The central factor in the pathogenesis of preeclampsia appears to be placental ischaemia which is supposed to be caused by an initial defective placentation. The impaired placental function leads to generalized endothelial cell dysfunction, which in its turn gives rise to hypertension, proteinuria, oedema, thrombocytopenia and hypoperfusion, especially of liver and kidneys. The link between placental ischaemia and endothelial dysfunction could consist of a toxic circulating 'factor X' and the multifactorial origin of the defective placentation. Impaired development of immunological tolerance may lead to an activated immune system during trophoblast invasion which then causes defective placentation. Genetic predisposition and maternal vascular pathology could be modulating factors in this process. The recent finding of latent abnormalities in haemostasis, in metabolism (giving rise to thrombophilia), and in volume homeostasis in patients with a history of preeclampsia in suggestive of an important role of these vascular mediators in the pathogenesis of preeclampsia.