Fibroblast growth factor 23 in hypophosphataemic HIV-positive adults on tenofovir

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?<?0.75?mmol/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 +/- 0.03?mmol/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.