Proteinuria Induced by Parenteral Iron in Chronic Kidney... : Clinical Journal of the American Society of Nephrology (original) (raw)

Original Articles: Original Articles

Proteinuria Induced by Parenteral Iron in Chronic Kidney Disease—A Comparative Randomized Controlled Trial

Agarwal, Rajiv*,†; Leehey, David J.‡,§; Olsen, Scott M.‖; Dahl, Naomi V.‖

*Division of Nephrology, Department of Medicine, Indiana University School of Medicine, and

†Richard L. Roudebush VA Medical Center, Indianapolis, Indiana;

‡Division of Nephrology, Department of Medicine, Loyola University Stritch School of Medicine, Maywood, Illinois;

§Edward Hines Jr. VA Medical Center, Hines, Illinois; and

‖Watson Laboratories, Inc., Morristown, New Jersey

Correspondence: Dr. Rajiv Agarwal, VA Medical Center, 111N, 1481 West 10th Street, Indianapolis, IN 46202. Phone: 317-554-0000, ext. 82241; Fax: 317-988-2171; E-mail: [email protected]

Received July 12, 2010

Accepted August 25, 2010

Abstract

Background and objectives

Among patients with chronic kidney disease (CKD), differences in proteinuria are seen between intravenous iron preparations after a single dose exposure. This study examined differences in proteinuria between two intravenous iron preparations after multiple doses.

Design, setting, participants, & measurements

Patients with iron-deficiency anemia and CKD, stratified by angiotensin converting enzyme inhibitor (ACEI)/angiotensin receptor-blocker (ARB) use, were randomized to iron sucrose or ferric gluconate. Each patient at 12 centers received 100 mg of study drug weekly for 5 weeks. Urine protein/urine creatinine ratio was measured before each dose and frequently thereafter for 3 hours.

Results

Postbaseline data were available from 33 patients receiving iron sucrose and 29 patients receiving ferric gluconate. Although neither preparation of intravenous iron increased the predose level of proteinuria, the proteinuric response to intravenous iron was dependent on the type of iron and ACEI/ARB use. Without ACEIs/ARBs, ferric gluconate tended to cause less proteinuria with repeated iron administration; iron sucrose did not mitigate or aggravate proteinuria. Among patients receiving ACEIs/ARBs, in contrast to ferric gluconate, which produced only mild transient proteinuria, iron sucrose produced a consistent and persistent proteinuric response that was on average 78% greater.

Conclusions

Although multiple doses of either intravenous iron did not increase basal levels of proteinuria, postdose proteinuria was greater with iron sucrose than with ferric gluconate. These data suggest that nephrotoxicity of iron may depend on type of intravenous iron and on ACEI/ARB use. The long-term effects on kidney function need to be further evaluated.