<prompt> A characteristic electron microscopic feature of minimal change disease:Mesangial depositsSplitting of basement membraneFusion of foot processes their effacementSubepithelial deposits  <response>: Ans. c Fusion of foot processes their effacement. Ref. Robbins pathologic basis of disease, 5th 935GLOMERULAR PATHOLOGYGlomerular pathologyFeaturesAcute post-streptococcal glomerulonephritis Nephritic syndrome Most frequently seen in children. Resolves spontaneously. Peripheral and periorbital edema, hematuria, hypertension Oliguria, azotemia.LM: Glomeruli and hypercellular neutrophils, lumpy-bumpy.EM: subepithelial humps.IF: granular patternRapidly progressive crescentic GNRapid course to renal failure.LM and IF: crescent moon shapeGoodpastures syndrome type II hypersensitivity--Hemoptysis, hematuria.IF; linear pattern, anti-GBM antibodies.Membranoproliferative glomerulonephritisSlowly progresses to renal failureEM: subendothelial humps, tram track.IgA nephropathy Bergers diseaseMild disease. Often postinfectious.IF and EM: mesangial deposits of IgAAlports syndromeSplit basement membraneCollagen IV mutation.Nerve deafness and ocular disordersNephrotic syndromeMassive proteinuria, hypoalbuminemia,Peripheral and periorbital edema, hyperlipidemia.Membranous glomerulonephritisA common cause of the adult nephrotic syndromeLM: Diffuse capillary and basement membrane thickening.IF: granular pattern.EM: spike and domeMinimal change diseaselipoid nephrosisMost common cause of childhood nephrotic syndrome. Responds to steroids.LM: normal glomeruli.EM; foot process effacementFocal segmental glomerular sclerosisMore severe disease in HIV patientsLM: segmental sclerosis and hyalinosis.Diabetic nephropathyLM: Kimmelstiel- Wilson wire loop lesions, basement membrane thickening.SLELM: In membranous glomerulonephritis.Wire-loop lesion with subendothelial deposits 