Table 3.
Effects of aPL antibodies and control antibodies on renal histology and function
| Ab | ↑ glomerular deposition/expression |
EM |
Thrombin generation and renal function |
Amelioration of GEC injury and renal failure |
||||||
|---|---|---|---|---|---|---|---|---|---|---|
| C3 | Fibrin | TF | GEC damage | ↑TAT | ↑BUN | ↑ACR | C5aR−/− mice | Low TF mice | Pravastatin | |
| FB1 (C′ activating Ab) | Yes | Yes | Yes | Yes | Yes | Yes | Yes | Yes | Yes | Yes |
| FC1 (anti-B2GPI Ab) | No | No | No | Yes | Yes | Yes | Yes | No | Yes | Yes |
| FD1 | No | No | No | No | No | No | No | NA | NA | NA |
| aPL-IgG | Yes | Yes | Yes | No | Yes | Yes | Yes | Partial | Yes | Yes |
| NH-IgG | No | No | No | No | No | No | No | NA | NA | NA |
Effects of FC1, FB1, FD1, aPL-IgG, and NH-IgG on glomerular C3 and fibrin deposition, TF expression and synthesis, plasma thrombin antithrombin III (TAT) levels, and renal function (BUN and ACR). The last 3 columns represent the effect of genetic deletion of C5aR, genetic diminution of TF, and pravastatin treatment on endothelial injury and renal failure.
C′ indicates complement; Ab, antibody; GEC, glomerular endothelial cell; and NA, not applicable.