Project Number: 5306-51530-018-30
Project Type: Reimbursable

Start Date: Aug 01, 2011
End Date: Feb 28, 2014

Objective:
Vitamin D deficiency causes loss of bone mineral density by impairing calcium and phosphate absorption. Parathyroid hormone (PTH) is a principal mediator of this effect of vitamin D and elevated PTH can be an indicator of vitamin D deficiency. In a just-completed study with the same research group we found that vitamin D supplementation improved vitamin D “status” in that serum vitamin D levels increased and serum PTH decreased, as expected. Interestingly, PTH decreased in subjects with “normal” vitamin D status. These subjects were HIV infected and were taking tenofovir (TDF)-containing anti-retroviral therapy. This observation suggested that TDF produced a functional vitamin D deficiency, requiring higher serum vitamin D levels to maintain “normal” PTH levels. Fibroblast growth-factor 23 (FGF23) mediates phosphate balance and changes in FGF23 (not measured originally) may explain some of the negative effects of TDF on calcium and phosphate balance, and the relationship of vitamin D to PTH. For this reason we propose to measure FGF-23 in serum samples from the just-completed study to address this question.

Approach:
Our research plan is to measure serum FGF23 (and some related markers of vitamin D metabolism and kidney function) in previously collected serum located at the WHNRC. Data analysis will be performed with research collaborators at a Westat, Medical College of Wisconsin and UCSF.