Abstract

Cardiovascular disease (CVD) is the leading cause of death in chronic kidney disease (CKD) patients. Elevated homocysteine levels in CKD patients were thought to be one of the causes. Folic acid supplementation, which was known to improve anemia in CKD patients, can also reduce homocysteine levels, which would reduce cardiovascular events. In this review we will discuss the pathophysiology of hyperhomocysteinemia in CKD patients and studies that explain the role of folic acid to lower homocysteine levels that can also lower the risk of CVD in CKD patients. There are some conflicting results among available studies, but folic acid still seems reasonable to be considered as a suitable supplementary therapy in individuals with CKD after a thorough evaluation of the patient's folate status.

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