
Hepcidin‐25 Concentrations Are Markedly Increased in Patients With Chronic Kidney Disease and Are Inversely Correlated With Estimated Glomerular Filtration Rates
Author(s) -
Troutt Jason S.,
Butterfield Anthony M.,
Konrad Robert J.
Publication year - 2013
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.21634
Subject(s) - hepcidin , renal function , medicine , endocrinology , kidney disease , ferroportin , creatinine , ferritin , anemia , transferrin , hemoglobin , kidney , chemistry
Background Hepcidin‐25 regulates iron homeostasis by binding the iron transporter ferroportin, causing its degradation. Increased hepcidin‐25 causes decreased intestinal iron absorption and release from intracellular stores. Our objective in this study was to measure hepcidin‐25 levels in patients with chronic kidney disease (CKD) to determine if they might contribute to the anemia of CKD. Methods We used a hepcidin‐25‐specific enzyme‐linked immunosorbent assay to measure hepcidin‐25 in 103 CKD patients and 100 healthy individuals. We assessed in CKD subjects the correlation of hepcidin‐25 with creatinine, estimated glomerular filtration rate (eGFR), hemoglobin, blood urea nitrogen, serum iron, transferrin, and ferritin. Results Hepcidin‐25 concentrations in CKD patients were significantly increased compared to healthy subjects (60.4 ± 6.1 μg/l vs. 3.0 ± 0.5 μg/l, P < 0.001). Hepcidin‐25 concentrations were directly correlated with creatinine ( R = 0.28, P = 0.004) and inversely correlated with eGFR ( R = −0.32, P = 0.001). Hepcidin‐25 levels were also correlated with transferrin ( R = −0.28, P = 0.004) and ferritin ( R = 0.80, P < 0.001). Conclusion The direct correlation of hepcidin‐25 with creatinine and its inverse correlation with eGFR suggest that hepcidin‐25 levels increase as renal function deteriorates, possibly due to decreased hepcidin‐25 renal clearance.