Prohepcidin, Inflammation and Iron Homeostasis in Hemodialysis Patients With Chronic Hepatitis C

Hepatitis C virus (HCV) infection is the most common cause of chronic liver disease in the world and also common among chronic hemodialysis (HD) patients. Patients with chronic HCV often have increased liver iron, a condition associated with reduced sustained response to antiviral therapy, more rapid progression to cirrhosis, and development of hepatocellular carcinoma; however, little is known about the mechanism of iron accumulation in the liver. Recently identified hepcidin, a 25-amino acid peptide hormone exclusively synthesized in the liver, is thought to be a key regulator for iron homeostasis and is induced by infection and inflammation. Hepcidin expression is modulated by iron stores, so that it decreases in iron deficiency to facilitate iron absorption while it increases in iron repletion to prevent pathological overload. Interleukin (IL)-6 has been proposed as a major inducer of hepcidin, via direct transcriptional activation of hepatic hepcidin expression by binding to its receptor complex containing gp130 to activate janus kinase (JAK) and activator of transcription 3 (STAT 3).

Inclusion criteria

• Chronic hemodialysis patients

Exclusion criteria

• Patients positive for hepatitis B virus surface antigen (HBsAg)
• Patients previously diagnosed nonrenal cause of anemia other than iron deficiency
• Patients with an evidence of active or occult bleeding
• Patients received blood transfusion within the past 4 months
• Patients with a history of malignancy, end-stage liver disease, or chronic hypoxia
• Patients with a history of recent hospitalization or infection requiring antibiotics within the past 4 weeks.