Iron Balance and the Role of Hepcidin in Chronic Kidney Disease

被引:122
作者
Ganz, Tomas [1 ]
Nemeth, Elizabeta [1 ]
机构
[1] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, CHS 37-055, Los Angeles, CA 90095 USA
基金
美国国家卫生研究院;
关键词
Anemia; inflammation; iron deficiency; renal failure; REGULATED EIF2-ALPHA KINASE; SERUM HEPCIDIN; MAINTENANCE HEMODIALYSIS; MAMMALIAN IRON; ANEMIA; FERROPORTIN; HOMEOSTASIS; DEFICIENCY; CKD; ERYTHROPOIESIS;
D O I
10.1016/j.semnephrol.2016.02.001
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:87 / 93
页数:7
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