Experimental Autoimmune Renal Cortical Tubulointerstitial Disease in Guinea Pigs Lacking the Fourth Component of Complement (C4)

Abstract

C4d guinea pigs develop experimental autoimmune renal tubulointerstitial disease indistinguishable from the disease observed in guinea pigs with circulating C4. These data demonstrate that an antibody-mediated autoimmune renal disease can occur in the absence of C4. We conclude: 1) complement may, at least in part, play a role in the pathogenesis, 2) complement activation does not occur via the classical sequence in this model, and 3) that activation and tissue injury may be mediated by an alternate complement pathway.