The Intensity in Pathogenesis of Mutual Burden of Non-Alcoholic Fatty Liver Disease and Chronic Kidney Disease with Obesity

The purpose of the study was to find out the possible intensity in the pathogenesis of the mutual burden of non-alcoholic fatty liver disease on the background of obesity, depending on its type and the presence of a comorbid chronic kidney disease. Material and methods. 384 patients with non-alcoholic fatty liver disease were examined: 84 of them with non-alcoholic fatty liver disease with obesity of the 1st degree (group 1), which contained 2 subgroups: 32 patients with non-alcoholic steatosis and 52 patients with non-alcoholic steatohepatitis; 270 patients with non-alcoholic fatty liver disease with comorbid obesity of the 1st degree and chronic kidney disease І-ІІІ stage (group 2), including 110 patients with non-alcoholic steatosis and 160 patients with non-alcoholic steatohepatitis. The control group consisted of 90 patients with chronic kidney disease of the І-ІІІ stage with normal body weight (group 3). Results and discussion. The study showed that the most significant metabolic changes for the development of non-alcoholic fatty liver disease on the background of obesity and chronic kidney disease are likely postprandial hyperglycemia, hyperinsulinemia, increased glycated hemoglobin, and primary tissue insulin resistance. The reason for the metabolic syndrome progression on the background of non-alcoholic fatty liver disease and chronic kidney disease is lipid distress syndrome with an increase in proatherogenic lipoproteins, anti-atherogenic high-density lipoproteins. The leading role in the development and progression of steatohepatitis is the disorders of the hepatic circulation that results in an increase in blood TG. Conclusions. The development of non-alcoholic fatty liver disease in patients with chronic kidney disease and obesity is accompanied by a significant disorder of hyperlipidemia with the highest among the groups compared with the increase in the content of low density proatherogenic lipoproteins, the probable decrease in anti-atherogenic high-density lipoproteins and the increase in the atherogenicity index.