FO002
FIBROBLAST GROWTH FACTOR 23 IS ASSOCIATED WITH FRACTIONAL SODIUM EXCRETION IN PATIENTS WITH CHRONIC KIDNEY DISEASE Free

INTRODUCTION AND AIMS: Fibroblast growth factor 23 (FGF23) regulates phosphate reabsorption and activation of vitamin D in the proximal tubule. Recent animal studies suggest that FGF23 increases apical membrane abundance of the sodium-chloride symporter (NCC) in the distal tubule, thereby reducing fractional sodium excretion (FENa), resulting in volume expansion and hypertension. Herein we investigated the associations of FGF23 to renal sodium handling and blood pressure in nondialysis CKD patients.

METHODS: Cross-sectional study in nondialysis CKD patients undergoing renal biopsy. Serum intact FGF23 levels, 24 h sodium excretion, FENa and blood pressure were measured at baseline. The association between FGF23 and renal sodium handling was explored by multivariate regression analysis.

RESULTS: 180 patients with a median age of 52.8 years, 60.6% male and a median eGFR of 50.6 ml/min/1.73 m² were included. In univariate analysis, FGF23 showed a positive association with FENa (Spearman's rho = 0.47; P < 0.001) and systolic blood pressure (rho = 0.17, P < 0.05), but not with plasma sodium, 24 h sodium excretion or mean arterial blood pressure. The association between FGF23 and FENa remained significant after adjustment for age, sex, BMI, eGFR, albuminuria, ischemic heart disease, diabetes and use of diuretics (multivariable adjusted β coefficient 0.62, P < 0.01). This association was most evident among the 102 individuals with eGFR <60 mL/minute/1.73 m² (β coefficient = 0.47; P < 0.05), and adjustment for iohexol clearence instead of eGFR did not alter the relationship.

CONCLUSIONS: FGF23 is positively associated with FENa in nondialysis CKD patients. These data do not support previously reported animal experiments, and suggest that FGF23 might contribute to maintaining normal sodium homeostasis during the progression of CKD.