Phosphate Binder Reduces FGF23 in CKD Patients

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Patients with non-dialysis chronic kidney disease and iron deficiency anemia treated with ferric citrate experienced significant declines in FGF23 regardless of change in serum phosphorus.
Patients with non-dialysis chronic kidney disease and iron deficiency anemia treated with ferric citrate experienced significant declines in FGF23 regardless of change in serum phosphorus.
The following article is part of conference coverage from Kidney Week 2017 in New Orleans hosted by the American Society of Nephrology. Renal & Urology News staff will be reporting live on medical studies conducted by nephrologists and other specialists who are tops in their field in acute kidney injury, chronic kidney disease, dialysis, transplantation, and more. Check back for the latest news from Kidney Week 2017.

NEW ORLEANS—Ferric citrate, an oral phosphate binder, can lower fibroblast growth factor 23 (FGF23) levels in patients with non-dialysis dependent chronic kidney disease (NDD-CKD) and iron deficiency anemia, regardless of change in serum phosphorus levels, according to study findings presented at the American Society of Nephrology's Kidney Week 2017.

The drug, which is FDA approved for controlling serum phosphorus levels in patients on dialysis, previously has been shown to improve hemoglobin and iron parameters in patients with NDD-CKD and iron deficiency anemia (IDA).

The latest study, led by Geoffrey Block MD, director of clinical research at Denver Nephrology, examined data from 233 patients with NDD-CKD and IDA randomly assigned to receive ferric citrate (117 patients) or placebo (116 patients) for 16 weeks. Ferric citrate was initiated at 3 1-g tablets per day and titrated to achieve a 1 g/dL or greater increase in hemoglobin levels from baseline (maximum dosing 12 g/day).

After 16 weeks of treatment, intact FGF23 levels significantly decreased in those with transferrin saturation (TSAT) above or below 20% and across all strata of baseline phosphorus other than those with levels below 3.5 mg/dL. C-terminal FGF23 decreased significantly in both TSAT strata (less than 20% and 20% or higher) and in all baseline phosphorus strata except for levels of 5.5 mg/dL or above. The changes in FGF23 occurred even in those who had no change in serum phosphorus, further supporting the view that ferric citrate acts via several distinct and potentially complementary mechanisms to reduce FGF23, according to Dr Block and colleagues.

“FGF23 is emerging as an important biomarker of chronic kidney disease,” Dr Block said. “A potential oral treatment option for iron deficiency anemia in patients with non-dialysis dependent CKD, which also reduces FGF23, could be important in the management of CKD.”

Visit Renal & Urology News' conference section for continuous coverage from Kidney Week 2017.


Reference

Block GA, Pergola PE, Uhlig K, et al. Ferric citrate reduced FGF23 in patients with non-dialysis dependent chronic kidney disease (NDD-CKD) and iron deficiency anemia (IDA) irrespective of the change in serum phosphate (P). Oral presentation at Kidney Week 2017 in New Orleans (Oct. 31-Nov. 5). Abstract TH-OR038.

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