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Semin Nephrol. 2016 Mar;36(2):87-93. doi: 10.1016/j.semnephrol.2016.02.001.

Iron Balance and the Role of Hepcidin in Chronic Kidney Disease.

Author information

1
Department of Medicine, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, CA. Electronic address: tganz@mednet.ucla.edu.
2
Department of Medicine, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, CA.

Abstract

The hepatic iron-regulatory hormone hepcidin and its receptor, the cellular iron exporter ferroportin, constitute a feedback-regulated mechanism that maintains adequate plasma concentrations of iron-transferrin for erythropoiesis and other functions, ensures sufficient iron stores, and avoids iron toxicity and iron-dependent microbial pathogenesis. In chronic kidney disease, inflammation and impaired renal clearance increase plasma hepcidin, inhibiting duodenal iron absorption and sequestering iron in macrophages. These effects of hepcidin can cause systemic iron deficiency, decreased availability of iron for erythropoiesis, and resistance to endogenous and exogenous erythropoietin. Together with impaired renal production of erythropoietin, hepcidin-mediated iron restriction contributes to anemia of chronic kidney disease.

KEYWORDS:

Anemia; inflammation; iron deficiency; renal failure

PMID:
27236128
PMCID:
PMC4884601
[Available on 2017-03-01]
DOI:
10.1016/j.semnephrol.2016.02.001
[Indexed for MEDLINE]
Free PMC Article

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