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This Article Full Text Full Text (PDF) All Versions of this Article: CJN.05931108v1 4/6/1051    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by Zaritsky, J. Articles by Salusky, I. B. PubMed PubMed Citation Articles by Zaritsky, J. Articles by Salusky, I. B. Related Collections Related Article

Hepcidin—A Potential Novel Biomarker for Iron Status in Chronic Kidney Disease

Joshua Zaritsky^*, Brian Young, He-Jing Wang, Mark Westerman, Gordana Olbina, Elizabeta Nemeth, Tomas Ganz, Seth Rivera, Allen R. Nissenson, and Isidro B. Salusky^*

^* Department of Pediatrics, Department of Medicine, and Department of Biomathematics, David Geffen School of Medicine, University of California–Los Angeles, Los Angeles, California; and Intrinsic Life Sciences, La Jolla, California

Correspondence: Joshua Zaritsky, A2-383 MDCC, 650 Charles Young Drive, Los Angeles CA 90095. Phone: 310-206-6987; Fax: 310-825-0442; E-mail: jzaritsky{at}mednet.ucla.edu

Background and objectives: Hepcidin is a key regulator of iron homeostasis, but its study in the setting of chronic kidney disease (CKD) has been hampered by the lack of validated serum assays.

Design, setting, participants, & measurements: This study reports the first measurements of bioactive serum hepcidin using a novel competitive ELISA in 48 pediatric (PCKD2–4) and 32 adult (ACKD2–4) patients with stages 2 to 4 CKD along with 26 pediatric patients with stage 5 CKD (PCKD5D) on peritoneal dialysis.

Results: When compared with their respective controls (pediatric median = 25.3 ng/ml, adult = 72.9 ng/ml), hepcidin was significantly increased in PCKD2–4 (127.3 ng/ml), ACKD2–4 (269.9 ng/ml), and PCKD5D (652.4 ng/ml). Multivariate regression analysis was used to assess the relationship between hepcidin and indicators of anemia, iron status, inflammation, and renal function. In PCKD2–4 (R² = 0.57), only ferritin correlated with hepcidin. In ACKD2–4 (R² = 0.78), ferritin and soluble transferrin receptor were associated with hepcidin, whereas GFR was inversely correlated. In PCKD5D (R² = 0.52), percent iron saturation and ferritin were predictors of hepcidin. In a multivariate analysis that incorporated all three groups (R² = 0.6), hepcidin was predicted by ferritin, C-reactive protein, and whether the patient had stage 5D versus stages 2 to 4 CKD.

Conclusions: These findings suggest that increased hepcidin across the spectrum of CKD may contribute to abnormal iron regulation and erythropoiesis and may be a novel biomarker of iron status and erythropoietin resistance.

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Hepcidin Assays: Ironing Out Some Details

Jolanta Malyszko
Clin. J. Am. Soc. Nephrol. 2009 4: 1015-1016. [Full Text] [PDF]

This article has been cited by other articles:

				B. Young and J. Zaritsky Hepcidin for Clinicians Clin. J. Am. Soc. Nephrol., August 1, 2009; 4(8): 1384 - 1387. [Abstract] [Full Text] [PDF]

				J. Malyszko Hepcidin Assays: Ironing Out Some Details Clin. J. Am. Soc. Nephrol., June 1, 2009; 4(6): 1015 - 1016. [Full Text] [PDF]