Heterozygosity for the factor V Leiden (G1691A) mutation predisposes renaltransplant recipients to thrombotic complications and graft loss

Background. Heterozygosity for a mutation in the coagulation factor V gene (factor V Leiden; FVL) leads to resistance to activated protein C and repre sents the, most common cause of inherited thrombophilia. FVL is associated with a high risk for thromboembolic events and might be a risk factor for v enous thrombosis and early graft loss in renal transplant recipients. Methods. We studied a cohort of 202 renal allograft recipients to assess th e impact of the FVL mutation on thrombotic events and graft loss within I y ear after transplantation. We recorded the occurrence of deep venous thromb osis, pulmonary embolism, early graft perfusion defect, and graft loss. The occurrence of these events was then correlated with the presence or absenc e of heterozygosity for the FVL mutation. Results. Heterozygosity for FVL was detected in 8 (4%) of 202 patients. The incidence of deep venous thrombosis or pulmonary embolism was higher in he terozygous compared with wild-type patients (25% vs. 5.7%, P = 0.09). Furth ermore, early graft perfusion defect (25% vs. 2.6%; P = 0.03) and graft los s within 7 days after transplantation (2/8 vs. 1/194; P = 0.004) were signi ficantly more frequent among heterozygous carriers of FVL. All eight FVL ca rriers were negative for protein C or S deficiency and antiphospholipid and anticardiolipin antibodies, and were not carriers of the G20210A prothromb in mutation. Conclusions. Heterozygosity for the FVL mutation predisposes renal allograf t recipients to venous thromboembolic complications, graft perfusion defect s, and early transplant loss. Screening for the FVL mutation and appropriat e peri- and postoperative anticoagulation after renal transplantation might prevent these thromboembolic complications.