Preeclampsia (PE) is a multisystemic disease that has been recorded as a complication in up to 15 % of pregnancies being lead cause of maternal mortality worldwide. Despite that PE pathophysiology has not been fully elucidated, it is currently believed that the endothelial dysfunction and pro-inflammatory status play a key role in its development, which account for impaired implantation processes as well as trophoblast invasion during placentation. Altogether, it results in developing generally accepted clinical symptoms “triad”: arterial hypertension, proteinuria, and edema. PE is also characterized by clotting disorders that cause an increased risk of maternal venous thromboembolism. It should be remembered that the related risk may be markedly elevated in the postpartum period. The mechanisms underlying the development of thrombosis high risk remain to be fully investigated, albeit upregulated expression of procoagulant factors, endothelial dysfunction, compromised endogenous anticoagulant activity, and increased platelet activity result in prothrombotic predisposition.