A complex analysis of acute kidney injury (AKI) in pregnant women shows that it is caused by the interaction of gestation-associated pathologies and beneficial signaling pathways activated by pregnancy. Studies report an increase in the regeneration of some organs during pregnancy. However, the kidney response to the injury during pregnancy has not been addressed. We investigated the mechanisms of the pregnancy influence on AKI. During pregnancy, the kidneys were shown to be more tolerant to AKI. Pregnant animals showed remarkable preservation of kidney functions after ischemia/reperfusion (I/R) indicated by the decrease of serum creatinine levels. The pregnant rats also demonstrated a significant decrease in kidney injury markers and an increase in protective markers. Two months after the I/R, group of pregnant animals had a decreased level of fibrosis in the kidney tissue. These effects are likely linked to increased cell proliferation after injury: using real-time cell proliferation monitoring we demonstrated that after ischemic injury, cells isolated from pregnant animal kidneys had higher proliferation potential vs. control animals; it was also supported by an increase of proliferation marker PCNA levels in kidneys of pregnant animals. We suggest that these effects are associated with hormonal changes in the maternal organism, since hormonal pseudopregnancy simulated effects of pregnancy.