Is there a link between Hepcidin, inflamation and atherosclerosis in patients with chronic kidney disease

Abstract

Objective: The major cause of death and morbidity in chronic kidney disease (CKD) patients is atherosclerotic cardiovascular disease. Iron build-up is enhanced in atherosclerotic lesions in arterial macrophages. The inhibition of hepcidin by binding and inactivating the iron export cell iron ferroportine from macrophages and iron absorption from Enterocytes. In this study, the relationship between hepcidin-25 serum and subclinical atherosclerosis is clarified in CKD patients.

Methods: 40 non hemodialysis CKD (non HD-CKD) and 40 hemodialysis CKD (HD-CKD) patients were registered in this study in adding to 20 subjects as a control group. In HD-CKD patients, the sample was collected at start of hemodialysis session after overnight fast. In non HD-CKD patients and the controls, the venous blood sample was also collected from a peripheral vein after overnight fast. These samples were centrifuged for 15 minutes at approximately 3000 rpm and stored at -70°C for the measurement of serum levels of hepcidin-25, TNF-α, IL-6, hs-CRP, ferritin, iron, and total iron binding capacity.

Results: In the non HD-CKD and HD-CKD groups compared to checks (P < 0.001 for each group) hepcidin-25 serum has been considerably elevated. In contrast to the non-HD-CKD group (P = 0.005) it was considerably elevated in HD-CKD groups. In non-HD-CKD, compared to control group (P = 0.002), CIMT has been considerably raised. In HD-CKD, compared with the control group (P = 0,001), it was also considerably elevated. In non HD-CKD and HD-CKD groups serum levels were raised substantially by hs-CRP (P<0,001 for each group), TNF-α (P<0,001, for each group,), and IL-6 (P <0,001 for each group) compared to the control group.

Conclusion: Our data suggest that in individuals with CKD hepcidin may be involved in cardiovascular disease and atherosclerotic pathogenesis.