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Background. Preeclampsia is a frequent complication of pregnancy. The literature data and the results of our own studies indicate the development of morphofunctional changes in the kidneys, ureters and bladder of fetuses and newborns that developed under maternal preeclampsia, in particular, sclerotic processes in these organs, morphogenesis of which is currently unknown. The purpose of the study was to search for the signs of epithelial-mesenchymal transition in the kidneys, ureters and bladder of fetuses and newborns, which developed under the conditions of maternal preeclampsia, and to evaluate its role in the development of sclerotic changes in these organs. Materials and methods. Study materials were the tissues of the kidneys, ureters and bladder of full-term fetuses and newborns. All materials were divided into the following groups: I — fetuses and newborns from mo­thers with physiological pregnancy; II — fetuses and newborns from mothers, whose pregnancy was complicated by mild preeclampsia; III — fetuses and newborns from mothers, whose pregnancy was complicated by moderate preeclampsia; IV — fetuses and newborns from mothers, whose pregnancy was complicated by severe preeclampsia. An immunohistochemical study was performed with monoclonal antibodies to vimentin, smooth muscle actin, desmin, cytokeratins 18 and 19. Results. A comprehensive analysis of the immunohistochemical reactions with monoclonal antibodies to vimentin, smooth muscle actin, desmin, cytokeratins 18 and 19 allowed to reveal in the kidneys, ureters and bladder of fetuses and newborns developed under the conditions of maternal preeclampsia of varying severity the signs of epithelial-mesenchymal transition, which increased with the increasing age of the child, aggravation of maternal preeclampsia. Epithelial-mesenchymal transition was characterized by increased expression of vimentin, smooth muscle actin, desmin and decreased expression of cytokeratins 18 and 19. Conclusions. In the kidneys, ureters and bladder of fetuses and newborns from mothers, whose pregnancy was complicated by preeclampsia of varying severity, the sclerotic changes are caused by the process of epithelial-mesenchymal transition, which becomes more significant from fetus to newborn and with the increasing severity of maternal preeclampsia. Chronic intrauterine hypoxia and activation of the macrophage system in these organs may influence the pathogenesis of epithelial-mesenchymal transition in the kidneys, ureters and bladder of fetuses and newborns developing under maternal preeclampsia.