Effect of Folate, Vitamin B 6, and Vitamin B 12 Intake and MTHFR C677T Polymorphism on Homocysteine Concentrations of Renal Transplant Recipients

Abstract

Plasma hyperhomocysteinemia (HHcy) is considered a risk factor for chronic allograft dysfunction (CAD), the main cause of functional loss in transplant recipients. Genetic polymorphisms that alter enzymes involved in homocysteine (Hcy) metabolism, such as methylenetetrahydrofolate reductase ( MTHFR), and vitamin deficiency can result in HHcy. The objectives of this study were to investigate the relationship between HHcy and CAD development, and to evaluate the effect of intake of folate and vitamins B 6 and B 12 as well as MTHFR C677T polymorphism on Hcy concentrations. Ninety-eight renal transplant recipients including 48 showing CAD and 50 with normal renal function (NRF), were included in this cross-sectional study. Peripheral blood samples were collected for plasma Hcy quantification by liquid chromatography/sequential mass spectrometry (LC-MS/MS), and for MTHFR polymorphism analysis using polymerase chain reaction-restriction fragment length polymorphism. Dietary intake was evaluated using a nutritional questionnaire. HHcy ( P = .002) and higher mean concentrations of Hcy ( P = .029) were associated with CAD. An association was observed between HHcy and 677T variant allele in the CAD group ( P = .0005). There was no correlation between Hcy concentration and folate, vitamin B 6 or vitamin B 12 intake in the CAD group. However, a negative correlation was observed between Hcy concentration and folate intake ( P = .043), and also between Hcy concentration and vitamin B 6 intake ( P = .030) in the NRF group. According to our study, HHcy is associated with CAD development. In patients with CAD, MTHFR polymorphism seems to have a greater effect on the Hcy concentration than the vitamin intake. Increased folate and vitamin B 6 intakes seem to reduce Hcy concentrations among transplant recipients with NRF, and could contribute to reducing the risk of CAD development.