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Name the nephrotic syndromes
- MCD
- Membranous glomerulonephritis
- FSGS
- Membranoproliferative glomerulonephritis
- Mesangial proliferation
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Name the nephritic syndromes
- IgA nephrophathy (Berger's disease)
- Poststreptococcal glomerulonephritis
- TTP-HUS
- Alport's
- Membranoproliferative glomerulonephritis
- Henoch-Schonlein purpura
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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)
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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
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Rapidly progressive glomerulonephritis
- Crescents on light microscopy and immunofluorescence
- Includes Goodpasture's, Wegener's, and microscopic polyarteritis
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Renal and lung disease with crescents on light microscopy and linear immunofluorescence
Goodpasture's
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Subendothelial immune complexes with wire loop capillary pattern on light microscopy and granular immunofluorescents
SLE
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Immune complex deposits in mesangium with symptoms of nephritic syndrome, following acute gastroenteritis or URI
Berger's disease, IgA nephropathy
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Alport's disease
Caused by a mutation in type IV collagen. Splitting of the basement membrane with ocular disorders and deafness
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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
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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
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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
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FSGS
- Causes nephrotic syndrome, seen in HIV patients and blacks
- Segmental sclerosis and hyalinization on light microscopy
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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
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Causes of calcium oxalate kidney stones
- Ethylene glycol poisoning or vitamin C overdose
- Treat with thiazides
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Radiolucent kidney stones
- Uric acid stones
- Struvite stones (may also be radioopaque)
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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
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Deletion of WT tumor suppressor gene on chromosome 11
Wilm's tumor--may also be associated with aniridia, genitourinary malformations, and retardation
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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
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Causes of acute tubular necrosis
- Ischemia
- Crush injury (causes myoglobinuria)
- Toxins
Granular, muddy brown casts in urine
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Renal papillary necrosis
- Presents with gross hematuria and proteinuria
- Associated with diabetes, acute pyelonephritis, chronic phenacetin use (e.g. acetaminophen), and sickle cell anemia
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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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