The major pathogenic mechanism of poststreptococcal glomerulonephritis (PSGN) is an in situ immune complex formation due to deposition of streptococcal nephritogenic antigens, such as nephritis-associated plasmin receptor (NAPlr) and Streptococcal pyrogenic exotoxin B (SPE B). Both are capable of activating the alternate pathway of the complement cascade and enhance the expression of adhesion molecules. SPE B also stimulates the production of chemotactic cytokines. NAPlr was isolated from group A streptococcus and was shown to bind plasmin(ogen). In the original report, 92 percent of Japanese patients with the acute PSGN had anti-NAPlr antibodies, and about 80% of renal biopsy samples showed deposits of NaPlr
