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International Journal of Nephrology
Volume 2012, Article ID 239476, 7 pages
http://dx.doi.org/10.1155/2012/239476
Clinical Study

Serum Hepcidin Levels and Reticulocyte Hemoglobin Concentrations as Indicators of the Iron Status of Peritoneal Dialysis Patients

1Department of Medicine IV, Tokyo Women's Medical University, Kawada-cho 8-1, Shinjuku, Tokyo 162-8666, Japan
2Department of Nephrology, Kameda Medical Center, Higashi-machi 929, Kamogawa, Chiba 296-8602, Japan
3Immunology & Chemistry Product Engineering, ICH Business Unit, Sysmex Corporation, Wakihama, Kaigandori 1-5-1, Chuou-ku, Koube, Hyogo 651-0073, Japan
4Clinical Development, Technology Development, Sysmex Corporation, Wakihama, Kaigandori 1-5-1, Chuou-ku, Koube, Hyogo 651-0073, Japan

Received 24 July 2012; Accepted 27 September 2012

Academic Editor: Kook-Hwan Oh

Copyright © 2012 Aya Eguchi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Hepcidin is the key mediator of renal anemia, and reliable measurement of serum hepcidin levels has been made possible by the ProteinChip system. We therefore investigated the iron status and serum hepcidin levels of peritoneal dialysis (PD) patients who had not received frequent doses of an erythrocytosis-stimulating agent (ESA) and had not received iron therapy. In addition to the usual iron parameters, the iron status of erythrocytes can be determined by measuring reticulocyte hemoglobin (RET-He). The mean serum hepcidin level of the PD patients was 80.7 ng/mL. Their serum hepcidin levels were significantly positively correlated with their serum ferritin levels and transferrin saturation (TSAT) levels, but no correlations were found between their serum hepcidin levels and RET-He levels, thereby suggesting that hepcidin has no effect on the iron dynamics of reticulocytes. Since low serum levels of CRP and IL-6, biomarkers of inflammation, were not correlated with the serum hepcidin levels, there is likely to be a threshold for induction of hepcidin expression by inflammation.