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[Hyperhomocysteinemia as a vascular risk factor in chronic hemodialysis patients]
Hernán Trimarchi1, Pablo Young, María L Díaz
1Servicio de Nefrología, Hospital Británico de Buenos Aires, Argentina. htrimarchi@hotmail.com
Insights
High homocysteine levels are common in dialysis patients and increase cardiovascular risk. Folic acid and methylcobalamin effectively reduce homocysteine, especially in MTHFR variants, lowering thrombosis risk.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Nutritional Biochemistry
Context:
- Hyperhomocysteinemia is a significant risk factor for cardiovascular disease and thrombosis, particularly in end-stage renal disease (ESRD) patients undergoing hemodialysis.
- Nearly 90% of dialysis patients exhibit elevated homocysteine levels, contributing to their increased morbidity and mortality.
- The C677T thermolabile variant of methylenetetrahydrofolate reductase (MTHFR) is associated with reduced enzyme activity and a higher requirement for folic acid to manage hyperhomocysteinemia.
Purpose:
- To investigate the efficacy of folic acid and methylcobalamin in reducing homocysteine levels in hemodialysis patients.
- To explore the influence of MTHFR gene variants on homocysteine levels and treatment response.
- To assess the relationship between hyperhomocysteinemia, MTHFR variants, and thrombotic events in renal failure patients.
Summary:
- Folic acid administration effectively decreases homocysteine levels, with intravenous methylcobalamin potentiating this effect in hemodialysis patients.
- Patients with homozygous or heterozygous C677T MTHFR variants require higher folic acid doses for hyperhomocysteinemia management due to reduced enzyme activity.
- While vascular-access thrombotic events were similar across MTHFR variants, treating hyperhomocysteinemia is suggested as key to reducing thrombosis risk. Hypohomocysteinemia, linked to malnourishment, is associated with higher mortality.
Impact:
- Vitamin therapy (folate, cobalamin) is well-tolerated and low-risk, suggesting routine monitoring of folate, cobalamin, and homocysteine levels in chronic renal patients.
- Prompt treatment to maintain homocysteine levels around 10 +/- 5 micromol/l may be beneficial in reducing vascular disease and thrombosis rates in this population.
- This study supports the clinical utility of vitamin supplementation for managing hyperhomocysteinemia and mitigating cardiovascular risks in patients with chronic kidney disease.
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.
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