Edema, for example, is common in normal pregnancy, partly as a result of compression of the inferior vena cava by the enlarged uterus. Moreover, in patients with a molar pregnancy, preeclampsia may be observed earlier than the 20th week, often during the first trimester. The pathogenesis of preeclampsia is incompletely understood. The earliest pathologic change is in the uteroplacental circulation, with decreased dilatation of the spiral arteries. The normal pregnancy-induced differentiation of the cytotrophoblasts to an endothelial cell phenotype is impaired in preeclampsia, which may explain this diminished vasodilatation.
Immunologic factors appear to be important in the pathogenesis of preeclampsia.
The development of this disorder may reflect altered or inadequate immunoprotection of fetoplacental tissue. This finding suggests that exposure to paternal antigens in the semen before pregnancy may permit the development of antibodies that can block a subsequent maternal immune response directed against tissue from the fetus or placenta. Supporting this hypothesis is the observation that preeclampsia is more common during first pregnancies and in women who have a subsequent pregnancy but with a different partner. The principal renal pathologic changes in preeclampsia are seen in the glomeruli. On light microscopy, swelling of endothelial cells and the resultant narrowing or obliteration of the glomerular capillary lumina are observed.