ACTIVITY OF CHRONIC INFLAMMATION AND ENDOTHELIAL DAMAGE IN PATIENTS WITH CARDIAC VALVE CALCIFICATION IN DIALYSIS–DEPENDENT CHRONIC KIDNEY DISEASE

The purpose of the research was to identify the role of chronic inflammation in mechanisms of cardiac valve calcification (CVC) in patients undergoing chronic hemodialysis (HD) by determining the relation of inflammatory markers with valve calcification and the correlation of the latter with endothelial damage indices. Methods. The research included 94patients undergoing chronic HD (males, 52, age, (46,4±11,2) years, duration of HD, (28,9±32,4) months). Patients with chronic glomerulonephritis (47,9 %) dominated. All subjects underwent echo– cardiographic examination for detection of CVC. The intensity of the inflammatory process was estimated by the serum content of fibrinogen (FG), amount of circulatory immune complexes (CICs), concentration of C–reactive protein (CRP) and middle molecules (MM). The nitric oxide (NO) production was studied on the plasma content of nitrite–anions (NO2–) by spectrophotometric method, the amount of circulating endothelial cells (CECs) in platelet rich plasma under the method (Hladovec J. et al., 1978), modified by (Susla A.B., Mysula I.R., 2011). Results. The CRP, FG, CICs indices in patients with CVC exceeded in those without the calcification by 44,2 (р=0,009), 18,4 (р<0,001) and 17,2 % (р=0,002) accordingly. The dynamic of the MM with wave length of 254 nm (MM/254) and 280 nm (MM/280) had identical direction. For the first time a group of patients with CVC (n=42) had been identified with correlations between CECs and CRP indices (Rs=0,42, р=0,006), FG (Rs=0,31, р=0,043), CICs (Rs=0,55, р<0,001), MM/254 (Rs=0,36, р=0,018), MM/280 (Rs=0,42, р=0,005) as well as between the values of NO2– and CRP (Rs=–0,55, р<0,001), FG (Rs=–0,41, р=0,007), CICs (Rs=–0,41, р=0,008), MM/254 (Rs=–0,38, р=0,014), MM/280 (Rs=–0,34, р=0,029). Conclusions. The valve calcification in HD patients combines with the activation of chronic inflammation, which manifests itself in accumulation of CRP, FG, CICs and MM, and the inflammation markers tightly correlate with endothelial damage and lack of NO