The thesis research dealt with study of morphological peculiarities of the kidneys, ureters and bladder in the foetuses and newborns, who developed in conditions of maternal preeclampsia, iron deficiency anaemia, experimental chronic intrauterine, acute postnatal and mixed hypoxias, experimental maternal abdominal subacute infectious inflammatory process caused by Escherichia coli. In order to achieve the target goal and solve problems the thesis research was conducted in several stages. At the first stage, it was found out that the indicators of morbidity and prevalence of the urinary system organs diseases in the child population of the Kharkiv region were higher versus the respective indicators for Ukraine by 32.0% and 42.0% and demonstrated undulating changes. In the structure of the urinary system organs diseases in the child population of the Kharkiv region there were many cases of infections, dysmetabolic nephropathy, congenital defects, glomerulonephritides, vesicoureteral reflux and neurogenic bladder dysfunction. At the second stage, the regional risk factors for the urinary system organs diseases development in the child population of the Kharkiv region (the female sex of the child, his/her living in the countryside, decreased mass and body length of the baby at birth, its parents' smoking before and during pregnancy, the parents' unemployment, abortions in the mothers' case history, their genital and extragenital pathology (genitourinary system diseases) as well as complications during pregnancies (placental insufficiency and preeclampsia) and delivery (abnormalities in delivery and placental abruption)) were identified. At the third stage, we constructed discriminative models, which made it possible to predict the probability of the urinary system organs diseases development for children from the Kharkiv region. At the fourth stage, we conducted a complex morphological examination of the experimental material. It was proved that acute postnatal hypoxia did not affect the mass of kidneys in the descendants, but chronic intrauterine and mixed hypoxias causing its reduction. Acute postnatal, chronic intrauterine and mixed hypoxias resulted in the development of respectively minimal, moderate and marked morphological changes in the kidneys, ureters and bladder of the foetuses and newborns, and these changes increasing in the newborns versus the foetuses in case of chronic intrauterine hypoxia. The kidneys revealed changes in their capsules, parenchymal and stromal-vascular components. The kidneys are characterized by primarily damage the stromal vessels, parenchyma where more marked changes took place in the tubules, collecting ducts. As for the ureters and bladder, the changes developed in all layers of the organ wall, the mucous membrane and vessels being primarily affected. Acute postnatal, chronic intrauterine and mixed hypoxias stimulated cells of the fibroblastic line, while chronic intrauterine and mixed hypoxias also induced the epithelial-mesenchymal transformation causing an excessive production of collagens and sclerosis development in the organs. Acute postnatal, chronic intrauterine and mixed hypoxias induced apoptosis and proliferation and resulted in an imbalance between them. Acute postnatal hypoxia did not influence T- and B-cell immunity, but activated the macrophage system, while chronic intrauterine and mixed hypoxias inhibited T- and B-cell immunity and stimulated the macrophage system. Maternal abdominal subacute infectious inflammatory process, caused by Escherichia coli, produced monotypic, apart from local immune responses, morphological changes in the kidneys, ureters and bladder of the descendants versus chronic intrauterine hypoxia with more marked changes. Local immune responses were characterized by inhibition of T-cell immunity, activation of B-cell immunity and the macrophage system. At the fifth stage, we conducted a complex morphological examination of autopsy material. It was revealed that severe iron deficiency anaemia and preeclampsia resulted in development of excessive embryonal lobulation of the kidneys in the foetuses and newborns. Preeclampsia of the moderate and severe degrees of severity caused excessive development of adipose capsules. The mass, length, width and thickness of the kidneys as well as the length of the ureters in the foetuses and newborns did not change in mild iron deficiency anaemia and preeclampsia, but decreased in moderate and severe iron deficiency anaemia and preeclampsia, a higher degree of severity of the maternal pathology resulting in a lower value of the organometric parameter of the organ. Mild maternal iron deficiency anaemia and preeclampsia did not affect the length and width of the bladder, but caused an increase of its thickness. Moderate and severe maternal iron deficiency anaemia and preeclampsia resulted in decreases of the bladder length and width, but increased its thickness. Iron deficiency anaemia and preeclampsia in the kidneys, ureters and bladder of the foetuses and newborns caused morpho-functional changes, which were more manifested in preeclampsia and increased with the child's age and a higher degree of severity of the maternal pathology. As for the kidneys, structural changes developed in their capsules, parenchyma and stroma with the primary damage of the organ's parenchyma and stroma vessels, the maximum changes of the parenchyma being observed in the tubular component of nephrons and in the collecting ducts. As for the ureters and bladder, the changes developed in all layers of the organ wall, the mucous membrane and vessels being primarily affected. Mild iron deficiency anaemia did not affect T- and B-cell immunity and at the same time stimulated the macrophage system, but the moderate and severe degrees of the above maternal pathology inhibited T- and B-cell immunity with activation of the macrophage system. All degrees of severity of maternal preeclampsia resulted in an extreme activation of the macrophage system, T- and B-cell immunity. Maternal iron deficiency anaemia and preeclampsia served as activators of apoptotic and proliferative processes with an imbalance between them, stimulators of the pool of fibroblastic line cells and inducers of the epithelial-mesenchymal transformation with resultant organs sclerosis.
