1. Intravascular coagulation has been assessed by following the catabolism of 131I-fibrinogen in relation to 125I-labelled antigen disposal during anaphylaxis and acute and chronic serum sickness glomerulonephritis in rabbits.
2. As a result of antigen challenge early in the bovine serum albumin (BSA) immunization schedule, in vivo formation of immune complexes caused platelet damage, intravascular coagulation shown as ‘rebound defibrination’ (that is a transient fall of labelled fibrinogen), and also activation of kinins and of fibrinolysis.
3. ‘Rebound defibrination’ was associated with precipitating antibody to BSA, with rapid removal of antigen, and with the appearance of fibrin microthrombi in the renal glomeruli. It also appeared to be related to the development of proliferative glomerular histology. Further, inhibition of fibrinolysis before antigen challenge may lead to patchy renal cortical infarction.
4. Florid ‘rebound defibrination’ occurred in animals with anaphylaxis and was accompanied by obstruction of the vasculature of lungs and kidneys by fibrin. These animals had high levels of precipitating antibody.
5. Animals which developed chronic proteinuria late in immunization had relatively more non-precipitating antibody to BSA and showed slower removal of antigen, no rebound effect and thus normal fibrinogen catabolism. Glomerular histology showed little proliferative response.
6. Long-term horse serum injection produced glomerulonephritis accompanied by fibrinoid vasculitis, and accelerated fibrinogen catabolism.