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Am J Kidney Dis. 2015 Sep;66(3):479-88. doi: 10.1053/j.ajkd.2015.03.013. Epub 2015 May 7.

The Phosphate Binder Ferric Citrate and Mineral Metabolism and Inflammatory Markers in Maintenance Dialysis Patients: Results From Prespecified Analyses of a Randomized Clinical Trial.

Author information

1
University of Texas Southwestern Medical Center, Dallas, TX. Electronic address: peter.vanburen@utsouthwestern.edu.
2
Vanderbilt University Medical Center, Nashville, TN.
3
University of Utah Medical Center, Salt Lake City, UT.
4
Duke University Medical Center, Durham, NC.
5
Henry Ford Medical Center, Detroit, MI.
6
Nephrology Specialists PC, Michigan City, IN.
7
Wake Forest University Medical Center, Winston-Salem, NC.
8
Ichilov Medical Center, Tel Aviv, Israel.
9
Kidney Associates PLLC, Houston, TX.
10
University of Pennsylvania Medical Center, Philadelphia, PA.
11
Rush University Medical Center, Chicago, IL.
12
Tufts Medical Center, Boston, MA.

Abstract

BACKGROUND:

Phosphate binders are the cornerstone of hyperphosphatemia management in dialysis patients. Ferric citrate is an iron-based oral phosphate binder that effectively lowers serum phosphorus levels.

STUDY DESIGN:

52-week, open-label, phase 3, randomized, controlled trial for safety-profile assessment.

SETTING & PARTICIPANTS:

Maintenance dialysis patients with serum phosphorus levels ≥6.0 mg/dL after washout of prior phosphate binders.

INTERVENTION:

2:1 randomization to ferric citrate or active control (sevelamer carbonate and/or calcium acetate).

OUTCOMES:

Changes in mineral bone disease, protein-energy wasting/inflammation, and occurrence of adverse events after 1 year.

MEASUREMENTS:

Serum calcium, intact parathyroid hormone, phosphorus, aluminum, white blood cell count, percentage of lymphocytes, serum urea nitrogen, and bicarbonate.

RESULTS:

There were 292 participants randomly assigned to ferric citrate, and 149, to active control. Groups were well matched. For mean changes from baseline, phosphorus levels decreased similarly in the ferric citrate and active control groups (-2.04±1.99 [SD] vs -2.18±2.25 mg/dL, respectively; P=0.9); serum calcium levels increased similarly in the ferric citrate and active control groups (0.22±0.90 vs 0.31±0.95 mg/dL; P=0.2). Hypercalcemia occurred in 4 participants receiving calcium acetate. Parathyroid hormone levels decreased similarly in the ferric citrate and active control groups (-167.1±399.8 vs -152.7±392.1 pg/mL; P=0.8). Serum albumin, bicarbonate, serum urea nitrogen, white blood cell count and percentage of lymphocytes, and aluminum values were similar between ferric citrate and active control. Total and low-density lipoprotein cholesterol levels were lower in participants receiving sevelamer than those receiving ferric citrate and calcium acetate. Fewer participants randomly assigned to ferric citrate had serious adverse events compared with active control.

LIMITATIONS:

Open-label study, few peritoneal dialysis patients.

CONCLUSIONS:

Ferric citrate was associated with similar phosphorus control compared to active control, with similar effects on markers of bone and mineral metabolism in dialysis patients. There was no evidence of protein-energy wasting/inflammation or aluminum toxicity, and fewer participants randomly assigned to ferric citrate had serious adverse events. Ferric citrate is an effective phosphate binder with a safety profile comparable to sevelamer and calcium acetate.

KEYWORDS:

Hemodialysis; adverse events; calcium acetate; end-stage renal disease (ESRD); ferric citrate; hyperphosphatemia; mineral bone disease; phosphate binder; protein-energy wasting (PEW)/inflammation; safety; sevelamer carbonate

PMID:
25958079
PMCID:
PMC4868355
DOI:
10.1053/j.ajkd.2015.03.013
[Indexed for MEDLINE]
Free PMC Article

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