The pathophysiology of preeclampsia involves altered levels of angiogenic factors promoted by hypoxia and autoantibody-mediated mechanisms.

Pre-eclampsia is a syndrome characterized by inadequate placentation, which is due to deficient trophoblastic invasion of the uterine spiral arteries. This deficiency can lead to placental hypoxia, secretion of proinflammatory cytokines, and release of angiogenic and antiangiogenic factors. Hypoxic conditions in the placenta can promote oxidative stress and the production of angiogenic factors that are antagonized by soluble receptors, which are also elevated in this syndrome. In addition to these factors, the development of hypertension in women with pre-eclampsia may be associated with the renin-angiotensin system and endothelial dysfunction. The presence of antiangiotensin II type 1 receptor autoantibodies is relevant in pre-eclampsia because it has been related to the secretion of antiangiogenic factors through cytokine pathways, indicating that autoimmune mechanisms may participate in the pathophysiology of this syndrome.