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Plasma activity of contact coagulation factors in patients with IgA nephritis
Intraglomerular coagulation, initiated by the local activation of contact coagulation factors, has been suggested as one possible factor causing glomerular injury in IgA nephritis. The plasma activity of factor XII, prekallikrein and high molecular weight (HMW) kininogen were measured in 24 patients with biopsy-proven IgA nephritis and in 123 normal controls, using an activated partial thromboplastin time assay with the appropriate factor-deficient plasma as substrate. IgA patients had significantly lower plasma activity of factor XII (45.5% +/- 28.3% against 80.7% +/- 31.8%; mean +/- standard deviation, P < 0.001), prekallikrein (37.7% +/- 24.5% against 119.8% +/- 37.7%; P < 0.001) and HMW kininogen (72.8% +/- 37.8% against 119.1% +/- 42.8%; P < 0.001) when compared with controls. In the IgA patients, there was no significant correlation between factor XII, prekallikrein and HMW kininogen activity and 24-hour total urinary protein excretion, suggesting that the reduced plasma activity was not due to increased urinary loss of the coagulation factors. One possible explanation for these results is that the intrinsic coagulation pathway is activated in patients with IgA nephritis.
Intraglomerular coagulation, initiated by the local activation of contact coagulation factors, has been suggested as one possible factor causing glomerular injury in IgA nephritis. The plasma activity of factor XII, prekallikrein and high molecular weight (HMW) kininogen were measured in 24 patients with biopsy-proven IgA nephritis and in 123 normal controls, using an activated partial thromboplastin time assay with the appropriate factor-deficient plasma as substrate. IgA patients had significantly lower plasma activity of factor XII (45.5% +/- 28.3% against 80.7% +/- 31.8%; mean +/- standard deviation, P < 0.001), prekallikrein (37.7% +/- 24.5% against 119.8% +/- 37.7%; P < 0.001) and HMW kininogen (72.8% +/- 37.8% against 119.1% +/- 42.8%; P < 0.001) when compared with controls. In the IgA patients, there was no significant correlation between factor XII, prekallikrein and HMW kininogen activity and 24-hour total urinary protein excretion, suggesting that the reduced plasma activity was not due to increased urinary loss of the coagulation factors. One possible explanation for these results is that the intrinsic coagulation pathway is activated in patients with IgA nephritis.