Abstract
Acute glomerulonephritis is now considered to be a nonsuppurative complication of infections with hemolytic streptococci of Lancefield's group A, although the exact mechanism by which the disease develops has not been clearly defined. As early as 1917, Ophuls1 indicated that only certain strains of streptococci appeared to have a definite nephritogenic action in man. Rammelkamp, Weaver and Dingle2 have reported evidence showing that the incidence of acute glomerulonephritis following group A streptococcal infections varied considerably from year to year, while that of acute rheumatic fever re-
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