铁平衡与铁调素在慢性肾脏病中的作用
Iron Balance and the Role of Hepcidin in Chronic Kidney Disease.
作者信息
Ganz Tomas, Nemeth Elizabeta
机构信息
Department of Medicine, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, CA.
Department of Medicine, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, CA.
出版信息
Semin Nephrol. 2016 Mar;36(2):87-93. doi: 10.1016/j.semnephrol.2016.02.001.
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.
肝脏铁调节激素铁调素及其受体——细胞铁输出蛋白铁转运蛋白，构成了一种反馈调节机制，该机制维持足够的血浆铁转铁蛋白浓度以支持红细胞生成及其他功能，确保充足的铁储备，并避免铁毒性和铁依赖性微生物致病。在慢性肾脏病中，炎症和肾脏清除功能受损会使血浆铁调素增加，抑制十二指肠铁吸收并将铁隔离在巨噬细胞中。铁调素的这些作用可导致全身性缺铁、红细胞生成可用铁减少以及对内源性和外源性促红细胞生成素产生抵抗。与肾脏促红细胞生成素生成受损一起，铁调素介导的铁限制导致了慢性肾脏病贫血。
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