Acute glomerulonephritis (AGN) is a representative disease of acute nephrit
ic syndrome characterized by the sudden appearance of edema, hematuria, pro
teinuria, and hypertension. The prototype of AGN is acute poststreptococcal
glomerulonephritis (APSGN), "Nephritogenic streptococci" are defined as or
ganisms that are cultured from a patient who develops AGN, Although only a
limited number of M-types of streptococci have been recognized as "nephrito
genic streptococci", all M-types of streptococci may have nephritogenic pot
ential because the genes for major putative nephritogenic antigens such as
SPEB and NAPlr are found to be present in all group A streptococci thus far
examined. Pathogenic mechanisms for APSGN involving both humoral and cell-
mediated immunity have been recently proposed. The role of humoral immunity
is presumed to be mediated by the in situ formation of nephritogenic strep
tococcal antigen-antibody complexes and circulating immune complexes. While
in the cellular immune component a role for delayed-type hypersensitivity
has been suggested to contribute to the pathogenesis of APSGN.