Tags

Type your tag names separated by a space and hit enter

[Hyperhomocysteinemia as a vascular risk factor in chronic hemodialysis patients].
Medicina (B Aires). 2005; 65(6):513-7.M

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+Show Affiliations

Servicio de Nefrología, Hospital Británico de Buenos Aires, Argentina. htrimarchi@hotmail.comNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article

Language

spa

PubMed ID

16433478

Citation

Trimarchi, Hernán, et al. "[Hyperhomocysteinemia as a Vascular Risk Factor in Chronic Hemodialysis Patients]." Medicina, vol. 65, no. 6, 2005, pp. 513-7.
Trimarchi H, Young P, Díaz ML, et al. [Hyperhomocysteinemia as a vascular risk factor in chronic hemodialysis patients]. Medicina (B Aires). 2005;65(6):513-7.
Trimarchi, H., Young, P., Díaz, M. L., Schropp, J., Forrester, M., & Freixas, E. (2005). [Hyperhomocysteinemia as a vascular risk factor in chronic hemodialysis patients]. Medicina, 65(6), 513-7.
Trimarchi H, et al. [Hyperhomocysteinemia as a Vascular Risk Factor in Chronic Hemodialysis Patients]. Medicina (B Aires). 2005;65(6):513-7. PubMed PMID: 16433478.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Hyperhomocysteinemia as a vascular risk factor in chronic hemodialysis patients]. AU - Trimarchi,Hernán, AU - Young,Pablo, AU - Díaz,María L, AU - Schropp,Juan, AU - Forrester,Mariano, AU - Freixas,Emilio, PY - 2006/1/26/pubmed PY - 2006/5/23/medline PY - 2006/1/26/entrez SP - 513 EP - 7 JF - Medicina JO - Medicina (B Aires) VL - 65 IS - 6 N2 - 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. SN - 0025-7680 UR - https://www.unboundmedicine.com/medline/citation/16433478/[Hyperhomocysteinemia_as_a_vascular_risk_factor_in_chronic_hemodialysis_patients]_ L2 - https://medlineplus.gov/bvitamins.html DB - PRIME DP - Unbound Medicine ER -