Serum Hepcidin as a Biomarker of Subclinical Atherosclerosis in Peritoneal Dialysis: A Cross-Sectional Study

Background: Cardiovascular disease (CVD) is the leading cause of mortality in peritoneal dialysis (PD) patients, with traditional risk factors failing to fully explain the accelerated atherosclerosis observed in this group. Hepcidin, a major regulator of iron metabolism and inflammation, has emerged as a potential contributor to vascular remodeling. Methods: We conducted a cross-sectional study of 82 PD patients to assess the relationship between serum hepcidin levels and carotid intima-media thickness (CIMT), a surrogate marker of subclinical atherosclerosis. Clinical, biochemical, and dialysis-related data were collected. Patients were stratified into tertiles by hepcidin levels, and correlation, regression, and ROC analyses were performed. Results: Serum hepcidin levels showed a strong positive correlation with CIMT (ρ = 0.788, p < 0.001). In multivariate linear regression, hepcidin (β = 0.0057, p = 0.012) and dialysis duration (β = 0.0018, p = 0.015) remained independent predictors of CIMT. ROC analysis demonstrated excellent discriminative ability of hepcidin for elevated CIMT (AUC = 0.922), which improved further with the inclusion of dialysis duration (AUC = 0.952). Conclusions: Serum hepcidin is a strong, independent predictor of subclinical atherosclerosis in PD patients. These findings suggest that iron dysregulation and inflammation may play a more prominent role than traditional cardiovascular risk factors in this population. Hepcidin may serve as a valuable biomarker for early vascular risk stratification and a potential therapeutic target.