Abstract
Vitamin D is an important nutrient involved in bone mineral metabolism, and vitamin D status is reflected by serum total 25-hydroxyvitamin D (25[OH]D) concentrations. Vitamin D deficiency is highly prevalent in patients with chronic kidney disease (CKD), and nutritional vitamin D supplementation decreases elevated parathyroid hormone concentrations in subgroups of these patients. Furthermore, vitamin D is supposed to have pleiotropic effects on various diseases such as cardiovascular diseases, malignancies, infectious diseases, diabetes, and autoimmune diseases. Indeed, there is cumulative evidence showing the associations of low vitamin D with the development and progression of CKD, cardiovascular complication, and high mortality. Recently, genetic polymorphisms in vitamin D-binding protein have received great attention because they largely affect bioavailable 25(OH)D concentrations. This finding suggests that the serum total 25(OH)D concentrations would not be comparable among different gene polymorphisms and thus may be inappropriate as an index of vitamin D status. This finding may refute the conventional definition of vitamin D status based solely on serum total 25(OH)D concentrations.
Highlights
Vitamin D is a fat soluble secosteroid that interacts with a specific nuclear receptor similar to other steroid hormones and plays a central role in calcium and phosphate homeostasis and musculoskeletal health [1]
(3) Compared to Caucasians, African-Americans had lower serum total 25(OH)D concentrations over all but had the similar concentrations of bioavailable 25(OH)D within the quintiles of parathyroid hormone (PTH) concentrations. These findings suggest that it may be inappropriate to determine vitamin D status of each individual by serum total 25(OH)D concentrations unless we examine the D-binding protein (DBP) phenotype
A large body of evidence concerns the beneficial effects of vitamin D on musculoskeletal health as well as various diseases
Summary
Vitamin D is a fat soluble secosteroid that interacts with a specific nuclear receptor similar to other steroid hormones and plays a central role in calcium and phosphate homeostasis and musculoskeletal health [1]. Ecological and observational studies have demonstrated that vitamin D deficiency, defined as a low serum total 25-hydroxyvitamin D (25[OH]D) concentration, is associated with increased risks of death and diseases such as various cardiovascular diseases, malignancies, infectious diseases, diabetes, autoimmune diseases, and kidney diseases [2]. Chronic kidney disease (CKD) has been identified as a risk factor for vitamin D deficiency. The prevalence of vitamin D deficiency or insufficiency is high among patients with CKD, especially patients with end-stage renal disease and kidney transplant recipients [3, 4]. Similar to the general population, vitamin D deficiency in these patients is associated with elevated concentrations of parathyroid hormone and bone turnover markers as well as low bone mineral density [5,6,7]. The importance and implications of a genetic polymorphism of vitamin D-binding protein, which potentially overturn the current concept of vitamin D status, are discussed
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