“…Among them; the presence of CMV infection and cyclosporine or rapamycine administration after transplantation are basically observations and the mechanism of thrombogenicity about these drugs and infection are not fully demonstrated in high-powered clinical trials [13-15]. In addition; pretransplant hypercoagulable states as vascular access thromboses, prior venous thromboembolism, essential thrombocytemia, ischemic heart disease on antiplatelet therapy, atrial fibrillation on vitamin K antagonist therapy, factor V Leiden and prothrombin G20210A mutation and the presence of antiphospholipid antibodies have all been defined as independant risk factors for renal allograft thrombosis but not for posttransplant SVT in patients with optimal graft function [13,16,17]. The impact of JAK2V617F mutation in the pathogenesis of splanchnic vein and peripheral venous thrombosis and thromboses in MPD has been disclosed in detail [5,7,8,18-20].…”