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25 Cards in this Set
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Acute post streptococcal glomerulonephritis Nephritic or Nephrotic? Light microscopy findings Electron microscopy findings Immunoflurorescence findings |
Nephritic LM: Glomeruli is enlarged and hypercellular EM: Subepithelial immune complex humps IF: Lumpy bumpy appearance/ starry sky granular appearance, due to deposition of IgG, IgM and C3 along GBM (subepithelial humps) |
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Rapidly progressive glomerulonephritis Nephritic or Nephrotic? Light microscopy findings Electron microscopy findings Immunoflurorescence findings |
LM and IF: Show crescent moon shape IF Pattern is linear Deposits of IgG and C3 are present |
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Diffuse proliferative glomerulonephritis Nephritic or Nephrotic? Light microscopy findings Electron microscopy findings Immunoflurorescence findings |
Nephritic eventiually progressing to nephrotic Seen in SLE Most of the glomeruli show endothelial and mesangial proliferation affecting the entire glomerulus, leading to diffuse hyperceullarity of the glomeruli. When extensive, immune complexes create an overall thickening of the capillary wall, resembling rigid "wire loops" on routine light microscopy. Electron microscopy reveals electron-dense subendothelial immune complexes (IgG and C3). Immunofluoresecence shows a granular fluorescent staining pattern |
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Membranoproliferative glomerulonephritis Nephritic or Nephrotic Light microscopy findings Electron microscopy findings Immunoflurorescence findings |
Nephritic-Nephrotic Immunofluorescence: shows granular deposits PAS stain and H&E: show tram track appearance due to splitting of the glomerular basement membrane caused by mesangial ingrowth |
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IgA nephropathy (Berger Disease) Nephritic or Nephrotic? Light microscopy findings Electron microscopy findings Immunoflurorescence findings |
Nephritic LM: Mesangial proliferation EM: Mesangial immune complex deposits IF: IgA based immune complex deposit in mesangium |
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Alport syndrome How does it present? What kind of inheritance? Defect in what? EM shows? |
Nephritic Inherited defect in type IV collagen; Most commonly X-linked dominant Results in thinning and splitting of the glomerular basement membrane Presents as isolated hematuria, sensorineural deafness, and ocular disturbances (retinopathy, lens dislocation) EM: Shows basket weave appearance due to splitting of the GBM |
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Minimal change disease Nephritic or Nephrotic? Light microscopy findings Electron microscopy findings Immunoflurorescence findings |
Nephrotic LM: Normal glomeruli EM: Effacement of the foot processes Immunofluorescence is negative |
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Focal segmental glomerulosclerosis Nephritic or Nephrotic? Light microscopy findings Electron microscopy findings Immunoflurorescence findings |
LM: Segmental sclerosis and hyalinosis of glomeruli
EM: Also shows effacement of foot processes like in MCD Immunofluoresence is often negative (positive in few cases due to deposition of IgM, C3 and C1) |
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Membranous nephropathy Nephritic or Nephrotic? Light microscopy findings Electron microscopy findings Immunoflurorescence findings |
LM: diffuse capillary and GBM thickening H&E: also shows thick GBM EM: Spike and dome appearance with subepithelial deposits Immunofluorescence shows granular appearance due to immune complex deposition |
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What diseases fall under RPGN? |
Goodpasture disease Wegener Granulomatosis Microscopic polyangiitis |
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What is RPGN? |
Nephritic syndrome that progresses to renal failure in days to weeks |
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Hallmark of RPGN? |
Presence of crescents in the glomerular/bowmans spaes. Crescents consist of fibrin and plasma proteins e.g. C3b |
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Pauci immune glomereulonephritis indicates |
Indicates that there is no Ig or C3 deposition Seen in Wegener's and microscopic polyangiitis |
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Good pasture disease pathogenesis involves: |
Type II hypersensitivity; there are antibodies against the alpha 3 chain of collagen IV. This affects the glomerular BM and also alveolar BM. Responsive to plasmapharesis |
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Explain MPGN I |
Type I---- Involves subendothelial immune complex deposits of complement components i.e. C1, C4, IgG/. This leads to activation of both classical and alternative pathway for complement and results in decreased serum levels of C1, C4, and C3. May be secondary to hep. B or C infection |
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Explain MPGN II |
Also known as dense deposit disease Intramembranous deposits associated with C3 nephriticfactor (autoantibody that stabilizes C3 convertase,leading to overactivation ofcomplement, inflammation, and low levels of circulating C3) |
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How does IgA nephropathy present |
Presents during childhood as episodic gross or microscopic hematuria with RBCcasts, usually following mucosal (Respiratory or GI) infections Basically involves deposition of IgA in the mesangium |
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In general nephrotic syndrome presents with which symptoms: |
Hypoalbuminemia---> Pitting edema Hypercoagulable state----> Due to loss of antithrombin III Hypogammaglobulinemia----> Increased risk of infection Hyperlipidemia and hypercholesterolemia---> May result in fatty casts in urine |
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Features of minimal change disease |
MCC of nephrotic syndrome in kids Rarely may be secondary to Hodgkin lymphoma Selective proteinuria i.e. loss of albumin but not immunoglobulin Excellent response to corticosteroids May be triggered by recent infection, immunization, immune stimulus |
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FSGS may be secondary to which other conditions |
HIV Sickle cell disease Heroin abuse Massive obesity Interferon treatment |
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FSGS is often found in which group of people |
African Americans and Hispanics |
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Membranous nephropathy is most common in which group of people |
Caucasians |
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Membranous nephropathy may be secondary to which conditions: |
SLE Drugs e.g. NSAIDS, penicillamine Infections e.g. HBV, HCV Solid tumors |
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Name the primary cause of membranous nephropathy |
Antibodies to phospholipase A2 receptor |
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Pathophysiology of diabetic glomerulonephropathy |
Nonenzymatic glycosylation of GBM----> Increased permeability and thickening of the basement membrane Nonenzymatic glycosylation of the efferent arterioles----> Increased GFR and mesangial expansion |
