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J Am Soc Nephrol. 2015 Feb;26(2):493-503. doi: 10.1681/ASN.2014020212. Epub 2014 Jul 24.

Ferric citrate controls phosphorus and delivers iron in patients on dialysis.

Author information

1
Divisions of Nephrology and Hypertension and Julia.lewis@vanderbilt.edu.
2
Divisions of Nephrology and Hypertension and.
3
Hematology/Oncology, Vanderbilt University Medical Center, Nashville, Tennessee;
4
Metrolina Nephrology Associates, Charlotte, North Carolina;
5
Kidney Care Associates, Augusta, Georgia;
6
Clinical Research Ltd., Canton, Ohio;
7
Nephrology Associates, Nashville, Tennessee;
8
Southeast Renal Research Institute, Chattanooga, Tennessee;
9
Pioneer Valley Nephrology, Holyoke, Massachusetts;
10
Washington Nephrology Associates, Bethesda, Maryland;
11
Western Nephrology, Westminster, Colorado;
12
Division of Nephrology, Medical College of Wisconsin, Milwaukee, Wisconsin;
13
Mountain Kidney and Hypertension Associates, Asheville, North Carolina;
14
Pines Clinical Research, Pembroke Pines, Florida;
15
Division of Nephrology and Hypertension, University of Cincinnati, Cincinnati, Ohio;
16
Houston Kidney, Houston, Texas; and.
17
Division of Epidemiology, University of Utah, Salt Lake City, Utah.

Abstract

Patients on dialysis require phosphorus binders to prevent hyperphosphatemia and are iron deficient. We studied ferric citrate as a phosphorus binder and iron source. In this sequential, randomized trial, 441 subjects on dialysis were randomized to ferric citrate or active control in a 52-week active control period followed by a 4-week placebo control period, in which subjects on ferric citrate who completed the active control period were rerandomized to ferric citrate or placebo. The primary analysis compared the mean change in phosphorus between ferric citrate and placebo during the placebo control period. A sequential gatekeeping strategy controlled study-wise type 1 error for serum ferritin, transferrin saturation, and intravenous iron and erythropoietin-stimulating agent usage as prespecified secondary outcomes in the active control period. Ferric citrate controlled phosphorus compared with placebo, with a mean treatment difference of -2.2±0.2 mg/dl (mean±SEM) (P<0.001). Active control period phosphorus was similar between ferric citrate and active control, with comparable safety profiles. Subjects on ferric citrate achieved higher mean iron parameters (ferritin=899±488 ng/ml [mean±SD]; transferrin saturation=39%±17%) versus subjects on active control (ferritin=628±367 ng/ml [mean±SD]; transferrin saturation=30%±12%; P<0.001 for both). Subjects on ferric citrate received less intravenous elemental iron (median=12.95 mg/wk ferric citrate; 26.88 mg/wk active control; P<0.001) and less erythropoietin-stimulating agent (median epoetin-equivalent units per week: 5306 units/wk ferric citrate; 6951 units/wk active control; P=0.04). Hemoglobin levels were statistically higher on ferric citrate. Thus, ferric citrate is an efficacious and safe phosphate binder that increases iron stores and reduces intravenous iron and erythropoietin-stimulating agent use while maintaining hemoglobin.

KEYWORDS:

anemia; clinical trial; dialysis; phosphate binders

PMID:
25060056
PMCID:
PMC4310662
DOI:
10.1681/ASN.2014020212
[Indexed for MEDLINE]
Free PMC Article

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