Trends and dynamics of changes in calcification score over the 1-year observation period in patients on peritoneal dialysis.

Background: Accelerated vascular calcification is an important cause of excess mortality in patients on dialysis therapy. The aim of the study was to evaluate the trends in coronary artery calcification (CAC) score (CaSc) during a 1-year period in a group of stable peritoneal dialysis (PD) patients and identify factors that may be associated with CaSc changes.
Methods: Sixty-one stable patients (28 women, 33 men) on PD therapy with a mean age of 50.4 +/- 13.6 years were included. Forty-seven patients survived the entire study period on PD therapy and were suitable for the final analysis. CaSc was assessed at baseline and after 12 months by using multislice spiral computed tomography. Proinflammatory cytokines (interleukin-6, tumor necrosis factor-alpha [TNF-alpha]), acute-phase proteins (C-reactive protein [CRP], fibrinogen), calcium-phosphate balance, and lipid profile were assessed at baseline and after 6 and 12 months.
Results: Median CaSc was 22.6 Agatston units (range, 0 to 5,502.8 Agatston units) at baseline and increased to 84 Agatston units (range, 0 to 5,001.3 Agatston units) at a 1-year follow-up (P < 0.05). In the entire group of patients, 3 subgroups were identified: patients with progression (n = 21; P = 0.02 for the difference between initial versus follow-up CaSc), patients with regression (n = 12; P = 0.05), and subjects without change in CaSc after 1 year (n = 14). Patients without progression showed no calcifications at baseline and follow-up and were younger, less overweight, and characterized by significantly lower mean TNF-alpha, leptin, and CRP levels during 1 year compared with both progressors and regressors. Mean serum phosphate and calcium x phosphate product (Ca x P) values were gradually increasing from regressors through the no-calcification group to progressors (P < 0.01 for phosphate levels, P < 0.02 for Ca x P product). Significant correlations were found between changes in CaScs and mean values for phosphate (R = 0.44; P < 0.0005) and Ca x P product (R = 0.38; P < 0.005).
Conclusion: Chronic nonspecific inflammation does not directly attribute to progression in CaScs. Calcium-phosphate balance abnormalities appear to be the only important factors promoting CAC, although a permissive or promoting role of inflammation cannot be ruled out.