Introduction. Cystatin C is one of the markers of acute kidney injury, which have a greater sensitivity than the level of blood creatinine. There are separate publications that the dynamic determination of the level of cystatin C in the blood can be useful for predicting the course of the pathological process and the risk of transition of acute injury (AKI) to chronic kidney disease (CKD).

Aim of study. In animal experiments determine the possibility predict the probability of AKI transition to CKD and the effectiveness of nephroprotective therapy based on the dynamic determination of the blood level of cystatin C.

Material and methods. The experiments were performed on 40 white mongrel male rats. AKI was induced by removal of the right kidney and ischemia of the remaining left kidney for 60 minutes (moderate damage) or 90 minutes (severe damage). In 20 rats, therapy was performed with the drug Cellex, which is a protein-peptide complex of stem cells of embryonic tissues, and 20 rats were not treated. After 3, 7 and 14 days, as well as after 3 months, the level of cystatin C in the blood was determined in comparison with the indicators of the functional state of the kidney (diuresis, blood creatinine level, glomerular filtration rate) during therapy and without it.

Results. In experiments without nephroprotective therapy, the level of cystatin C in the blood increased proportionally to the deterioration of the functional state of the kidney 3 days after ischemia. With moderate AKI (60 minutes of ischemia), the level of cystatin C decreased after 14 days with improved kidney function, whereas with severe AKI (90 minutes of ischemia), the level of cystatin C remained persistently elevated, although the organ function improved somewhat during this period. 3 months after the 60-minute ischemic exposure, the level of cystatin C did not significantly differ from the norm with complete normalization of functional parameters. After 90-minute ischemia, it exceeded normal values by almost 4 times, which was accompanied by the preservation of pronounced renal dysfunction in all animals of this group, which can be regarded as the development of CKD. In experiments with nephroprotective therapy with Cellex, there was a more pronounced improvement in the functional parameters of the kidney in both moderate and severe AKI. At the same time, the dynamics of the level of cystatin C with moderate AKI was the same as without therapy, whereas with severe AKI, the level of cystatin C significantly decreased by 14 days, in contrast to control experiments. At the same time, signs of CKD were detected in 40% of rats in this group, while in the control – in 100%.

Conclusion. Dynamic determination of the level of cystatipn C in the blood allows not only to detect AKI at an early stage, but also to predict the likelihood of developing CKD, as well as to evaluate the effectiveness of nephroprotective therapy.