Preeclampsia represents a severe pregnancy disorder associated with premature delivery and fetal growth retardation in about 15 per cent of premature births. The clinical symptoms are high blood pressure, proteinuria and edema. This disease may progress into serious complications such as eclampsia, whereby the main problem is represented by convulsions. Other complications may include kidney failure and development of a HELLP syndrome, which includes hypertension, a disruption of the liver, and a significant decrease of red blood cells and platelets. Consequently, the continuously increasing complications during this pregnancy-associated disorder can be life threatening for the mother and the fetus. Whereby the fetal death rate has decreased in recent times, perinatal morbidity continues to be a major problem due to clinically indicated interventional prematurity. Although the sources and specific prognostic markers for this severe pregnancy disorder remain unclear, women with a persistently high resistance in uterine arteries have an increased risk of the subsequent development of a preeclampsia. Doppler ultrasound investigation of the uterine artery in the second trimester of gestation provides a non-invasive method for the study of the uteroplacental blood flow and for the prediction of abnormal outcomes in risk pregnancies with high negative predictive values. Particularly in high-risk women, uterine artery Doppler waveform analysis performs best in the prediction of preeclampsia. In this context, uteroplacental insufficiency, placental abruption and interventional prematurity exhibit major causes of perinatal morbidity and mortality. Moreover, the gestational age at delivery represents a key factor for the neonate, whereby neonatal sepsis remains a cause for concern. In the search for prognostic markers, several research activities at the molecular levels suggested the development of preeclampsia as a multifactorial interplay between oxidative stress products and distinct immunological imbalances. Considering the fetus as an allogene transplant, a continuously increasing accumulation of reactive oxygen species (ROS) together with an enhanced immunological barrier may contribute to endothelial dysfunctions and high blood pressure due to a reduced placental supply followed by placental and fetal growth retardation. Certain growth factors and their cellular receptors have been suggested to contribute to a proper endothelial function, however, imbalances leading to the development of preeclamptic symptoms remain unclear. Likewise, appropriate therapeutic approaches for preeclampsia are still unavailable to date.