Acute glomerulonephritis that results from streptococcal infections is the best-studied immune complex-mediated glomerulonephritis. Initially described in the convalescence of scarlet fever, the incidence of acute post streptococcal glomerulonephritis (APSGN) has decreased worldwide, particularly in developed countries where it is now rare and is limited to adult patients who have debilitating conditions. In developing countries, the annual burden of APSGN remains at a level of least 9 cases per 100,000 inhabitants. Two antigenic fractions of the streptococcus (streptococcal GAPDH/nephritis-associated plasmin receptor, and streptococcal pyrogenic exotoxin B and its zymogen precursor) are currently under scrutiny as putative nephritogens. Glomerulonephritis results from the glomerular deposition of circulating immune complexes and by the in situ formation of immune complexes. In-situ formation of immune complexes is a characteristic associated with cationic antigens that have a charge-facilitated penetration through the polyanionic glomerular basement membrane. The plasmin-binding capacity of streptococcal antigens favors immune complex deposition and inflammation. The typical pathological changes are endocapillary proliferation with varying degrees of leukocyte infiltration, and C3, IgG, and IgM immune deposits. Electron microscopy shows the hallmark lesion of subepithelial electron dense deposits (“humps”). The immediate prognosis is excellent in children, but adults have a significant early mortality, which partially results from cardiovascular disease. The long-term development of end-stage renal disease is exceptional in children. However, studies in aboriginal communities indicate that patients with a history of APSGN have a higher incidence of albuminuria, and that APSGN represents a risk factor for the subsequent development of chronic renal failure, if associated with diabetes and obesity.