| [ Summary ] |
Hyperhomocysteinemia has recently been found to be a risk factor for atherosclerotic disease. Plasma homocysteine concentrations in patients with chronic renal failure are twice to four times higher as compared to normal subjects, which may explain a high incidence of cardiovascular disease in renal failure. Although the exact mechanism for an increase in plasma homocysteine in patients with renal failure is unknown, a low clearance of homocysteine, deficiency or metabolic disturbance in vitamin B-groups, methylene tetrahydrofolate reductase gene mutation, or other abnormalities of homocysteine metabolism may cause hyperhomocysteinemia associated with chronic renal failure. To effectively reduce high plasma homocysteine levels in patients with end-stage renal failure,supplementation with higher doses of vitamin B-complex, folic acid, vitamin B12 and B6 is required. In particular, at least 10 mg daily of folic acid lowers fasting plasma homocysteine levels incases of chronic renal failure. The question remains unanswered as to whether long-term treatment with these vitamins reduces hyperhomocysteinemia effectively and safely or prevents atherosclerotic disease in chronic renal failure. Further clinical studies are needed to establish the best way to treat hyperhomocysteinemia in uremic disease. |