The pathogenesis of acute proliferative glomerulo-nephritis-
immune complex disease in which tissue injury is primarily caused by complement activation by the classical pathway. Typical features of immune complex disease, such as hypocomplementemia and granular deposits of IgG and complement on the GBM, are seen. The relevant antigens probably are streptococcal proteins. Specific antigens implicated in pathogenesis include streptococcal exotoxin B (Spe B) and streptococcal GAPDH. Both activate the alternative complement pathway and have an affinity for glomerular proteins and plasmin. It is not clear if immune complexes are formed mainly in the circulation or in situ. Ref: Robbins basic pathology 9th edition page529
Cytotoxic T-cell mediated
Immune complex mediated
Antibody mediated
Cell-mediated (Typer IV)
Urinary tract