Effect Of Folate, Vitamin B6, And Vitamin B12 Intake And Mthfr C677t Polymorphism On Homocysteine Concentrations Of Renal Transplant Recipients

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 B6 and B12 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 B6 or vitamin B12 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 B6 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 B6 intakes seem to reduce Hcy concentrations among transplant recipients with NRF, and could contribute to reducing the risk of CAD development. © 2007 Elsevier Inc. All rights reserved.391031633165Matas, A.J., Humar, A., Gillingham, K.J., Five preventable causes of kidney graft loss in the 1990s: a single-center analysis (2002) Kidney Int, 62, p. 704Finkelstein, J.D., The metabolism of homocysteine: pathways and regulation (1998) Eur J Pediatr, 157 (2 SUPPL), p. 40Haddad, R., Mendes, M.A., Hoehr, N.F., Amino acid quantitation in aqueous matrices via trap and release membrane introduction mass spectrometry: homocysteine in human plasma (2001) Analysis, 126, p. 1212Abdel-Rahman, S.Z., Nouraldeen, A.M., Ahmed, A.E., Molecular interaction of [2,3-14C] acrylonitrile with DNA in gastric tissue of rat (1994) J Biochem Toxicol, 9, p. 121Bova, I., Chapman, J., Sylantiev, C., The A677V methylenetetrahydrofolate reductase gene polymorphism and carotid atherosclerosis (1999) Stroke, 30, p. 2180Ribeiro, A.B., Cardoso, M.A., Construção de um questionário de freqüência alimentar como subsidio para programas de prevenção de doenças crônicas não transmissi{dotless}́veis (2002) Rev Nutr, 15, p. 239(1998) Dietary reference intakes for thiamin, riboflavin, niacin, vitamin B6, folate, vitamin B12, pantothenic acid, biotin, and choline, , Institute of Medicine, National Academy Press, Washington, DCde Alvarenga, M.P., Pavarino-Bertelli, E.C., Abbud-Filho, M., Combination of angiotensin-converting enzyme and methylenetetrahydrofolate reductase gene polymorphisms as determinant risk factors for chronic allograft dysfunction (2007) Transplant Proc, 39, p. 78Gonin, J.M., Folic acid supplementation to prevent adverse events in individuals with chronic kidney disease and end stage renal disease (2005) Curr Opin Nephrol Hypertens, 14, p. 27