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Published ahead of print on March 29, 2006
Clin J Am Soc Nephrol 1: 475-482, 2006
© 2006 American Society of Nephrology
doi: 10.2215/CJN.01541005

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Clinical Nephrology

Effect of Intravenous Iron Sucrose in Peritoneal Dialysis Patients Who Receive Erythropoiesis-Stimulating Agents for Anemia: A Randomized, Controlled Trial

Harmeet Singh*, John Reed{dagger}, Sylvia Noble{ddagger}, Jose L. Cangiano§, David B. Van Wyck||; for the United States Iron Sucrose (Venofer) Clinical Trials Group

* Western Nephrology & Metabolic Bone Disease, PC, Lakewood, Colorado; {dagger} Nephrology Associates, Columbus, Mississippi; {ddagger} Northwestern Louisiana Nephrology, Shreveport, Louisiana; § Puerto Rico School of Medicine, San Juan, Puerto Rico; and || University of Arizona College of Medicine, Tucson, Arizona

Address correspondence to: Dr. David B. Van Wyck, Kidney Health Institute LLC, 6720 N. Nanini Drive, Tucson, AZ 85704-6128. Phone: 520-906-8262; Fax: 520-498-5027; E-mail: dvanwyck{at}sprynet.com

Although iron therapy is essential to optimize use of erythropoiesis-stimulating agents (ESA), randomized, controlled trials have heretofore been unavailable to evaluate reliably the efficacy of intravenous iron as an adjuvant to ESA treatment in peritoneal dialysis (PD) patients. In a multicenter trial, patients who had anemia, PD-dependent chronic kidney disease, stable ESA therapy, and a broad range of iron status (ferritin ≤500 ng/ml, transferrin saturation ≤25%) were randomly assigned to receive either 1 g of iron sucrose intravenously in three divided doses (300 mg over 1.5 h on days 1 and 15, 400 mg over 2.5 h on day 29) or no supplemental iron. No serious adverse drug events occurred after intravenous iron administration. The primary end point, peak hemoglobin increase, was higher (1.3 ± 1.1 versus 0.7 ± 1.1, mean ± SD; P = 0.0028), and anemia intervention (transfusion, increase in ESA dose, or intravenous iron therapy not called for in protocol) occurred later (P = 0.0137) and less often in intravenous iron–treated patients compared with untreated control subjects (one of 66 [1.3%] versus five of 30 [16.7%]). Among patients who did not require intervention, iron-treated patients showed a calculated net ESA dose decrease compared with untreated control subjects. Baseline iron status did not predict responsiveness to intravenous iron therapy. Intravenous iron sucrose is an effective adjunct to ESA therapy in anemic patients with PD-dependent chronic kidney disease and is administered safely as 300 mg over 1.5 h or 400 mg over 2.5 h. Evidence of iron deficiency at baseline is not required to demonstrate intravenous iron efficacy.


Related Article

Intravenous Iron Therapy in Peritoneal Dialysis Patients: Short-Term Efficacy and Long-Term Issues
Richard A. Zager
Clin. J. Am. Soc. Nephrol. 2006 1: 353-355. [Full Text] [PDF]






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