Association of Serum Visfatin Levels with Coronary Artery Disease and Biochemical Parameters in Patients Undergoing Maintenance Hemodialysis

Background: Cardiovascular disease is a major cause of morbidity and mortality in patients with end-stage kidney disease receiving maintenance hemodialysis. Visfatin is a pro-inflammatory adipokine involved in metabolic and inflammatory pathways; however, its relationship with established coronary artery disease (CAD) in hemodialysis patients remains uncertain. This study evaluated the associations of serum visfatin concentrations with hemodialysis status, clinically documented CAD, and selected metabolic and biochemical parameters. Methods: This cross-sectional study included 130 non-diabetic adults classified into four groups: healthy controls (n = 40), participants with preserved renal function and established CAD (n = 28), maintenance hemodialysis patients without CAD (n = 30), and maintenance hemodialysis patients with established CAD (n = 32). Demographic, anthropometric, and laboratory variables were recorded. Serum visfatin concentrations were measured using an enzyme-linked immunosorbent assay. Between-group comparisons and exploratory correlation analyses were performed. Analysis of covariance was additionally used to assess between-group differences in visfatin after adjustment for age, sex, hypertension, and BMI, with body fat percentage substituted for BMI in a sensitivity analysis. Results: Median serum visfatin concentration was higher in the pooled hemodialysis groups than in the pooled non-hemodialysis groups (35.75 vs. 30.51 ng/mL, p = 0.014). In unadjusted pairwise comparisons, healthy controls had lower visfatin concentrations than participants with preserved renal function and CAD (p = 0.007), hemodialysis patients without CAD (p = 0.001), and hemodialysis patients with CAD (p = 0.004). However, visfatin concentrations did not differ between hemodialysis patients with and without established CAD (p = 0.972). After adjustment for age, sex, hypertension, and BMI, the overall between-group effect was no longer statistically significant (F(3, 122)= 2.054, p = 0.110, partial η2 = 0.048). The result was similar in the sensitivity analysis replacing BMI with body fat percentage (p = 0.060). In exploratory analyses of the pooled hemodialysis population, visfatin was positively correlated with fasting insulin (r = 0.269, p = 0.039), HOMA-IR (r = 0.277, p = 0.033), and serum uric acid (r = 0.263, p = 0.039). Conclusions: Higher serum visfatin concentrations were observed in patients receiving maintenance hemodialysis in unadjusted analyses, but the overall between-group difference was attenuated after adjustment for demographic and body-composition variables. Visfatin did not distinguish hemodialysis patients according to established CAD status. These findings do not demonstrate an independent association of circulating visfatin with either hemodialysis status or clinically documented CAD. Given the cross-sectional design and exploratory nature of the correlation analyses, further prospective studies with larger samples and standardized assessment of coronary disease burden are warranted.