<prompt> If renal biopsy shows distinct crescents, diagnosis isRPGNMPGNPSGNMinimal change disease  <response>: Ans. a RPGN Ref. Robbins Pathology 7th 976, and H-18thch. 283RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS RPGN is severe glomerular injury with necrosis and GBM breaks and subsequent proliferation of parietal epithelium crescents. RPGN may be immune mediated, as when autoantibodies develop to the GBM in anti-GBM antibody disease or when it develops consequent to immune complex deposition; it can also be pauci-immune, associated with antineutrophil cytoplasmic antibodies. RPGN is defined by 2 criteria:- Presence of epithelial crescents in more than 70 of glomeruli- Occurrence of rapidly progressive renal failure. End stage disease occurs within months. Causes of Crescentic Glomerulonephritis Type I Anti-GBM Antibody- Idiopathic- Goodpasture syndrome Type 11 Immune Complex- Idiopathic- Postinfectiousinfection related- Systemic lupus erythematosus- Henoch-Schonlein purpuraIgA nephropathy Type III Pauci-immune ANCA Associated- Idiopathic- Wegener granulomatosis- Microscopic angiitisDiseaseMost Frequent clinical presentationPathogenesisLight MicroscopyFluorescence MicroscopyElectronPost strepto- coccal GNAcute nephritisAntibody mediated; circulating or planted antigenDiffuse proliferation; leukocytic infiltrationGranular IgG and C3 in GBM and mesangiumSubepithelial humpsGood pasture syndromeRapidly progressive glomerulo- nephritisAnti-GBM COL4-A3 antigenProliferation; crescentsLinear IgG and C3; fibrin in crescentsNo deposits; GBM disruptions; fibrinIdiopathicRPGNRapidly progressive glomeru- lonephritisAnti-GBM antibodyProliferation; focal necrosis; crescentsLinear IgG and C3No deposits Immune complex Granular IgG or IgA or IgMDeposits may be present In situ antibody- mediated; antigen unknownDiffuse capillary wall thickenningNegative or equivocalNo depositsMembranous glomerulo-pathyNephrotic syndrome Granular IgG and C3; diffuseSubepithelial depositsMinimal change diseaseNephrotic syndromeUnknown, loss of glomerular polyanion; podocyte injuryNormal; lipid in tubulesNegativeLoss of foot process; No depositsFocal segmental glomerulo- nephritisNephrotic syndrome non-nephrotic proteinuriaUnknown, Ablation nephropathy plasma factor ?; podocyte injuryFocal and segmental sclerosis and hyalinosisFocal; IgM and C3Loss of foot processes; epithelial denudationMembrano- proliferative glomerulone- phritis MPGNNephrotic syndrome1 Immune complex I lgG C3;Clq C4l subendothelial deposits Mesangial pro- liferation; basement membrane thickening; splitting Dense deposit diseaseMPGN1HematuriaII Autoantibody: alternative alter- native complement pathway II C3lgG; no CLq or C4II Dense deposits Chronic renal failure IgA NephropathyRecurrent hematuria or proteilnuriaUnknown; see textFocal proliferative glomerulonephritis; mesangial wideningIgA -lgG, IgM, and C3 in mesangiumMesangial and paramesangial dense depositsChronic glomerulo- nephritisChronic renal failureVariableHyalinized glomeruliGranular or negative 