An association between coronary artery calcification score, lipid profile, and selected markers of chronic inflammation in ESRD patients treated with peritoneal dialysis

Abstract

Background: Chronic uremia is considered a proinflammatory state associated with high cardiovascular morbidity and mortality. The aim of the present study is to evaluate the potential relationship between the prevalence of coronary artery calcification (CAC) and selected factors that may be involved in the process of atherogenesis (lipid profile, acute-phase reactants, growth factors, and cytokines).

Methods: The study group consisted of 43 patients (19 women, 24 men) with a mean age of 50.6 +/- 13.4 years treated with peritoneal dialysis (PD) for a median period of 15 months (range, 2 to 96 months). Only patients with sinus rhythm were included. CAC score (CaSc) was measured using multirow spiral computed tomography (MSCT). As parameters of lipid profile, total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, and triglycerides were assayed. C-reactive protein (CRP) and fibrinogen represented the level of acute-phase activation. Proinflammatory cytokines (interleukin-6 [IL-6] and tumor necrosis factor-alpha [TNF-alpha]), leptin, and basic fibroblast growth factor (bFGF) also were measured.

Results: Median CaSc equaled 17.9 Agatston units (range, 0 to 5,502 Agatston units). No calcification was detected in 20 subjects (46.5%; CaSc < 10 Agatston units). CaSc correlated with age (R = 0.57; P < 0.0001), body mass index (R = 0.42; P < 0.005), and serum leptin (R = 0.3; P < 0.05) and CRP levels (R = 0.38; P < 0.05). The correlation with PD therapy duration was borderline statistically significant (P = 0.063). Patients with the greatest values for CaSc (> 400 Agatston units) were characterized by significantly greater levels of IL-6, bFGF, and CRP compared with subjects with a CaSc less than 10 Agatston units (P < 0.05 for all). Patients with history of coronary artery disease (CAD) had significantly greater CaSc values (median, 778.6 versus 3.3 Agatston units; P < 0.001) compared with those without CAD. Serum triglyceride levels were significantly greater and HDL cholesterol levels were significantly lower in patients with CAD. The first group also was characterized by significantly greater serum TNF-alpha (P < 0.01) and CRP levels (P < 0.005). In multiple regression analysis, only age was independently associated with CaSc (beta = 0.45; P = 0.002).

Conclusion: Our results may suggest an association between CAC and chronic inflammation activity in the mentioned group of patients. To our knowledge, this is the first study reporting the prevalence of CAC in PD patients using the MSCT method. The association between CaSc results and classic, as well as inflammatory, risk factors for CAD found in this study should be interpreted with caution because of its method limitations (cross-sectional design, heterogeneity of study population, and small number of studied patients).