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Acute kidney injury (AKI) is major factors of mortality in the clinic. AKI occurs in 20% of patients hospitalized with acute illnesses, and the mortality rate can reach 40%. Pregnancy is a major factor which affects AKI: during pregnancy AKI can reach 10% of all pregnancies and the mortality rate of pregnant women can reach 18%. On the other hand, studies report an increase in regeneration rate of some tissues during pregnancy. An obvious contradiction emerges: pregnancy is a major risk factor for kidney pathologies, but fundamental studies suggest, that it might be vice versa. These points can both be valid: complications can affect the outcome more, than the initial pathology. We have shown, that during pregnancy kidneys are more protected from AKI. Pregnant animals have shown remarkable preservation of kidney functions after ischemia/reperfusion (model of AKI), indicated by the drop of serum creatinine levels, compared to the non-pregnant group. The pregnant group also has a significant decrease in kidney damage marker NGAL and lipids damage marker MDA levels. Two months after ischemia pregnant group has drastically decreased rate of fibrosis formation in kidney tissue. These effects are likely linked to increased cell proliferation in pregnant kidneys tissue after injury: using real-time cell proliferation monitoring we have shown, that after ischemic injury cells, isolated from pregnant animals kidneys, increase their proliferation rate significantly more, than cells from control animals. It is also supported by increase of proliferation marker PCNA levels both in kidney tissue and cell culture. These effects must be due to changes in mothers organism since hormonal pseudopregnancy mimic pregnancy’s effects. Results of our work show, that kidney during pregnancy are more tolerant to ischemic damage and suggest, that clinical outcome might be more affected by complications, rather than initial pathology.