Nesen A. The pathogenic mechanisms and diagnostically-therapeutic strategy at combination of atherosclerosis and chronic kidney disease.

Dissertation work is devoted to the decision of problem modern therapy - to development the conception of synthropic cooperation of pathogenesis mechanisms which predetermine comorbidity of atherosclerosis and chronic kidney disease on the basis of visualization of atherosclerotic injuries, investigation of renal blood stream and tissue structure of kidney, determination of specific of oxidizations, fermentative, inflammatory mechanisms taking into account the state of the renin-angiotensin system and structural changes of endothelial and on this basis is developed the diagnostically-therapeutic strategy, directed by the correction of risk factors, associated with development and progress as to atherosclerosis so chronic kidney disease. The present research lead to that therapeutic strategy which are directed on the correction of arterial pressure, dyslipidaemia, to the renal blood flow, endothelial dysfunction, oxidizations, fermentative and immunoinflammatory processes can slow down the progress of comorbidity pathology, and development of newest methods of diagnostics and treatment, allow considerably to extend possibilities of primary and second prophylaxis of chronic kidney insufficiency and second prophylaxis of atherosclerosis. In first was offered and included in medical practice of recommendation from the therapeutic correction of violations of filtrations function of kidney and endothelial dysfunction, estimation of forming of structural violations of endothelial of vessels of kidney and efficiency of therapy on the basis of research of functional reserve of kidney, prophylaxis of cardio-vascular complications at comorbidity atherosclerosis and chronic kidney disease. The estimation of dynamics of indexes of peroxide oxidization of lipids, lipids spectrum of blood and amount of the lipid-containing leucocytes is conducted during the developed complex therapy and certainly influence of pharmacological blockade of angiotensin II on the secretion of interleukin's.