Is hepcidin‐25 a predictor of atherosclerosis in hemodialysis patients?

Abstract

Atherosclerotic cardiovascular disease is an important cause of mortality and morbidity in hemodialysis patients. Iron accumulation in arterial wall macrophages is increased in atherosclerotic lesions. Hepcidin is a key hepatic hormone regulating iron balance. It inhibits iron release from macrophages and iron absorption from enterocytes by binding and inactivating the cellular iron exporter ferroportin. The aim of this study is to investigate the relation of hepcidin-25, iron parameters, and atherosclerosis measured by carotid intima media thickness (CIMT) in hemodialysis patients. Eighty-two hemodialysis patients were enrolled in this cross-sectional study. Predialysis blood samples were centrifuged at 1500 g and 4°C for 10 minutes and stored at -80°C for the measurement of hepcidin-25. DRG hepcidin enzyme-linked immunosorbent assay kit was used for the measurement of hepcidin-25. Ultrasonographical B-mode imaging of bilateral carotid arteries was performed with a high-resolution real-time ultrasonography (Mindray DC7). Mean age of the study population was 57.90 ± 16.08 years and 43.9% were men. Total study population was grouped into two according to median value of hepcidin-25. There was no difference between groups with respect to age, dialysis vintage, and C-reactive protein. CIMT was found to be statistically significantly higher in low hepcidin-25 group. In correlation analysis, CIMT was found to be correlated with age (P < 0.01, R = 0.33) and hepcidin-25 (P < 0.01, R = 0.46). In linear regression analysis, age (β = 0.31) and hepcidin-25 (β = 0.44) were found to be the determinants of CIMT in hemodialysis patients. Our results implicate that hepcidin may take part in pathophysiology of atherosclerosis and cardiovascular disease in hemodialysis patients.