Etiology

• Type I: anti-GBM glomerulonephritis: anti-glomerular basement membrane antibody disease (Goodpasture syndrome)
• Type II: immune complex-mediated glomerulonephritis
  • IgA nephropathy
  • Membranoproliferative nephropathy
  • IgA vasculitis
  • Lupus nephritis
  • Poststreptococcal glomerulonephritis (PSGN)
• Type III: glomerulonephritis associated with vasculitis (pauci-immune GN, ANCA-associated)
  • Granulomatosis with polyangiitis
  • Microscopic polyangiitis
  • Eosinophilic granulomatosis with polyangiitis

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Pathophysiology

• Breaks in the glomerular capillary wall and dysfunction of the glomerular basement membrane (GBM) → leakage of plasma proteins (e.g., coagulation factors) and passage of inflammatory cells (macrophages, T cells) into Bowman space
• Release of inflammatory cytokines → damage to the membrane of Bowman space and passage of cells from the interstitium into Bowman space
• This causes the formation of fibrin clots and proliferation of cells (e.g., macrophages, fibroblasts, neutrophils, epithelial cells) → crescent moon formation → compression of the glomerulus → renal dysfunction

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Clinical features

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Diagnostics

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Treatment

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