[7] Most types of RPGN are characterized by severe and rapid loss of kidney function with marked hematuria; red blood cell casts in the urine; and proteinuria sometimes exceeding three grams in twenty-four hours, a range associated with nephrotic syndrome.

[2] It is thought that antineutrophil cytoplasmic antibodies (ANCA) interact with antigens in the cytoplasm of neutrophils to cause an early[citation needed] degranulation, triggering the release of lytic enzymes at the site of injury[8] and leading to the formation of glomerular crescents that consist primarily of parietal epithelial cells from Bowman's capsule and in some cases podocytes.

Some cases are associated with antibodies directed against the basement membrane of lung alveoli, producing Goodpasture syndrome.

[2] Characterized by deposition of immune complexes in glomerular tissues, type II RPGN accounts for 40[11]% of cases.

Any immune complex disease—including systemic lupus erythematosus, acute proliferative glomerulonephritis, Henoch–Schönlein purpura, and IgA nephropathy—that involves the glomerulus may progress to RPGN if severe enough.