Understanding and exploiting hepcidin as an indicator of anemia due to chronic kidney disease

Derek S. Larson, Daniel W. Coyne

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


Hepcidin, produced by the liver, is the master regulator of iron balance. Serum hepcidin is increased by high iron stores, blocks intestinal iron absorption, and impairs storage iron release. Conversely, iron deficiency lowers hepcidin levels and enhances intestinal iron absorption and the release of storage iron. As with ferritin, hepcidin is an acute phase reactant. Consequently, inflammation increases hepcidin and leads to impaired iron absorption, lowers serum iron and transferrin saturation, and contributes to the anemia of chronic kidney disease (CKD). We review the physiology of iron absorption, its relationship to hepcidin and the transmembrane iron transporter ferroportin, the role of hepcidin in CKD related anemia, and the possible diagnostic implications and limitations of using hepcidin as a marker of iron status.

Original languageEnglish
Pages (from-to)11-15
Number of pages5
JournalKidney Research and Clinical Practice
Issue number1
StatePublished - Mar 2013


  • Anemia
  • Chronic kidney disease
  • Hepcidin
  • Iron


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