Serum FGF23 levels in normal and disordered phosphorus homeostasis

Area of Science:

• Endocrinology
• Nephrology
• Genetics

Background:

• X-linked hypophosphatemic rickets (XLH) is caused by PHEX mutations leading to renal phosphate wasting.
• Fibroblast growth factor 23 (FGF23) is a phosphaturic hormone implicated in autosomal dominant hypophosphatemia.
• The role of FGF23 in XLH pathogenesis remains to be fully elucidated.

Purpose of the Study:

• To investigate circulating FGF23 levels in subjects with XLH.
• To determine the correlation between FGF23 levels and hypophosphatemia in XLH.
• To compare FGF23 levels in XLH with those in end-stage renal disease (ESRD) and other hypophosphatemic conditions.

Main Methods:

• Fasting serum FGF23 levels were measured using ELISA in subjects with XLH, hypophosphatemia of unknown cause, ESRD, and age-matched controls.
• Serum biochemical parameters, including phosphorus and calcium, were analyzed.
• Statistical analyses included Spearman's correlation coefficient and linear regression.

Main Results:

• FGF23 levels were not significantly different between XLH subjects and controls.
• FGF23 levels were significantly elevated in ESRD subjects.
• FGF23 showed a strong inverse correlation with serum phosphorus and Ca x P product in XLH.
• FGF23 demonstrated a strong positive relationship with phosphorus and Ca x P product in ESRD.

Conclusions:

• FGF23 may play a role in mediating hypophosphatemia in XLH and tumor-induced osteomalacia (TIO).
• Overlapping FGF23 levels in hypophosphatemic disorders and normal subjects suggest independent regulation of serum phosphorus.
• FGF23 is markedly increased in ESRD, highlighting its role in phosphate homeostasis in kidney disease.