Abstract
The aim of the study. To establish the mechanisms of mutual burden and progression of non-alcoholic steatohepatitis (NASH) and chronic kidney disease (CKD) in patients with obesity.Material and methods. 114 patients with NASH were examined against the background of І-ІІ degree obesity, including: 52 patients with NASH (group 1) (without accompanying CKD), 62 patients with NASH with a comorbid CKD І-ІІ degree (group 2). The average age of patients was (45.8 ± 3.81) years. The control group consisted of 20 practically healthy persons (PHPs) of the corresponding age and sex. Results. The obtained data testify that under the conditions of the H2S deficit and hyperproduction of homocysteine for the comorbidity of NASH from CKD I-II degree the synthesis and resorption of collagen are activated, but the anabolism processes predominate as a result of the activation of the fibroblasts system, with a significant hyperproduction of acute phase proteins, fibronectin, a higher degree of hyperthyroidism and dyslipidemia with predominance of proatherogenic lipoprotein fractions, and a higher degree of endothelium dysfunction.Conclusions. A significant increase in the synthesis of collagen and glycoproteins (fibronectin) in patients with NASH, which was observed on the background of obesity, was established, which is accompanied by an ineffective resorption of newly formed collagen due to inhibition of collagenolysis against activation of proteinase inhibitors (α2-MG), accompanied by hyperproduction of the fibroblast growth factor, homocysteine, endothelin‑1, deficiency in the liberation of hydrogen sulfide and nitrogen monoxide.
Highlights
A significant increase in the synthesis of collagen and glycoproteins in patients with non-alcoholic steatohepatitis (NASH), which was observed on the background of obesity, was established, which is accompanied by an ineffective resorption of newly formed collagen due to inhibition of collagenolysis against activation of proteinase inhibitors (α2-MG), accompanied by hyperproduction of the fibroblast growth factor, homocysteine, endothelin‐1, deficiency in the liberation of hydrogen sulfide and nitrogen monoxide
The obtained data indicate that in patients with NASH, which arose on the background of obesity, a significant increase in the synthesis of collagen and glycoproteins was observed in the comorbidity with chronic kidney disease (CKD), which was accompanied by an ineffective resorption of newly formed collagen due to insufficient activation of collagenolysis and proteolysis, a significant imbalance in the metabolism system of the connective tissue, which leads to progressive fibrosis of the liver and kidneys and the violation of their functions
1.In patients with NASH, which arose on the background of obesity, a significant increase in the synthesis of collagen and glycoproteins was observed, which was accompanied by an ineffective resorption of newly formed collagen due to inhibition of collagenolysis (CLA) on the background of activation of proteinase inhibitors (α2-MG), accompanied by hyperproduction fibroblast growth factor, homocysteine, endothelin-1, deficiency in the liberation of hydrogen sulfide and nitrogen monoxide
Summary
FEATURES OF THE NONALCOHOLIC STEATOHEPATITIS AND CHRONIC KIDNEY DISEASE COURSES, PATHOGENETIC CORRECTION EFFICIENCY. To establish the mechanisms of mutual burden and progression of non-alcoholic steatohepatitis (NASH) and chronic kidney disease (CKD) in patients with obesity. The steady increase in the frequency of cases of comorbid flow of non-alcoholic steatohepatitis (NASH) against the background of obesity and chronic kidney disease (CKD) in persons of working age in Ukraine and in the world [1,2,3,4,5,6,7,8] necessitates conducting research on mechanisms of mutual burden and the search for new factors of pathogenesis of progression of this comorbid pathology [1,2,3,4,5, 7, 8]. The results of the researches show that the processes of fibrosing of organs in a strong interdependence correlate with the violation of the endogenous synthesis of H2S, and with the decrease in the activity of H2S-generating enzymes in plasma and directly in tissues [1,2,3,4, 5]
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