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

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

Nephritic syndrome

Decrease in urine output within days to weeks → possibly anuria

Fatigue

Pulmonary symptoms (e.g., hemoptysis) may occur (see “Differential diagnosis of pulmonary-renal syndromes”).