Iron Balance and the Role of Hepcidin in Chronic Kidney Disease.
Iron Balance and the Role of Hepcidin in Chronic Kidney Disease.
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DOI：
10.1016/j.semnephrol.2016.02.001
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发表时间：
2016-03
影响因子：
3.3
通讯作者：
Nemeth E
中科院分区：
文献类型：
--
作者：
Ganz T;Nemeth E
肝脏铁调节激素肝蛋白及其受体，细胞铁出口剂铁托蛋白构成了一种反馈调节的机制，该机制保持了促红细胞生成的铁转化蛋白的血浆浓度和其他功能，并确保了足够的铁储存，并避免了足够的铁毒性和铁依赖性铁依赖性铁依赖性的铁含量。在慢性肾脏疾病中，炎症和肾脏清除受损会增加血浆肝素的血浆，抑制巨噬细胞中的十二指肠铁吸收和隔离铁。肝素的这些作用会导致全身性铁缺乏症，促进促红细胞生成的铁的可用性以及对内源性和外源性促红细胞生成素的耐药性。加上促红细胞生成素的肾脏产生，肝素介导的铁限制有助于慢性肾脏疾病的贫血。
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.