Elevated plasma total homocysteine (ptHcy) or hyperhomocysteinemia (hHcy) independently predicts cardiovascular disease in predialysis chronic kidney disease (pCKD). Folate status is one of the known nutritional determinants of ptHcy. In the era of folic acid food fortification, this cross-sectional study aimed to describe in pCKD subjects (n=48): 1) Prevalence of hHcy. 2) Intake and status of nutrients involved in homocysteine metabolism. 3) Determinants of ptHcy. The prevalence of hHcy was 93.8% (95% CI: 81.8 to 98.4). Median (25th, 75th percentile) total folate intake from food and supplements was 389 (282,640) µg DFE/d. No subject was folate deficient (red blood cell < 317 nmol/L). Red blood cell folate (r = - 0.406, p=0.004) and energy-protein undernutrition (r = 0.357, p=0.013) independently predicted ptHcy. To conclude, total folate intake among subjects with pCKD was sufficient to prevent folate deficiency but not able to prevent a high prevalence of hHcy.

Elevated plasma total homocysteine (ptHcy) or hyperhomocysteinemia (hHcy) independently predicts cardiovascular disease in predialysis chronic kidney disease (pCKD). Folate status is one of the known nutritional determinants of ptHcy. In the era of folic acid food fortification, this cross-sectional study aimed to describe in pCKD subjects (n=48): 1) Prevalence of hHcy. 2) Intake and status of nutrients involved in homocysteine metabolism. 3) Determinants of ptHcy. The prevalence of hHcy was 93.8% (95% CI: 81.8 to 98.4). Median (25th, 75th percentile) total folate intake from food and supplements was 389 (282,640) µg DFE/d. No subject was folate deficient (red blood cell < 317 nmol/L). Red blood cell folate (r = - 0.406, p=0.004) and energy-protein undernutrition (r = 0.357, p=0.013) independently predicted ptHcy. To conclude, total folate intake among subjects with pCKD was sufficient to prevent folate deficiency but not able to prevent a high prevalence of hHcy.