Moving Points in NephrologyVitamin D in Health and DiseaseHeaney, Robert P. Author Information Creighton University, Omaha, Nebraska Correspondence: Dr. Robert P. Heaney, Creighton University, 601 N. 30th Street, Suite 4841, Omaha, NE 68131. Phone: 402-280-4029; Fax 402-280-4751; E-mail: [email protected] Clinical Journal of the American Society of Nephrology 3(5):p 1535-1541, September 2008. | DOI: 10.2215/CJN.01160308 Buy Metrics Abstract Vitamin D functions in the body through both an endocrine mechanism (regulation of calcium absorption) and an autocrine mechanism (facilitation of gene expression). The former acts through circulating calcitriol, whereas the latter, which accounts for more than 80% of the metabolic utilization of the vitamin each day, produces, uses, and degrades calcitriol exclusively intracellularly. In patients with end-stage kidney disease, the endocrine mechanism is effectively disabled; however, the autocrine mechanism is able to function normally so long as the patient has adequate serum levels of 25(OH)D, on which its function is absolutely dependent. For this reason, calcitriol and its analogs do not constitute adequate replacement in managing vitamin D needs of such patients. Optimal serum 25(OH)D levels are greater than 32 ng/mL (80 nmol/L). The consequences of low 25(OH)D status include increased risk of various chronic diseases, ranging from hypertension to diabetes to cancer. The safest and most economical way to ensure adequate vitamin D status is to use oral dosing of native vitamin D. (Both daily and intermittent regimens work well.) Serum 25(OH)D can be expected to rise by about 1 ng/mL (2.5 nmol/L) for every 100 IU of additional vitamin D each day. Recent data indicate that cholecalciferol (vitamin D3) is substantially more potent than ergocalciferol (vitamin D2) and that the safe upper intake level for vitamin D3 is 10,000 IU/d. Copyright © 2008 The Authors. Published by Wolters Kluwer Health, Inc. All rights reserved.
