Figure 3
Figure 3. Impaired renal function and increased TAT levels in mice treated with FB1, FC1, and aPL-IgG. (A) Urinary ACR. FB1, FC1, and aPL-IgG induced albuminuria compared with mIgG- and NH-IgG-treated mice. FD1-treated mice did not show increased ACR compared with mIgG. (B) BUN. BUN levels in FB1-, FC1-, and aPL-IgG -treated mice were higher than in mIgG- or NH-IgG-treated mice. Mice treated with FD1 did not show increased BUN levels compared with mIgG-treated mice. (C) TAT complex. TAT levels were increased in FB1-, FC1-, and aPL-IgG–treated mice compared with control mice (mIgG- and NH-IgG-treated mice). *Different from mIgG-treated mice (P < .01). #Different from NH-IgG-treated mice (P < .01).

Impaired renal function and increased TAT levels in mice treated with FB1, FC1, and aPL-IgG. (A) Urinary ACR. FB1, FC1, and aPL-IgG induced albuminuria compared with mIgG- and NH-IgG-treated mice. FD1-treated mice did not show increased ACR compared with mIgG. (B) BUN. BUN levels in FB1-, FC1-, and aPL-IgG -treated mice were higher than in mIgG- or NH-IgG-treated mice. Mice treated with FD1 did not show increased BUN levels compared with mIgG-treated mice. (C) TAT complex. TAT levels were increased in FB1-, FC1-, and aPL-IgG–treated mice compared with control mice (mIgG- and NH-IgG-treated mice). *Different from mIgG-treated mice (P < .01). #Different from NH-IgG-treated mice (P < .01).

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