The differential diagnosis of glomerulonephritis without systemic disease includes poststreptococcal glomerulonephritis, IgA nephropathy, rapidly progressive glomerulonephritis (RPGN), and membanoproliferative glomerulonephritis (MPGN). Glomerular inflammation is probably induced directly by a nephritogenic streptococcal protein in poststreptococcal glomerulonephritis, and by mesangial deposition of abnormally glycosylated IgA1-containing immune aggregates in IgA nephropathy. In crescentic RPGN the role of cellular rather than humoral immune mechanisms is now becoming clear. Many patients with MPGN have chronic hepatitis C infection. There is no effective disease-specific therapy for poststreptococcal glomerulonephritis or IgA nephropathy. RPGN benefits from high-dose steroids and cytotoxic drug therapy with the addition of plasma exchange in disease induced by antibody to glomerular basement membrane. Antiviral therapies reduce the severity of MPGN due to hepatitis C virus. However, various new therapies directed at specific cytokines, growth factors, fibrin deposition, and other mediators of injury are being developed, as well as more specific and less toxic forms of immunotherapy.