{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T22:55:55Z","timestamp":1793228155439,"version":"4.5.0"},"reference-count":103,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["CJASN"],"published-print":{"date-parts":[[2016,6]]},"abstract":"<jats:p>Preeclampsia is becoming an increasingly common diagnosis in the developed world and remains a high cause of maternal and fetal morbidity and mortality in the developing world. Delay in childbearing in the developed world feeds into the risk factors associated with preeclampsia, which include older maternal age, obesity, and\/or vascular diseases. Inadequate prenatal care partially explains the persistent high prevalence in the developing world. In this review, we begin by presenting the most recent concepts in the pathogenesis of preeclampsia. Upstream triggers of the well described angiogenic pathways, such as the heme oxygenase and hydrogen sulfide pathways, as well as the roles of autoantibodies, misfolded proteins, nitric oxide, and oxidative stress will be described. We also detail updated definitions, classification schema, and treatment targets of hypertensive disorders of pregnancy put forth by obstetric and hypertensive societies throughout the world. The shift has been made to view preeclampsia as a systemic disease with widespread endothelial damage and the potential to affect future cardiovascular diseases rather than a self-limited occurrence. At the very least, we now know that preeclampsia does not end with delivery of the placenta. We conclude by summarizing the latest strategies for prevention and treatment of preeclampsia. A better understanding of this entity will help in the care of at-risk women before delivery and for decades after.<\/jats:p>","DOI":"10.2215\/cjn.12081115","type":"journal-article","created":{"date-parts":[[2016,4,19]],"date-time":"2016-04-19T22:58:45Z","timestamp":1461106725000},"page":"1102-1113","source":"Crossref","is-referenced-by-count":514,"title":["Preeclampsia: Updates in Pathogenesis, Definitions, and Guidelines"],"prefix":"10.2215","volume":"11","author":[{"given":"Elizabeth","family":"Phipps","sequence":"first","affiliation":[{"name":"Department of Nephrology\/Medicine, Jacobi Medical Center at Albert Einstein College of Medicine, Bronx, New York; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Devika","family":"Prasanna","sequence":"additional","affiliation":[{"name":"Department of Nephrology\/Medicine, Jacobi Medical Center at Albert Einstein College of Medicine, Bronx, New York; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wunnie","family":"Brima","sequence":"additional","affiliation":[{"name":"Department of Medicine, James J. Peters Veterans Affairs Medical Center, New York, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Belinda","family":"Jim","sequence":"additional","affiliation":[{"name":"Department of Nephrology\/Medicine, Jacobi Medical Center at Albert Einstein College of Medicine, Bronx, New York; and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2016,4,19]]},"reference":[{"issue":"Suppl A","key":"B1-20230813","doi-asserted-by":"crossref","first-page":"S32","DOI":"10.1016\/j.placenta.2008.11.009","article-title":"The two stage model of preeclampsia: Variations on the theme","volume":"30","author":"Roberts","year":"2009","journal-title":"Placenta"},{"key":"B2-20230813","doi-asserted-by":"crossref","first-page":"1200","DOI":"10.1016\/0002-9378(89)90665-0","article-title":"Preeclampsia: An endothelial cell disorder","volume":"161","author":"Roberts","year":"1989","journal-title":"Am J Obstet 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