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.
OBJECTIVES: Hypophosphataemia is common in HIV-positivepatients, 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-positivepatients on tenofovir. METHODS:Calcium and phosphate metabolism was studied in 36 HIV-positivepatients 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-positivepatients on TDF. The data suggest that a PTH-like factor may be involved.
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Authors: Peter L Havens; Rohan Hazra; Charles B Stephensen; Jennifer J Kiser; Patricia M Flynn; Craig M Wilson; Brandy Rutledge; James Bethel; Cynthia G Pan; Leslie R Woodhouse; Marta D Van Loan; Nancy Liu; Jorge Lujan-Zilbermann; Alyne Baker; Bill G Kapogiannis; Catherine M Gordon; Kathleen Mulligan Journal: Antivir Ther Date: 2014-02-17
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