Abstract

One of the most common complications of acute respiratory distress syndrome is acute kidney injury, the mechanisms of development of which remain not completely clarified. The purpose of this study is to examine morphofunctional changes in the kidneys of rats with induced acute respiratory distress syndrome at various time intervals after modelling the pathology. For the study, 56 healthy sexually mature male rats weighing 200-220 g were used, divided into 7 groups: control, 6, 24 hours, 3, 7, 14, and 28 days of the experiment. Respiratory distress in animals was caused by inhalation of lipopolysaccharide (5 mg/kg body weight). The kidneys of intact rats had a typical histological structure without specific features. Histological changes in the renal parenchyma of rats in the study groups included compaction of Malpighian bodies, damage and desquamation of epithelial cells of the nephron tubules, and the appearance of signs of disseminated intravascular coagulation. A month after the start of the experiment, both pathological changes in the nephrons and restored or preserved structural components of the kidney are observed, which indicates activation of intracellular reparative processes. The expression of TGF-β1 fibrosis marker as well as CD68 panmacrophage marker increased on days 3 and 7 of the experiment. The number of macrophages in the kidney samples remained consistently high until the end of the experiment, while the level of TGF-β1 decreased on day 28, indicating the start of the resolution phase. Biochemical analysis of renal markers showed an undulating course of inflammatory processes in the kidneys of experimental rats. The maximum concentration of creatinine, urea, and uric acid in the blood serum was observed at 24 hours of the experiment, which indicated the onset of acute kidney injury as a complication of respiratory distress. Preclinical examination of morphofunctional changes in the kidneys during acute respiratory distress syndrome will help choose an effective method for treating this pathological condition in humans in the future

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