Abstract
FGF23 is a novel phosphaturic hormone; we aimed to assess the FGF23 levels and its association with dietary phosphate intake and indices of renal handling of phosphate in this study. Prospective study was conducted in which dietary phosphate intake was assessed by food frequency questionnaire (FFQ) along with blood and spot urine samples were collected after overnight fast for determining serum phosphate, FGF23, fractional excretion of phosphate (FePO4) and tubular maximum for phosphate (TmP/GFR). FGF23 (C-Term) was measured by a sandwich ELISA. The mean dietary phosphate intake of eighty healthy adults (mean age of 29 ± 5 years) was 1220 ± 426 mg; median FGF23 was 49.9 RU/ml (IQR=33, 76) and mean FePO4 was 7 ± 4.7. Subjects were stratified into two groups according to serum phosphate levels. Significant difference was not found in dietary phosphate intake and FGF23 levels in the two groups. However, TmP/GFR and creatinine were significantly different in the two groups. FePO4 was high in both the groups. Overall a rising pattern of FGF23 levels was seen with increasing serum phosphate levels. Significant positive correlation was found between FGF23 and dietary phosphate (r=0.22, p<0.05) and negative correlation was seen between FGF23 and FePO4 (r=-0.260, p<0.05).
Highlights
Fibroblast 23 (FGF23) is primarily expressed in osteocytes and in endothelial cells lining the venous sinusoids of bone marrow and thymus [1]
Mean TmP/GFR was low and FEPO4 was high in subjects with hypophosphatemia
Similar findings are seen in the 25 healthy Swiss subjects with high phosphate intake of 1400 ± 100 mg, median Fibroblast Growth Factor 23 (FGF23) of 48.3 ± 4.6 RU/ml and serum phosphate of 3.90 ± 0.09 mg/dl (Table 4)
Summary
Fibroblast 23 (FGF23) is primarily expressed in osteocytes and in endothelial cells lining the venous sinusoids of bone marrow and thymus [1]. Most of its functions occur in the kidney through an FGF receptor (FGFR)/Klotho complex; and it acts opposite to vitamin D by inhibiting 1 alpha hydroxylase and stimulating 24 hydroxylase enzymes in the renal tubule. The expression of type II sodium-dependent phosphate cotransporters (mainly NPT2a and NPT2c) is inhibited by FGF23 in cells of renal proximal tubules which reduces phosphate reabsorption and increases urinary phosphate excretion. FGF 23 interacts negatively with PTH mRNA in contrast to CKD, where increased FGF23 is associated with secondary hyperparathyroidism. Due to these opposing verdicts; local and systemic confounding factors have been projected to modify FGF23 levels and taken together, it is advocated that PTH and FGF23 axis is similar to vitamin D-FGF23 loop [2]
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