The aim: To study the distribution and influence of coagulation factor gene polymorphisms, endothelial dysfunction, blood pressure regulator on the development of obstetric and perinatal complications in women with preeclampsia (PE). Materials and methods: The prospective cohort study included 46 women with PE and maternal or fetal complications and 87 pregnant women with PE, without complications. Genetic polymorphisms of coagulation factors and fibrinolysis (1691 G→A FVL, 20210 G→A prothrombin, 675 5G/4G PAI-1, 455 G→A fibrinogen β), endothelial dysfunction (192 Q→R PON-1, 677 C→T MTHFR) and blood pressure regulator (235 M→T angiotensinogen II) were studied with the help of allele-specific polymerase chain reaction Results: Markers of predisposition to the development of obstetric and perinatal complications in pregnant women with PE are the following genotypes: 1691 GA by V Leiden factor gene – increases the risk in 2.9 times (95% CI 1.94-4.33), 20210 GA by prothrombin gene – in 2.36 times (95% CI 1.54-3.6), 20210 AA by prothrombin gene – in 3.12 times (95% CI 2.4-4.0). Pathological polymorphisms in the genes of angiotensinogen II 235 M→T, PAI-1 5G/4G, fibrinogen β 455 G→A, paraoxonase-1 192 Q→R do not significantly affect the development of complications during preeclampsia. Conclusions: The development of PE against the background of the existence of acquired and hereditary types of thrombophilia is associated with a more severe course, early-onset and the development of life-threatening complications for a mother and fetus.