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Streptococcal infection remains almost the sole cause of the clinical syndrome of acute glomerulonephritis in African children. Evidence for this is in elevated levels of antistreptolysin "O" (ASO) titre in 93% of 28 patients and growth of Group Abeta haemolytic streptococci from the skin and throat in 32%. Spread of infection from the skin, where lesions were present in all patients, to the throat would account for positive cultures at both sites and the frequent and vigorous antistreptolysin "O" responses. Clinical recovery occurred in most within seven days and in all within 60 days of admission. IgG and IgA, but not IgM, were increased in patients; C4 was normal in the majority and low in seven out of 24 (29%), C3 was diminished in 26 out of 28 (93%) and the mean level of C3 PA was lower than in controls. Total haemolytic complement paralleled C3 values; C3 breakdown products were not detected in any patient. Renal biopsies in seven out of 28 patients showed typical histological changes of diffuse exudative proliferative glomerulonephritis on light microscopy and fibrinogen and C3 on immunofluorescent staining. These findings suggest that events leading to glomerular damage in acute post-streptococcal nephritis in African children involve activation of both classical and alternative pathways of complement proteins and also confirm the well recognized and predictable nature of the disease, irrespective of geographical distribution.