Factor V Leiden mutation: potential thrombogenic role in renal vein, dialysis graft and transplant vascular thrombosis

Abstract

Factor V is an important blood coagulation factor, the procoagulatory activity of which is inhibited by activated protein C. The factor V Leiden mutation is due to a single base-pair change (G1691A), which alters the initial cleavage site for activated protein C. The impaired degradation of factor V by activated protein C yields a hypercoagulable state that confers a lifelong increased risk of thrombosis in heterozygous and homozygous individuals. The factor V Leiden mutation represents the most common cause of inherited thrombophilia, and enhances the risk for venous thrombosis by approximately sevenfold. In normal Western populations, heterozygosity for the factor V Leiden mutation is present in 2-5%, whereas in patients with venous thrombosis and a family history of thrombotic disease this figure may reach 50-60%. The presence of the mutation markedly increases the risk for renal vein thrombosis, particularly in neonates. Heterozygosity for factor V Leiden mutation does not appear to be a major risk factor for dialysis access clotting. The presence of factor V Leiden mutation is most devastating in kidney transplant recipients. In these patients the mutation predisposes to renal transplant vein thrombosis and early graft loss. The risk for acute vascular rejection is also enhanced in transplant recipients who are heterozygous for the mutation. Routine screening for factor V Leiden mutation by polymerase chain reaction, and appropriate perioperative and postoperative anticoagulation after renal transplantation might be a valuable strategy to prevent thromboembolic complications in transplant recipients.