Summary
Starting from a hypothesis according to which disseminated intravascular coagulation might be an intermediary mechanism in the production of acute renal failure, investigations were made in 94 cases of anuria of different etiology, in order to detect signs of a consumption coagulopathy. After an average lapse of time of 48 h since the onset of anuria, the most frequently encountered hemostatic defect was a decreased platelet adhesiveness. In vitro experiments and clinical observations suggest that in the early stage of acute renal failure caused by a septic abortion, deficient platelet adhesiveness is due, mainly to platelet damage caused by intravascular coagulation or by bacterial toxins and not by the retention of metabolites. Euglobulin lysis time was prolonged, but a significant decrease of the plasminogen level indicates that an activation of fibrinolysis might have occured in the evolution of the process.
