MECHANISMS OF PREGNANCY COMPLICATION DEVE LOPMENT IN ESSENTIAL-HYPERTENSION AND GLOMERULONEPHRITIS

Pregnancy complications have been analyzed in 124 females suffering fr om essential hypertension (EH) and chronic glomerulonephritis (CGN). S uch complications, as late gestosis (8.9%), ablation placentae (1.6%), premature delivery (14.5%), intrauterine growth retardation (14.5%) o ccurred more frequently than in population. Pre- and perinatal deaths were encountered with the same frequency as in the population. Morphol ogically, the placentas had in many cases histological evidence of mod erate placental insufficiency (PI). In more than 60% of the patients t here were uteroplacental and fetoplacental hemodynamic defects. Placen tal circulatory disorders and PI ran subclinically in most of the case s as they were compensated. In EH and CGN pregnant women, compared to healthy controls, red cells acquired abnormal forms more frequently, s erum thromboxane B2 levels got elevated, lactate hydrogenase activity became enhanced. Erythrocytic damage and platelet activation in EH and CGN pregnant women may indirectly confirm the existence of systemic a ngiopathy. It is suggested that ischemic placenta may produce endothel ial toxin, that systemic endothelial damage in EH, CGN, PI may be syne rgetic which potentiates its clinical appearance in the form of the ab ove pregnancy complications.