Topchii Ivan I, Kirienko Alexander N, Kirienko Denis A, Yakovtsova Iryna I, Gavriluk Alla A, Danyliuk Svitlana V, Ivakhno Igor V, Tovazhnianska Vira D
Government Institution "L.T. Malaya Therapy National Institute of the National Academy of Medical Sciences of Ukraine", Kharkiv, Ukraine.
State Institution "Zaycev V.T.Institute of General And Urgent Surgery of Nams of Ukraine" , Kharkiv, Ukraine.
Wiad Lek. 2019;72(7):1269-1273.
Introduction: Vascular endothelium function interruption has the main role among mechanisms of development and progression of chronic kidney disease. In numerous experimental and clinical studies, it was proved that activated vascular endothelium is a structural and functional unit that matches processes of inflammation with intravascular coagulation, fibrinolysis and haemorheological disorders. The aim: To identify special features of endothelium morphological structure in kidney vessels, coronary arteries and aorta during chronic kidney disease.
Materials and methods: Based on autopsy materials, we conducted a morphological study of patients (n = 20) aged 45 to 55 years who were observed in cardiac and neurological hospitals for 5-7 years. We removed kidney, heart and aorta samples from patients. For the study, a histological and immunohistochemical methods were used.
Results and conclusions: Morphological study of vessels endothelium of kidneys, heart and aorta demonstrated that in the majority of observations intima underwentprofound pathological changes, manifested by different degrees of disorganization of endothelial lining and violations of structural and functional organization of the endotheliocytes, subendothelial layer, basal membrane. These pathological processes in all cases had similar features with the development of immune inflammation. Inflammatory infiltration was represented by macrophages, mast cells, plasma cells. Biological mediators of the presented cells can aggravate the damage to endothelial cells. Indirect signs of low ability to restore the structure of the vessel wall and endothelial lining may be a weak expression of the VEGF and bcl-2 vascular endothelial growth factor.
