FB1, FC1, and aPL-IgG induced glomerular histologic lesions characteristic of TMA. (A) Binding of antibody FB1 (i), FC1 (ii), FD1 (iii), mouse IgG (iv), aPL-IgG (v), and NH-IgG (vi) to renal glomeruli after in vivo administration. Note that all mouse aPL antibodies and human aPL antibodies bind to glomeruli. (B) Transmission electron micrographs of glomeruli (original magnification ×7000). Swelling of glomerular capillary loops endothelial cells (*) and loss of fenestrations (#) were observed in glomeruli from FB1- (i), FC1- (ii), and aPL-IgG–treated mice (iii). Note the numerous red blood cells (RC) trapped between swollen endothelial cells. No signs of endothelial injury, well-preserved fenestrations (—), and widely patent glomerular capillary lumina are observed in kidneys from mouse IgG- (iv) and NH-IgG-treated mice (v; control groups). Similar to kidneys from mouse IgG-treated mice, no signs of endothelial injury were observed in glomeruli from FD1-treated mice. In FD1-treated mice (vi), glomerular capillary lumina are patent, fenestrations are well preserved (—), and endothelial cells are not swollen. Six or 7 mice were studied in each experimental group. (C) Glomerular injury scores. EM was evaluated in a semiquantitative way. These scores were obtained by independent study by 2 scientists, and the scoring of all tissues was conducted in a blinded manner. FB1, FC1, and aPL indicate that IgG-treated mice showed the higher glomerular injury scores compared with control mice.