Genetic deletion of C5aR prevents glomerular injury and renal failure in FB1-treated mice. (A) Transmission electron micrograph of glomeruli from C5aR-deficient mice treated with FB1 (i), FC1 (ii), and aPL-IgG (iii). In C5aR^−/− mice treated with FB1, no signs of glomerular endothelial injury were found. The capillary lumina were patent, the endothelial cells were normal in appearance, and the fenestrations were abundant and well preserved (—). However, C5aR deficiency did not prevent FC1- or aPL-IgG–induced endothelial injury. Glomerular capillary loops show endothelial cell swelling (#) and absence of fenestrations (*) in these mice (original magnification ×7000). Six or 7 mice were studied in each experimental group. (B) Glomerular injury scores. (C) Urinary ACR. FB1-induced, increased ACR was not observed in C5aR-deficient mice compared with wild-type mice. *Different from wild-type mice (P < .001). C5aR deficiency did not prevent increased ACR in FC1-treated mice. Albuminuria was ameliorated in C5aR^−/− mice treated with aPL-IgG, but ACR values in these mice were still different from control values. (D) BUN. BUN levels in FB1-treated C5aR^−/− mice were lower than in FB1-treated wild-type mice. *Different from wild-type (P < .005). C5aR^−/− mice were not protected from FC1-induced BUN increase. A partial protection was observed in aPL-IgG–treated, C5aR-deficient mice. (E) TAT complex. TAT levels were diminished in FB1-treated C5aR^−/− mice. *Different from wild-type (P < .01). FC1-treated C5aR^−/− mice showed high TAT levels comparable with wild-type mice. aPL-treated C5aR^−/− mice showed a slight diminution in TAT values compared with wild-type mice.