Kidney Transplantation from Donors with Severe Disseminated Intravascular Coagulation

Disseminated intravascular coagulation (DIC) is a syndrome characterized by massive formation of thrombin, which can lead to renal dysfunction or failure. Many transplant centers are reluctant to accept the kidneys from donors with DIC especially if renal dysfunction is present. We developed protocol of machine perfusion followed by tissue plasminogen activator (tPA) infusion in order to treat and evaluate DIC kidneys prior to transplantation. The kidneys were placed on machine preservation with tPA added to the perfusate prior to transplantation. Three kidneys were transplanted from two donors who sustained gunshot injuries to the brain. A biopsy at the time of organ recovery documented widespread fibrin thrombi in approximately 80% of the glomeruli. Serial biopsies showed interval improvement following machine perfusion and a normal appearing kidney three months after successful transplantation. The histological presence of DIC in a deceased organ donor, even if associated with renal dysfunction, is not a contraindication to renal transplantation. Machine perfusion and tPA infusions may contribute to the recovery and successful transplantation of such kidneys. 1. Introduction In the 1970s, several authors observed an association of traumatic brain injury and disseminated intravascular coagulation (DIC), a syndrome characterized by massive formation of thrombin [1, 2]. When the circulation is exposed to large amounts of tissue factor, coagulopathy may develop resulting in widespread deposition of intravascular fibrin and ultimately leading to thrombosis of small and midsize vessels. The spectrum of DIC can range from laboratory abnormalities of no clinical significance, including decrease in platelet count and prolongation of clotting time, to fulminant activation of clotting cascade with multiple organ failure [3]. Clinical manifestations of DIC are variable and may include petechiae, purpura and other signs of abnormal bleeding, fever, hypotension, proteinuria, and hypoxia. Microvascular thrombosis can result in cardiac, pulmonary, renal, hepatic, and CNS dysfunction [4]. Establishing the diagnosis of DIC is problematic. The subcommittee on DIC of the International Society of Haemostasis and Thrombosis (ISHT) defined DIC as an acquired syndrome characterized by the intravascular activation of coagulation with loss of localization arising from different causes. It can originate from and cause damage to the microvasculature, which if sufficiently severe can produce organ dysfunction. The ISHT further proposed a simple scoring algorithm using the