期刊
SEMINARS IN NEPHROLOGY
卷 36, 期 2, 页码 87-93出版社
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.semnephrol.2016.02.001
关键词
Anemia; inflammation; iron deficiency; renal failure
资金
- Will Rogers Fund
- National Institutes of Health [R01 DK 065029-11, R01 DK107309]
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. (C) 2016 Elsevier Inc. All rights reserved.
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