title: Preeclampsia: pathophysiology and practice considerations for the consulting nephrologist.
abstract: Abnormal placental implantation presumed to be secondary to maternal genetic susceptibility or immune maladaptation is considered to be fundamental to the pathogenesis of preeclampsia. The reduced placental perfusion resulting in placental ischemia is hypothesized to cause the known endothelial dysfunction, which leads to the clinical manifestations of this disease. Oxidative stress is a postulated linking factor, an aberration that possibly has its genesis via cytokines released from the abnormally implanted and perfused placenta. Clearly the maternal pathophysiologic changes that subsequently produce what is recognized as preeclampsia are present long before the disease makes its clinical appearance.
authors.affiliation: University of Mississippi Medical Center, Jackson, MS 39216-4505, USA.
authors.forename: Christy M
authors.initials: CM
authors.lastname: Isler
authors.forename: James N
authors.initials: JN
authors.lastname: Martin
mesh_terms: D016207:Cytokines / Q000378:metabolism; D005260:Female; D006801:Humans; D007511:Ischemia / Q000503:physiopathology; D018384:Oxidative Stress; D010920:Placenta / Q000098:blood supply / Q000378:metabolism; D011225:Pre-Eclampsia / Q000235:genetics / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology*; D011247:Pregnancy
chemical_list: D016207:Cytokines