One of two patients in whom early homograft rejection developed after renal transplantation had many antidonor antibodies before operation. By the measurement of gradients across intracorporeal and extracorporeal homografts in this patient, the new kidneys were shown to sequester host immunoglobulins, platelets, white cells and clotting factors. Moreover, the renal venous blood then contained fibrinolytic activity. This presensitized recipient, as well as a second patient who did not have detectable preformed humoral antibodies, gave evidence from clinical observation and from the various clotting tests of disseminated intravascular coagulation with fibrinolysis and a severe bleeding, diathesis. Immunofluorescent and histologic studies revealed a laying down of fibrin in the homograft vessels that continued in some cases to cortical necrosis of the transplanted kidneys or, alternatively, receded at the time fibrinolysis occurred. The variety of rejection seen in these patients has been characterized as an immunologically induced coagulopathy.When a kidney homograft is revasculurized in a recipient who is presensitized to donor antigens there is a substantial risk of either accelerated or hyperacute rejection of the transplant. [1][2][3][4][5] The mechanism of the immediate destruction has been disputed. Two years ago in this journal, a clinical report from our institutions 5 suggested that an instantaneous antigen-antibody reaction or other mechanisms could precipitate a coagulopathy like that of the Shwartzman reaction and that the consequent fibrin thrombi could occlude the renal micro-vasculature and be responsible for cortical necrosis. The principal evidence in support of this contention was from special histologic examinations. Unfortunately, clotting assays were not obtained in these patients.A subsequent publication by Colman and Merrill and their associates confirmed that there were massive fibrin deposits in two human kidneys that had been hyperacutely rejected by apparently presensitized recipients. 6 However, no systemic clotting changes could be detected in either of their patients, nor was there an arteriovenous gradient of any of the measured coagulation factors across the kidney in the most completely studied of these cases. Because of the negative findings, there was no satisfactory explanation even for the local in intravascular coagulation that the authors postulated and no evidence whatever that there had been a systemic clotting disorder at any time. In contrast, studies from our laboratories have shown that noteworthy alterations in local or systemic coagulation regularly occur in presensitized dogs after the transplantation of the kidney, liver or spleen. 7 The same thing has been seen in two recently treated patients whose renal homografts failed promptly. In both these human recipients, studies obtained revealed consumption of clotting factors either within the kidney or systemically, as well as fibrinolysis and a bleeding diathesis. MethodsThe technics of renal transplantation a...