title: Serum hepcidin levels are associated with serum triglycerides and interleukin-6 concentrations in patients with end-stage renal disease.
abstract: Hepcidin has emerged as a peptide with a key role in the regulation of iron homeostasis in patients with chronic kidney disease (CKD), having a strong dependence on inflammation. Recent studies reveal that hepcidin may be also associated with the progression of atherosclerosis. This study was performed to analyze the relation of hepcidin to markers of atherosclerosis and inflammation in patients on dialysis. A total of 90 individuals were enrolled. Sixty patients with end-stage renal disease, who were on hemodialysis (HD) (N = 30) and peritoneal dialysis (N = 30) were compared with 30 normal controls (NC). Age, body mass index, time on dialysis, serum lipids, C-reactive protein (CRP) and interleukin-6 (IL-6) were measured and analyzed in correlation with hepcidin concentration. It was found that patients on HD and peritoneal dialysis have significantly higher (P < 0.0001) levels of hepcidin, CRP and IL-6 than NC. Hepcidin in dialysis patients is significantly related to age (r = 0.373, P = 0.012), serum triglycerides (r = 0.401, P = 0.005), HDL-C (r = -0.268, P = 0.048), CRP (r = 0.436, P = 0.0007) and IL-6 (r = 0.569, P < 0.0001). In multiple regression analysis, hepcidin correlated independently with triglycerides (β = 0.402, P = 0.041) and IL-6 (β = 0.559, P = 0.006). Moreover, patients with high triglycerides in combination with high IL-6 levels have significantly increased concentrations of hepcidin than those with low triglycerides and low IL-6 levels (P < 0.0001). Elevated levels of hepcidin in patients with CKD on dialysis may be related to the occurrence of high triglycerides and high IL-6 serum concentrations. This probably suggests that hepcidin may play a role to the progression of atherosclerosis and inflammation, but this hypothesis should be further evaluated.
authors.affiliation: Biochemical Department, "Alexandra" General Hospital, Athens, Greece.
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Samouilidou
authors.forename: Konstantinos
authors.initials: K
authors.lastname: Pantelias
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Petras
authors.forename: George
authors.initials: G
authors.lastname: Tsirpanlis
authors.forename: Joulia
authors.initials: J
authors.lastname: Bakirtzi
authors.forename: George
authors.initials: G
authors.lastname: Chatzivasileiou
authors.forename: Helen
authors.initials: H
authors.lastname: Tzanatos
authors.forename: Eirini
authors.initials: E
authors.lastname: Grapsa
mesh_terms: D000328:Adult; D000367:Age Factors; D000368:Aged; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D064451:Hepcidins / Q000097:blood*; D006801:Humans; D015850:Interleukin-6 / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010530:Peritoneal Dialysis / Q000379:methods; D012044:Regression Analysis; D006435:Renal Dialysis / Q000379:methods; D051436:Renal Insufficiency, Chronic / Q000628:therapy*; D014280:Triglycerides / Q000097:blood*
chemical_list: D064451:Hepcidins; D015850:Interleukin-6; D014280:Triglycerides; D002097:C-Reactive Protein
keywords: Atherosclerosis; Hemodialysis; Hepcidin; Inflammation; Peritoneal dialysis