The correlation between hepcidin levels and iron parameters in patients with end-stage renal disease on regular hemodialysis successfully treated from hepatitis C virus by directly acting antiretrovirals

Background Hepcidin is a polypeptide secreted from the liver. It regulates iron metabolism by blocking further iron absorption when iron stores are high. Hepcidin levels are usually higher than the normal range in hemodialysis (HD) patients. Hepatitis C virus (HCV) infection leads to lowering of hepcidin levels, leading to more iron overload. The objectives were to determine whether there is a correlation between iron stores and hepcidin levels in HD patients after HCV treatment and to assess the level of hepcidin in those patients who were treated from HCV compared with those who have chronic HCV infection. Patients and methods In total, 60 patients on regular HD were recruited and 30 healthy controls . Group I: 30 patients who have been successfully treated from HCV by directly acting antiretroviral drugs with a persistently negative PCR for at least 3 months, group II: 30 patients with chronic HCV infection, and 30 healthy controls form group III. Serum hepcidin levels, iron profile, and complete blood count were compared in all groups. Results Hepcidin levels were significantly higher in the HCV-treated group versus the HCV-infected group (mean 226.77±144.13 and 87.77±40.77 ng/dl), respectively, significantly higher transferrin-binding capacity (TIBC), and mean levels 410.5±74.65 and 310.93±122.57 μg/dl . Ferritin levels were higher in the HCV-infected group (355.13±196, 899.5±1522 ng/dl) than in HCV-treated. There was a significant correlation between hepcidin and serum iron, TIBC, and transferrin saturation in the HCV-treated group. On regression analysis, only TIBC and transferrin saturation correlated significantly. Conclusions Post HCV treatment with directly acting antiretroviral drugs, hepcidin levels are higher than during HCV-infection state and correlate significantly to higher TIBC . Further studies are needed to establish the effect of iron supplementation on hepcidin level in this subgroup of patients.