole increases GFR
    • LM shows mesangial expansion and nodular glomerulosclerosis
  13. FSGS
    • Causes nephrotic syndrome, seen in HIV patients and blacks
    • Segmental sclerosis and hyalinization on light microscopy
  14. Membranoproliferative glomerulonephritis
    • Can present as nephritic or nephrotic syndrome
    • Subendothelial immune complex deposition
    • Type I is associated with hep B and C, and shows tram track appearance (BM splitting)
    • Type II is associated with C3 nephritic factor and shows dense deposits on EM
  15. Causes of calcium oxalate kidney stones
    • Ethylene glycol poisoning or vitamin C overdose
    • Treat with thiazides
  16. Radiolucent kidney stones
    • Uric acid stones
    • Struvite stones (may also be radioopaque)
  17. Von Hippel Lindau syndrome
    • AD, caused by deletion of a tumor suppressor gene on chromosome 3
    • Presents with cerebellar hemangioblastoma, pheochromocytoma, and renal cell carcinoma
  18. Deletion of WT tumor suppressor gene on chromosome 11
    Wilm's tumor--may also be associated with aniridia, genitourinary malformations, and retardation
  19. Drug induced interstitial nephritis
    • Acute inflammation of the renal interstitium with papillary necrosis
    • Presents with fever, rash, and hematuria
    • Elevated eosinophil count
    • Can be induced by NSAIDs, penicillin, sulfonamides, and rifampin
  20. Causes of acute tubular necrosis
    • Ischemia
    • Crush injury (causes myoglobinuria)
    • Toxins

    Granular, muddy brown casts in urine
  21. Renal papillary necrosis
    • Presents with gross hematuria and proteinuria
    • Associated with diabetes, acute pyelonephritis, chronic phenacetin use (e.g. acetaminophen), and sickle cell anemia
  22. Fanconi's syndrome
    • Decreased PCT transport of amino acids, glucose, phosphate, uric acid, and electrolytes
    • Can be congenital or drug induced (cyclophosphamide, expired tetracycline)
    • Associated with Wilson's disease
    • Decreased bicarb absorption can cause type II renal tubular acidosis
    • Compensatory increased Na reabsorption causes K wasting
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shosh: renal pathology
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