Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3896309 | Seminars in Nephrology | 2016 | 6 Pages |
Abstract
Ferric citrate (FC) is an iron-containing phosphate binder that has been shown to effectively decrease serum phosphate, increase hemoglobin, and replete iron stores in patients with chronic kidney disease. Intestinal absorption of iron from FC results in increases in serum iron, ferritin, and transferrin saturation, effects that occur over 12 to 24 weeks and subsequently appear to plateau. As a result, use of erythropoiesis-stimulating agents and intravenous iron is reduced significantly and in clinical trials in patients receiving hemodialysis, the majority of subjects were able to discontinue intravenous iron use completely. One-year safety data have indicated that FC-treated subjects have reduced rates of hospitalization and reduced serious adverse events related to gastrointestinal, infectious, and cardiovascular causes, although the mechanism for this finding is unclear. The large doses of oral iron administered and lack of precise information on relative absorption over time or on the potential effect of FC on intestinal epithelial function should prompt continued clinical investigation. Although not yet approved for use in the United States for patients with non-dialysis-dependent chronic kidney disease, FC is a welcome addition to the available treatment options for decreasing phosphate concentrations. The multifaceted favorable effects on anemia and phosphate in combination with the erythropoiesis-stimulating agent and intravenous iron-sparing data support the use of FC as a first-line treatment option when phosphate-decreasing therapy is indicated.
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Authors
Geoffrey A. MD,