Abstract
The role of intravascular coagulation in the progression of immune complex induced nephritis (BSA nephritis) was examined in the albino rabbits, and the effects of urokinase and ancrod were tested.
Non-treated group revealed hyperfibrinogenemia, high level of serum FDP and low plasminogen activator activity accompanying endocapillary proliferation after BSA treatment.
By daily infusion of urokinase (3, 000U/day), the activity of plasminogen activator was conserved and the glomeruli showed more mild lesions than that of non-treated group.
By ancrod infusion (2U/kg/day; iv), the degree of endocapillary proliferation decreased accompanying hypofibrinogenemia.
These results suggest that intravascular coagulation plays an important role of BSA nephritis.
