Fibrin and Fibrinolysis in Liver, Kidney, and Lung Transplantation

Organ transplantation represents a unique environment in which the donor organ undergoes a systemic insult worsened by procurement that is followed by ischemia-reperfusion injury on revascularization. Historically, microvascular thrombosis during sequential injury was considered a cause of organ dysfunction. However, recent data challenge the concept that fibrin deposition in organs drives pathology and instead suggest that the hemostatic system may play an important role in organ recovery. Although fibrin may be protective in the early setting of organ injury, persistent fibrin deposition augments inflammatory leukocyte recruitment that propagates tissue damage. Because the timing of fibrin deposition within the transplanted organ influences both damage and repair, the fibrinolytic system plays an essential role in organ recovery after transplantation. Dysfunctional fibrinolysis is linked to adverse outcomes in many diseases but has received less attention in organ transplantation. This review covers the physiological and pathological role of fibrin formation in liver, kidney, and lung transplantation and discusses how activation of the fibrinolytic system may ultimately modulate outcome.