|Holden, Rachel - Kingston General Hospital|
|Morton, Ross - Kingston General Hospital|
|Garland, Jocelyn - Kingston General Hospital|
|Booth, Sarah - Jean Mayer Human Nutrition Research Center On Aging At Tufts University|
Submitted to: Journal of the American Society of Nephrology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/1/2010
Publication Date: 4/1/2010
Citation: Holden, R.M., Morton, R.A., Garland, J.S., Booth, S.L. 2010. Vitamins K and D status in patients with stages 3-5 chronic kidney disease. Journal of the American Society of Nephrology. 5(4):590-597.
Interpretive Summary: Vitamins K and D may be involved in the regulation of calcification in chronic kidney disease (CKD). To test this hypothesis, vitamin K and D status was measured as dietary intake and various biochemical markers used to assess nutritional status in 172 patients with earlier stages of CKD (defined as stages 3-5). A subjective assessment of overall nutritional status was also determined. Sub-clinical vitamin K deficiency criteria were met by up to 97% of patients, depending on the criterion used, whilst 58.3% and 8.6% had vitamin D insufficiency and deficiency respectively. Higher dietary vitamin K intakes were associated with higher vitamin K status as measured by two biochemical measures. High circulating measures of vitamin K were associated with stable weight and the absence of subcutaneous fat loss or muscle wasting. Circulating measures of vitamin D were positively associated with stable weight and biochemical measures of overall nutritional status and mineral metabolism. These data indicate that a suboptimal vitamin K and D status is prevalent in patients with CKD. Sufficiency of both vitamins K and D was similarly predicted by measures of overall improved nutritional status.
Technical Abstract: Background and Objectives: Vitamin K, vitamin K-dependent (VKD) proteins and vitamin D may be involved in the regulation of calcification in chronic kidney disease (CKD). Design, setting, participants and measurements: Vitamin K and D status was measured as dietary intake, plasma phylloquinone, serum percent uncarboxylated osteocalcin (%ucOC), proteins induced by vitamin K absence (PIVKA-II), Vitamin K Epoxide Reductase single nucleotide polymorphism, apolipoprotein E (apoE) genotype and plasma 25-hydroxyvitamin D (25(OH)D) in 172 subjects with stages 3-5 CKD. Nutritional status was determined by subjective global assessment (SGA). Results: Sub-clinical vitamin K deficiency criteria was met by 8% (phylloquinone), 60% (%ucOC) and 97% (PIVKA-II) of subjects whilst 58.3% and 8.6% had 25(OH)D insufficiency and deficiency respectively. Dietary vitamin K intake was associated with higher phylloquinone (p=0.05) and lower PIVKA-II (p=0.05). There were positive correlations between phylloquinone and the presence of stable weight (p=0.02), and the absence of subcutaneous fat loss (p=0.02) or muscle wasting (p=0.01). 25(OH)D levels were positively associated with stable weight (p=0.03) and albumin (p<0.001). PIVKA-II levels were associated with apoE genotype (p=0.02). Higher %ucOC and lower 25(OH)D were similarly associated with CKD stage, parameters of mineral metabolism and urine albumin:creatinine ratio. Conclusions: These data indicate that a suboptimal vitamin K and D status is prevalent in patients with CKD. Sufficiency of both vitamins K and D was similarly predicted by measures of overall improved nutritional status. Proteinuria was associated with both a suboptimal vitamin D status as well as worse peripheral vitamin K status.