Objectives: Hypophosphataemia is common in HIV-positive patients, in particular in those using tenofovir disoproxil fumarate (TDF). Its pathogenesis is not well understood. The importance of fibroblast growth factor 23 (FGF-23), the most potent phosphaturic hormone known today, has not been studied in these patients. The aim of the study was to investigate whether FGF-23 might be involved in the aetiology of hypophosphataemia in HIV-positive patients on tenofovir. Methods: Calcium and phosphate metabolism was studied in 36 HIV-positive patients on TDF. Hypophosphataemia was defined as a serum phosphate level<0.75mmol/L. Results: Fifteen patients (42%) had hypophosphataemia (group 1), and 21 had a normal serum phosphate level (group 2). The renal phosphate reabsorption threshold [tubular maximum phosphate reabsorption per glomerular filtration rate (TmP/gfr)] was significantly lower in group 1 than in group 2 (0.58±0.04 vs. 0.91±0.03mmol/L, respectively; P<0.0001). The serum phosphate concentration was strongly correlated with TmP/gfr (R=0.71; P<0.0001). Both groups had normal serum FGF-23 levels, and serum phosphate and TmP/gfr were not related to serum parathyroid hormone (PTH) or FGF-23 levels. Conclusion: FGF-23 is not involved in the pathogenesis of hypophosphataemia in HIV-positive patients on TDF. The data suggest that a PTH-like factor may be involved. © 2012 British HIV Association.
CITATION STYLE
Bech, A., Van Bentum, P., Nabbe, K., Gisolf, J., Richter, C., & De Boer, H. (2012). Fibroblast growth factor 23 in hypophosphataemic HIV-positive adults on tenofovir. HIV Medicine, 13(9), 558–563. https://doi.org/10.1111/j.1468-1293.2012.01015.x
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