Abstract
Objective: Vitamin D deficiency is estimated to affect one billion people worldwide. In the United States, 9-12% of healthy children have vitamin D deficiency. Renal calcium and phosphate excretion in healthy people is a sensitive indicator of total body mineral balance. We explored the possibility of using urine calcium-to-creatinine (Uca/Ucr) and urine phosphate-to-creatinine (Uphos/Ucr) as noninvasive biomarkers of vitamin D deficiency in at risk children. Patients and methods: This was an observational study of children with one or more risk factors for vitamin D deficiency. Anthropometric data and a physical exam were obtained in all children and skin pigmentation, sunlight exposure, dietary history, and frequency of vitamin supplementation of both mother and child were determined by parent report. We measured serum levels of calcium, phosphate, magnesium, intact PTH, 25-hydroxyvitamin D, alkaline phosphatase, and creatinine. A random urine sample was collected for calcium, phosphate and creatinine. Results: A total of 60 healthy children were recruited. Mean age of the subjects was 1.4 (range 0.5 to 2.9) years. Twenty percent of the children were regularly given vitamin D supplements. The prevalence of vitamin D deficiency (25-hydroxyvitamin D < 50 nmol/L) was 3.4%, vitamin D insufficiency (≥ 50 and < 80 nmol/L) was 28.6% and vitamin D sufficiency (≥ 80 nmol/L) was 68%. One subject had biochemical evidence of rickets. Linear regression analysis showed no correlation between 25-hydroxyvitamin D levels and random Uca/Ucr or Uphos/Ucr. Conclusion: Random urine calcium or phosphate levels offer little promise as screening tools for vitamin D deficiency in children.
Highlights
Vitamin D deficiency is extremely common worldwide and is estimated to affect one billion humans [1]
Linear regression analysis showed no correlation between 25-hydroxyvitamin D levels and random urine calcium-to-creatinine (Uca/Ucr) or Uphos/Ucr
Vitamin D is converted to 25-hydroxyvitamin D in the liver [13]. 25-hydroxyvitamin D is the storage form of vitamin D the vitamin D receptor does bind it with reduced affinity [15]. 25-hydroxyvitamin D is converted to the active 1,25-dihydroxyvitamin D primarily in the kidney, by an enzyme tightly regulated by parathyroid hormone (PTH) and to a lesser extent by hypocalcemia, hypophosphatemia, insulin, growth hormone and other factors
Summary
Vitamin D deficiency is extremely common worldwide and is estimated to affect one billion humans [1]. Vitamin D deficiency may lead to nutritional rickets, which is considered to be the most common non-communicable disease of children worldwide [1,2,3]. Conversion takes place in other tissues, but this does not play a major role in calcium homeostasis.1,25-dihydroxyvitamin D acts by binding the vitamin D receptor. The primary action of vitamin D is to increase calcium uptake in the small intestine [16]. It plays a role in calcium reuptake in the kidney and has a direct effect on growth plate chondrocytes and osteoblasts mediated through insulin-like growth factor-I [17]
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