title: [Hyperhomocysteinemia as a vascular risk factor in chronic hemodialysis patients].
abstract: Homocysteine is an independent risk factor for cardiovascular disease in the general population. In addition, it plays a main role in the development of atherogenesis and thrombosis, particularly in end-stage renal disease patients. Therefore, hemodialysis patients are under the burden of homocysteine toxic effects, present in nearly 90% of dialysis patients. Our group found that folic acid is an efficient therapeutic approach to decrease homocysteine levels, and the addition of intravenous methylcobalamin potentiates this effect; however, methylcobalamin alone was unsuccessful to normalize homocysteine levels. With time a group of patients required a higher dose of folic acid to reduce hyperhomocysteinemia. Patients homozygous and, to a lesser extent heterozygous, to the C677T thermolabile variant of methylenetetrahydrofolate reductase (MTHFR) presented a reduced catalytic activity and required a higher folic acid dose. Vascular-access thrombotic events were similar in all patients according to the variants of the enzyme, suggesting that treating hyperhomocysteinemia was the key to lower the risk of thromboses. Noteworthy, hypohomocysteinemia, generally acompanying malnourishment, is associated to higher mortality. Albeit hyper-homocysteinemia is considered a vascular risk factor in renal failure patients, it has not yet been established in this population if its correction is associated with a decrease in the rate of vascular disease and thrombosis. However, given the mentioned evidence about the low risk and good tolerance of vitamin therapy, we believe it useful to know folate, cobalamin and homocysteine blood levels in chronic renal patients and start a prompt treatment, which may proof adequate to maintain homocysteine levels of 10 +/- 5 micromol/l.
authors.affiliation: Servicio de Nefrología, Hospital Británico de Buenos Aires, Argentina. htrimarchi@hotmail.com
authors.forename: Hernán
authors.initials: H
authors.lastname: Trimarchi
authors.forename: Pablo
authors.initials: P
authors.lastname: Young
authors.forename: María L
authors.initials: ML
authors.lastname: Díaz
authors.forename: Juan
authors.initials: J
authors.lastname: Schropp
authors.forename: Mariano
authors.initials: M
authors.lastname: Forrester
authors.forename: Emilio
authors.initials: E
authors.lastname: Freixas
mesh_terms: D050197:Atherosclerosis / Q000209:etiology* / Q000378:metabolism; D005492:Folic Acid / Q000378:metabolism / Q000627:therapeutic use*; D006710:Homocysteine / Q000097:blood / Q000187:drug effects; D006801:Humans; D020138:Hyperhomocysteinemia / Q000150:complications* / Q000188:drug therapy / Q000378:metabolism; D007676:Kidney Failure, Chronic / Q000188:drug therapy / Q000378:metabolism; D042965:Methylenetetrahydrofolate Reductase (NADPH2) / Q000378:metabolism / Q000627:therapeutic use; D006435:Renal Dialysis / Q000009:adverse effects*; D012307:Risk Factors; D013927:Thrombosis / Q000209:etiology* / Q000378:metabolism; D014805:Vitamin B 12 / Q000031:analogs & derivatives / Q000378:metabolism / Q000627:therapeutic use; D014803:Vitamin B Complex / Q000378:metabolism / Q000627:therapeutic use*
chemical_list: D006710:Homocysteine; D014803:Vitamin B Complex; D005492:Folic Acid; C019476:mecobalamin; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D014805:Vitamin B 12