(NEPHIRITIC SYRDROME. Asani, Olga Hanes, pert Modes Potash [Alport Syndrome |» Recunent | Structualdefeetin Looks nommal [FM.=negatve [Symptoms | Progiesses toenal hhematusia before | Collagen IV leads to appear | faze ereditary Nephritis) | 3g020 Jeaky batement before age + Hypertension membranes EM.=glomeniar |20 2 Deatess and BM splting ‘cular problems Benign Familial + Recurent Reduced thickness | Looksuomal | FM. =negatve HHematuria hhematuna of glomerular BM + Most fequent (Thin BM Disease) | Lanse of EM, «reduced ‘asymptomatic slomerular BM. hematuria thickness [Acute Post. + Acute nepiuits + Tmmunecomples |+ Glomerular [FM.="lumpy- [Common [Retum to nonmalin Streptococcal) + Aoupt Inediated Typeil | hyperceliuanty bumpy" granular renal | 8 weeks. Glomeralonephritis | otiguna hypersensitivity, | + -Increaseim | deposits of1gG and disease in hematuuafacial + Occus after | endotheliaeels, | C3, etnldnood edema, Sueptococeal mesangial cell, and Complete recovery hypertension. pharyngitis or PMN’: ‘without teatment Hepatitis B + Noimereasein | EM. = Subepithelial (especially in kids) + itch ASO-tter, | epithelia cells | Masubendothelial vein 3 years lowes No BM. humps,” oherwase Imnckening normal appearing BM [SLE Nephropathy Degiee ofidney | Anti ds DNA (+ WHOL Noma | FM.=1gM,IeG-+ volvement aitbodies + WHOIL cs conelates with Increased mesangial [+ Type: Granular prognosis in SLE mats appearance + WHO: Focal |e Type-ll Pseudo- proliferation Timea appearance * WHOTY, Dittuse proliferation, worst = WHOY: Identical to /Membranous ‘Nephropathy TeANepluopaty Cuculatng [e+ [+ Mesangiaicell [FM=Granular | Young (Geiger Disease): | sbronectn (due to | proliferation appearance,1gG+ | men 15-30 Most conmon chronic liver 3 nay disease) lonepbtis 8 pat EM. =Mesangial deposits Henoch-Sehonlein ames above, plus |+ Mesangialcell [FM.=Granular | Children Focal Segmental Hen . pura systemic disease: | proliferation, more | appearance, IeG + Glomerulonephritis pupusa of Serious than above. |C3 extiemties, atts colicky abdominal pan EM. =Mesamgial deposits Endocarditis |S. aureus ‘+ Subepitielial | FM. = Granular Kiduey disease Jmmue deposits | appearance, IgG +3, resolves when Infection is cured. [Rapidly Progressive + Wegener + ‘Inflamed + Cells accumulate [FM = Pauc- ‘Must be teated or Crescentie Tadney+ upper | glomerular jn Bowman's smmune. negular st val go to renal Glomerulonephritis |zespuatory act. capllaies Capsule false within - anna SANCAG@) [+ Fibun tappedin wees. + Oliguna Homer EM, = winking Epithelial cet | discontinuity of BM. proliferation + Maciophage, PMN iniates Goodpasture Tung (Bemoptysis) | Anu-BM. Shar t© FM. =Lincarpattem, [Males 25- [Responds to [syndrome kidneys amitbodies, against | Crescentic 1G +c3 30 ammunosuppressive (@emattia) Type lV collagen | glomerulonephritis, therapy and (Ant-BM Antibody se above. plasmapheresis Disease) EM, = Noimaune complex deposit [Membranoproliferative (+ BM.thickening | EM.=Tram-tack™ Glomerulonephritis nd cellular appearance, resulting proliferation ‘fom double-layer (Mesangiocapillary + Mesangial —_| appearance of Glomerulonephris) xpansion makes | glomerular BM. slomerular BM. appear as though it Were mn two layers