A growing transplanted kidney

to thrombectomy and finally to thrombolytic therapy with anticoagulation, which is currently the standard treatment of choice [1]. Here, we present a young woman with bilateral RVT. Her case constituted the first clinical report of heterozygous MTHFR mutation with RVT, which was her only risk factor for the disease. MTHFR is a key enzyme for intracellular folate homeostasis and metabolism that catalyses the reduction of 5,10-methylenetetrahydrofolate to 5methyltetrahydrofolate, the main circulating form of folate and the methyl donor for the vitamin B12-dependent remethylation of Hcy to methionine. Results from previous studies showed that the 677TT MTHFR genotype can be considered as an independent risk factor for both arterial and venous thrombosis and may itself increase the risk for thrombosis even in the absence of other thrombophilic risk factors [3,4]. Recently, a novel MTHFR polymorphism, 1298A3C, which changes glutamic acid into an alanine residue, was shown to be associated with decreased enzyme activity but did not result in decreased folate plasma levels or increased plasma Hcy concentrations in homozygous or heterozygous members of neural tube defect families [5]. Also, others have reported that MTHFR 1298CC and MTHFR 1298AC had no effect on the risk for vein thrombosis [6]. In contrast, we present the first adult case that shows a relation between RVT and MTHFR-1298.