ePrints

New aspects in the pathophysiology of preeclampsia

Lookup NU author(s): Emeritus Professor John Davison

Downloads

Full text for this publication is not currently held within this repository. Alternative links are provided below where available.

Abstract

Preeclampsia, the de novo occurrence of hypertension and proteinuria after the 20th week of gestation, continues to exert an inordinate toll on mothers and children alike. Recent clinical trials, new physiologic insights, and novel observations on pathogenesis have altered the thinking about preeclampsia. The mechanisms surrounding relaxin and its effects on the circulation and on matrix metalloproteinases have been elucidated. The growth factor's receptor, fms-like tyrosine kinase 1, has been shown to exist in a soluble form that is able to inactivate vascular endothelial-derived growth factor and human placental growth factor. Compelling evidence has been brought forth suggesting that fms-like tyrosine kinase 1 is a circulating factor that can cause preeclampsia. Preeclamptic women have high circulating levels of asymmetric dimethyl arginine that could account for the generalized endothelial dysfunction observed in preeclampsia. Preeclamptic women also produce novel autoantibodies that may serve to activate angiotensin receptors. These new observations raise the possibility that the treatment of preeclamptic women will soon be improved.

Publication metadata

Author(s): Davison JM, Homuth V, Jeyabalan A, Conrad KP, Karumanchi SA, Quaggin S, Dechend R, Luft FC

Publication type: Review

Publication status: Published

Journal: Journal of the American Society of Nephrology

Year: 2004

Volume: 15

Issue: 9

Pages: 2440-2448

ISSN (print): 1046-6673

ISSN (electronic): 1533-3450

URL: http://dx.doi.org/10.1097/01.ASN.0000135975.90889.60

DOI: 10.1097/01.ASN.0000135975.90889.60

PubMed id: 15339993

Share