Folic acid supplementation to prevent adverse events in individuals with chronic kidney disease and end stage renal disease

The causes of hyperhomocysteindemia in renal failure remain obscure. The possibilities include impairment of both renal and extrarenal metabolic pathways by uraemia. Hyperhomocysteindemia is associated in some but not all studies with an increased risk for cardiovascular disease. A low homocysteine may reflect malnutrition and predict a poor outcome. Folate achieves modest reductions of homocysteine in some but not all studies. There are no data to support therapy with very high-dose folic acid. Hyperhomocysteindemia impairs endothelial function which is not adequately reversed by folate.