Effect of a non-calcium-based phosphate binder on fibroblast growth factor 23 in chronic kidney disease

Elevated fibroblast growth factor 23 (FGF23) levels are associated with progression of chronic kidney disease (CKD) and increased mortality. Studies in individuals without CKD suggest that FGF23 levels are regulated by dietary phosphorus; however, the effect of pharmacologic phosphorus restriction on FGF23 in CKD patients is uncertain.

We performed a prospective cohort study examining the effect of phosphorus reduction with sevelamer carbonate on FGF23 levels in CKD patients. Adults with an estimated glomerular filtration rate <60 ml/min/1.73 m(2) according to MDRD (Modification of Diet in Renal Disease) and hyperphosphatemia were enrolled. Subjects were started on sevelamer carbonate 800 mg by mouth with meals and the dose was titrated to achieve a serum phosphorus between 2.7 and 4.6 mg/dl for those with CKD stages III and IV, and between 3.5 and 5.5 mg/dl for CKD stage V. FGF23 levels were measured at baseline and 3 months. Results were analyzed as percent change from baseline.

40 patients completed the study. Mean estimated glomerular filtration rate by MDRD at entry was 21.2 ± 10.5, serum phosphorus 4.8 ± 0.8, and FGF23 level 602.3 ± 1,074.6. Mean serum phosphorus and FGF23 levels after 3 months were 4.4 ± 0.9 and 599.2 ± 720.9, respectively. No significant difference was seen in FGF23 (p = 0.76) despite a significant difference in phosphorus (p = 0.001).

The patients treated with sevelamer carbonate did not have a significant change in plasma FGF23 levels despite a significant reduction in phosphorus. It is possible that once overt hyperphosphatemia develops, FGF23 levels may not be reduced by phosphorus reduction alone in CKD patients.