Supplementation eases inflammation, lowers cardiac risk, and improves glycemic controls.
Deficiency in 25-hydroxyvitamin D [25(OH)D] is common in CKD. Although the endocrine functions of vitamin D in bone mineral metabolism are well known, the effects of autocrine and paracrine functions on insulin production and resistance, immunity, and CVD are receiving increased attention.
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Since an estimated 75% of “activated” vitamin D (1,25[OH]2D3) is produced in extra-renal sites close to where it is used for cellular “non-bone” functions, low serum levels of the required substrate 25(OH)D may negatively impact health outcomes particularly for people with CKD. The National Kidney Foundation (NKF) Kidney Disease Outcomes Quality Initiative (K/DOQI) clinical practice guidelines for bone metabolism and disease in CKD recognize the need for further research in this area.
With natural food sources of vitamin D (D3, cholecalciferol) limited mainly to fatty fish and fish oils, the body’s ability to convert ultra-violet B (UVB) rays from sunlight into pre-vitamin D provides its main supply. Factors impeding adequate 25(OH)D levels in CKD patients include reduced vitamin D3 in the skin as glomerular filtration rate (GFR) declines and as a result of aging; decreased activity and sunlight exposure resulting from fatigue and dialysis schedules; and higher melanin content in at-risk populations (African Americans, Hispanics).
Foods commonly fortified with vitamin D (D2, ergocalciferol) such as milk and other dairy products are often restricted due to high phosphorus content, so supplementation with vitamin D is being investigated as a remedy for CKD patients.
Evidence of the possible benefits of ergocalciferol in dialysis patients is mounting. In a study by Shah et al. (Perit Dial Int. 2005;25:362-366), 29 peritoneal dialysis patients were examined with regard to serum 25(OH)D levels and effects of ergocalciferol supplementation.
All but one patient were vitamin D deficient (less than 15 ng/mL [multiply by 2.496 to convert to nmol/L] and 25 had undetectable levels (less than 7 ng/mL). After receiving 50,000 IU of ergocalciferol weekly for four weeks, all were vitamin D replete except one patient who required an additional course. The investigators observed no significant change in serum calcium, phosphorus, and PTH.
A retrospective study by my colleagues and me (J Ren Nutr. 2008;18:375-382) examined the prevalence of vitamin D deficiency in 344 maintenance hemodialysis patients and the effects of supplementation with ergocalciferol (50,000 IU/week for 24 weeks) for 25(OH)D levels less than 40 ng/mL. Ninety-two percent of patients were vitamin D deficient based on these criteria, with 80% less than 31 ng/mL and 24% below 11 ng/mL. Baseline subgroup analysis showed lower levels of 25(OH)D associated with higher glycosylated hemoglobin (HbA1c).
Supplementation with ergocalciferol resulted in significant improvement in mean serum 25(OH)D from baseline (18.4 ng/mL) to six months (42 ng/mL), and improved glycemic control as reflected by lower mean HbA1c (6.9% vs. 6.4%).
