UREMIC ENCEPHALOPATHY: MAIN FACTORS CONTRIBUTING TO ITS OCCURRENCE

The review is devoted to the pathogenesis of uremic encephalopathy. An analysis of experimental and clinical studies, clinical guidelines, literature reviews from the eLIBRARY, Springer, Pubmed, Google Scholar databases was conducted using the terms: chronic kidney disease, pathogenesis, blood-brain barrier, urea, dysbiosis, encephalopathy, review. Chronic kidney disease is a common and long-term disease characterized by a gradual loss of kidney structure and function. Kidney dysfunction leads to accumulation, including protein-bound uremic toxins, which are poorly excreted by renal replacement therapy. This systemic retention of toxic metabolites, known as uremic syndrome, affects other organs and systems. The diagnosis of uremic encephalopathy is often based on a retrospective assessment of the patient’s condition, and the corresponding defining clinical and laboratory parameters are not yet used in routine studies. Complications develop due to hemodynamic disturbances and dysfunction of the blood-brain barrier, changes in the intestinal microbiome, and the reverse effect of urea. Uremic toxins can have an indirect effect on the brain through vascular dysfunction and hemostasis, as well as a direct effect - toxicity for neuronal cells, neuroinflammation and oxidative stress for glial cells and disruption of the blood-brain barrier. Anther way, during the hemodialysis procedure, delayed equilibration of the urea level between blood and cerebrospinal fluid leads to cerebral edema and the appearance of neurological disorders. The composition of the microbiome and the intestinal environment in chronic kidney disease, undergo changes and dysbiosis is formed, which leads to increased protein fermentation and a subsequent increase in the concentration of uremic toxins.