TERMINAL COMPLEMENT COMPLEXES IN ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS

Activation of the complement cascade occurs in most cases of acute pos tstreptococcal glomerulonephritis (APSGN) and results in the formation of the terminal complement complexes (TCC). To examine the possible r ole of TCC in the pathogenesis of glomerular injury in APSGN, we studi ed 30 patients with the clinical diagnosis of APSGN. All patients had an elevated plasma SC5b-9 concentration at the onset of clinical nephr itis. Serial plasma concentrations showed an inverse linear relationsh ip with time after onset of clinical disease (r = -0.59, P = 0.0008), while plasma C3 concentrations showed a positive linear relationship ( r = 0.78, P = 0.0001). Renal biopsies of 5 patients demonstrated co-lo calization of C5b-9, S-protein, and C3 deposition in a glomerular capi llary loop and mesangial distribution. Urinary excretion of TCC in the acute phase of APSGN was not elevated and was not a useful marker of disease activity. These data suggest that in APSGN with terminal compl ement pathway activation the local generation of TCC may contribute to the pathogenesis of the disease.