Abstract <p>Acute kidney injury (AKI) is a syndrome characterized by asharp decline in kidney function due to the death of nephron cells.Various experimental models are used to study AKI, including unilateral ureteralobstruction (UUO), which adequately reproduces the clinical presentationof obstructive nephropathy. Meanwhile, the morphological and functionalchanges in the kidneys that occur after the restoration of urineflow are currently insufficiently studied. The aim of this workwas to elucidate the mechanisms of inflammation and renal injuryin a rat model of UUO at different time points after temporary ureteralclamping. The study was conducted on male Wistar rats divided intothe following experimental groups: intact (control); with a three-day UUO(3UUO) without urine flow restoration; with a three-day reversibleUUO combined with contralateral nephrectomy and tissue samplingone and three days after ureteral obstruction relief (3UUO+1 and 3UUO+3,respectively). Serum creatinine and urea levels were measured toassess kidney function. The kidney tissue levels of the markersof inflammation, renal injury, and epithelial-mesenchymal transition (EMT)IL-18, PCNA, and alpha-smooth muscle actin (α-SMA) were determinedusing Western blotting, and an analysis of morphological changesin kidney tissue was carried out. One day after obstruction relief,AKI was shown to develop with maximum serum creatinine and urinelevels, which declined by day three. A similar pattern was shown forthe AKI and inflammation marker IL-18, while the elevated α-SMAlevel in the 3UUO+1 group indicated the development of EMT. Histological analysisrevealed a progressive tubular dilation, which persisted after obstructionrelief in the renal cortex while decreasing in the medulla. Thus,the obtained results show that the severity of AKI peaks 24 h afterthe cessation of ureteral obstruction. This model can serve as aconvenient tool for studying the sequelae of obstructive nephropathyin clinical practice.</p>