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Hepcidin excess is not the mechanism for impaired iron absorption in chronic kidney disease

Hepcidin (HC) excess has been suggested to be contributing to anemia in chronic kidney disease (CKD). High levels of HC could impair iron (Fe) absorption from diet and Fe mobilization from stores. Blocking HC could improve Fe availability. Three patients with hereditary hemochromatosis (HMC) developed end‐stage renal disease (ESRD). In all mutation of the gene encoding HMC protein HFE was present. All developed Fe deficiency anemia requiring i.v. Fe to maintain Hgb within K‐DOQI standard. These findings suggest that absence of HC does not improve Fe availability in ESRD. Thus HC excess is not the likely mechanism of impaired Fe absorption in ESRD.