Authors
Kalinin R.E., Suchkov I.A., Egorov A.A., Kamaev A.A.
Ryazan State Medical University, Ryazan
Abstract
Programmed hemodialysis is the primary method in the treatment of patients with terminal chronic kidney disease. Adequate vascular access is required for adequate hemodialysis. The lack of this access leads to serious complications during renal replacement therapy. One of the main reasons for the cessation of the functioning of permanent vascular access is its thrombosis. Objective of this study was to identify and evaluate markers of endothelial dysfunction and systemic inflammation in patients with thrombosis of permanent vascular access.
Methods. This study included 60 patients with arterio-venous fistulas. 30 patients with acute fistula thrombosis constituted the main group. The control group included 30 patients with a functioning access in the form of a native arterio-venous fistula for more than three years. Such indicators as intercellular adhesion molecules, selectin, superoxide dismutase, angiotensin, endothelin, etc. were studied.
Results. In the serum of patients with thrombosis, the total peroxide concentration increases as the level of oxistat increases significantly in this group compared with the control group (646.75 and 187.76 μmol / l, respectively). In patients with thrombosis, adhesion of lymphocytes, monocytes and eosinophils to activated endothelium occurs with their subsequent migration to the inflammatory focus, as evidenced by an increase in the concentration of intercellular adhesion molecules relative to the indicators of patients with working fistulas (842.65 and 382.35 ng / ml respectively).
Conclusion. A significant increase in the concentrations of all the studied markers in the serum of patients with acute thrombosis of permanent vascular access was detected compared with the control group. This fact suggests the development of endothelial dysfunction and systemic inflammation in patients with thrombosis.
Keywords: permanent vascular access, arterio-venous fistula, hemodialysis, endothelial dysfunction.
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