Division of Nephrology and Dialysis, Department of Medicine III, Medical University of Vienna, Vienna, Austria.
Nephrol Dial Transplant. 2014 Jun;29(6):1141-4. doi: 10.1093/ndt/gft467. Epub 2013 Nov 27.
Persistent hepatitis C virus (HCV) infection is a major cause of chronic liver disease including fibrosis, cirrhosis and hepatocellular carcinoma (HCC). Chronic hepatitis C (CHC) is also a problem in patients with chronic kidney disease (CKD), particularly in those on haemodialysis. Excessive iron in the liver of CHC patients contributes to hepatic fibrosis, cirrhosis and finally HCC, while iron depletion is beneficial. In CHC patients without CKD, in HCV-infected experimental animals and in cell culture studies, serum hepcidin levels and/or cellular hepcidin expression are low and directly suppressed by HCV, radical oxygen species, growth factors and/or transcription factors. In contrast, antiviral therapy (e.g. with pegylated interferon-alpha combined with ribavirin) raises hepcidin levels and reduces iron overload in patients with CHC. Hepcidin directly inhibits HCV replication mediated by STAT3 activation. HCV circumvents hepatic innate antiviral defence by lowering hepcidin. If hepcidin is also low in CKD patients with CHC, iron supplementation should be avoided even in CKD patients with CHC treated with erythropoiesis-stimulating agents.
持续性丙型肝炎病毒 (HCV) 感染是慢性肝病的主要病因，包括纤维化、肝硬化和肝细胞癌 (HCC)。慢性丙型肝炎 (CHC) 也是慢性肾脏病 (CKD) 患者的一个问题，特别是在血液透析患者中。CHC 患者肝脏中的铁过多会导致肝纤维化、肝硬化，最终导致 HCC，而铁耗竭则有益。在无 CKD 的 CHC 患者、HCV 感染的实验动物和细胞培养研究中，血清铁调素水平和/或细胞铁调素表达水平较低，并直接受到 HCV、活性氧、生长因子和/或转录因子的抑制。相比之下，抗病毒治疗（例如聚乙二醇干扰素-α联合利巴韦林）会提高 CHC 患者的铁调素水平并减少铁过载。铁调素通过激活 STAT3 直接抑制 HCV 复制。HCV 通过降低铁调素来规避肝脏固有抗病毒防御。如果 CKD 合并 CHC 患者的铁调素也较低，即使在接受促红细胞生成素刺激剂治疗的 CKD 合并 CHC 患者中，也应避免补充铁剂。
