Folic acid supplementation to prevent adverse events in individuals with chronic kidney disease and end stage renal disease.
OBJECTIVE
This review summarizes our current understanding of the role of folate in the treatment of hyperhomocysteindemia and the prevention of cardiovascular disease in patients with chronic kidney disease and end stage renal disease. Relevant papers published between 2003 and 2004 are referenced.


RESULTS
With the exception of one paper, recent therapeutic studies supported previous findings that folate therapy achieves only a modest reduction in plasma homocysteine and seldom normalizes homocysteine. Large prospective studies are under way to evaluate the causal relationship between homocysteine and cardiovascular risk. Recent work supports earlier data that suggested that homocysteine inflicts its damage by oxidative stress. A newly described consequence of hyperhomocysteindemia is DNA hypomethylation and alteration of gene expression. A recent study in the general population suggested that while folate may lower homocysteine it does not improve endothelial function in individuals without cardiovascular disease.


CONCLUSIONS
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.
Gonin
Joyce M
JM
Georgetown University Hospital, Washington, DC 20007, USA. goninj@gunet.georgetown.edu
D002318:Cardiovascular Diseases / Q000209:etiology / Q000517:prevention & control*; D002908:Chronic Disease; D019587:Dietary Supplements; D005492:Folic Acid / Q000627:therapeutic use*; D006801:Humans; D020138:Hyperhomocysteinemia / Q000150:complications; D007674:Kidney Diseases / Q000188:drug therapy*; D007676:Kidney Failure, Chronic / Q000188:drug therapy
D005492:Folic Acid