ENDOTHELIAL DYSFUNCTION IN PROGRAM HEMODIALYSIS-DEPENDENT PATIENTS

Background. The problem of treatment of patients with the end stage of chronic renal failure stems from a constantly growing number of patients needing program hemodialysis, and a high rate of complications related with functioning of the permanent vascular access. At present no ideal vascular access for hemodialysis exists. The main reasons leading to stoppage of its functioning and to the necessity of repeated surgeries is development of stenosis of arteriovenous anastomoses and of fistula veins. Endothelial dysfunction is considered to be one of the important factors in development of restenosis of the reconstruction zone. Aim. The level of markers of the endothelial dysfunction in patients with chronic kidney disease receiving program hemodialysis. Materials and Methods. The study included 12 patients diagnosed as having chronic kidney disease as a consequence of glomerulonephritis, who received program hemodialysis 4 hours a day 3 times a week. The average time of taking dialysis was 5 years. Vascular access in all patients was implemented through a native arteriovenous fistula. Blood sampling was performed before and after dialysis. The following biochemical parameters were used as markers of endothelial function: nitric oxide metabolites (II) (NO), malondialdehyde (MDA) and superoxide dismutase (SOD). Results. In the course of work a statistically significant increase in the SOD activity was found in the patients after dialysis (p=0.010863) from 49.02 [40.35; 54.17] rel.un/ml to 83.33 [66.67; 141.67] rel.un/ml. Concentration of MDA (p=0.015157) increased from 3.5 [2.38; 4.04] μmol/l to 4.18 [2.73; 5.58] μmol/l. Dynamics of the content of NO metabolites in blood plasma was statistically insignificant (р=0.953) and varied from 57.48 [56.3; 72.73] μmol/l to 61.78 [53.57; 69.6] μmol/l. Conclusions. In hemodialysis increase in the level of MDA and SOD of blood plasma was noted that can be characterized as development of endothelial dysfunction. Development of endothelial dysfunction may promote hyperproliferation of smooth muscle cells and may lead to restenosis of arteriovenous fistula and to thrombosis.