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26 Cards in this Set
- Front
- Back
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Nephrotic syndrome: clinical presentation |
Proteinuria: > 3.5 g/day Lipiduria, hyperlipidemia Hypoalbuminemia Edema (if diffuse podocyte injury) |
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Nephritic syndrome: clinical presentation |
"HAvE HOpe" Hematuria Azotemia Edema Hypertension Oliguria |
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Nephrotic syndrome: main types |
Minimal change disease Membranous nephropathy Focal segmental glomerulosclerosis (FSGS) |
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Acute nephritic syndrome: broad mechanism |
Sub endothelial deposits --> inflammation Preserved FPs |
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Acute nephritic syndrome: main types |
Post-strep glomerulonephritis Lupus nephritis Membranoproliferative glomerulonephritis |
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Rapidly progressive GN: common features (symptoms, microscopy) |
Clinical picture: nephritic but no edema, hypertension (time for equilibration) Light microscopy: focal necrotizing and crescentic GN |
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Rapidly progressive GN: main types |
ANCA diseases Anti-GBM disease |
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Hematuric syndromes: clinical presentation |
Hematuria, proteinuria normal renal function early in course Lack of edema or HTN |
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Hematuric syndromes: main types |
IgA nephropathy Thin basement membrane disease Hereditary nephritis |
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Systemic diseases: main types |
Diabetes mellitus Amyloidosis |
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Minimal change disease: classification, mechanism, microscopy |
Nephrotic syndrome Mechanism: idiopathic (infection, immune stimulation), secondary (drugs: NSAIDs, lymphoma, insect bites, SLE) - responds to steroids LM: normal; IF: negative EM: diffuse foot process effacement |
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Membranous nephropathy: classification, mechanism, microscopy |
Nephrotic syndrome Mechanism: in situ immune complex formation: (1) idiopathic: anti PLA2R, THSD7A (2) autoimmune (3) infection: hepatitis B/C, syphilis (4) drugs (5) tumors LM: GBM thickening, silver stain spikes IF: granular IgG (IgG4); C3, C1q negative EF: subepithelial deposits |
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FSGS: classification, mechanism, microscopy |
Class: nephrotic syndrome Mechanism: permeability factor --> foot process simplification LM: focal segmental glomerulosclerosis, hyalinosis IF: IgM aggregates, C3 positive EM: foot process effacement, mesangial expansion, podocyte loss |
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Post-strep glomerulonephritis: classification, clinical picture |
Class: acute nephritic Picture: ~2 weeks post strep Group A, resolves spontaneously, low C3 in serum |
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PSGN: microscopy |
LM: diffuse proliferative: all glomeruli enlarged, hypercellular, capillary occlusion by PMNs IF: granular IgG in capillaries and mesangium (polyclonal), C3+, C1q- (alternative pathway), fibrin+ (active inflamm) EM: sub-endothelial deposits, sub-epithelial humps |
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Lupus nephritis: class, microscopy |
Either acute or as RPGN (see focal necrotizing and crescentic lesions) LM: mononuclear hypercellularity, wire loops IF: granular IgG, C3+, C1q+ (classical complement) EM: large subendothelial, mesangial deposits |
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Membranoproliferative GN: class, light microscopy findings |
Nephritic syndrome LM: hypercellularity, duplicated basement membrane |
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MPGN: subtypes, IF and EM findings |
Infection, autoimmune: polyclonal Ig, C3+, C1q+ Paraprotein: monoclonal Ig, C3+, C1q+ Dense deposit, GN C3: no Ig, C3+, C1q- Thrombotic angiopathy: no Ig, fibrin+ (EM: membrane duplication) |
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ANCA diseases: class, mechanism, microscopy |
Class: RPGN Mechanism: autoimmune PMN activation LM: focal necrotizing and crescentic IF: "pauci-immune" EM: radiolucent subendothelial GBM expansion |
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ANCA: subtypes |
Based on anti-neutrophil staining c-ANCA: Ab against proteinase 3; association with polyangiitis with granulomatosis p-ANCA: Ab against myeloperoxidase; association with polyangiitis, Churg-Strauss |
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Anti-GBM disease: class, mechanism, microscopy |
Class: RPGN Mechanism: ADCC against ColIV alpha3 IF: linear IgG along capillary wall EM: delicate basement membrane, no deposits |
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IgA nephropathy: class, mechanism, microscopy |
Class: hematuric syndrome - manifestation of HS purpura Mechanism: IgA glycosylation defect -> less clearance, more aggr, autoantibodies LM: mesangioproliferative IF: IgA positive mesangial deposits EM: mesangial deposits |
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Thin basement membrane disease: class, mechanism, microscopy |
Class: hematuric syndrome Mechanism: mutation in ColIV gene -- benign, kidney function maintained LM: normal IF: negative EM: thin basement membrane |
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Hereditary nephritis: class, mechanism, microscopy |
Class: hematuric Mechanism: mutation in alpha3, 4, 5 Col IV genes (Alport syndrome) "Can't see, pee, hear buzzing bee" LM: global sclerosis IF: negative EM: basket weave appearance GBM |
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Amyloidosis: mechanism, microscopy |
Mechanism: aggregation in beta-pleated sheets LM: positive Congo red, green birefringence with polarized light IF: depends on type EM: depends on type - deposition |
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Amyloidosis: main types, causes |
Reactive: SAA: chronic inflamm state AL/AH: light chain, heavy chain: B cell lymphoproliferative disorder Hemodialysis-associated: beta2 microglobulin: trapped by dialysis filter Hereditary: mutation: predisposed to misfold |
