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NDT Advance Access originally published online on November 27, 2008
Nephrology Dialysis Transplantation 2009 24(1):31-33; doi:10.1093/ndt/gfn534
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Low catechol-O-methyltransferase and 2-methoxyestradiol in preeclampsia: more than a unifying hypothesis*

Duska Dragun and Anja Haase-Fielitz

Department of Nephrology and Intensive Care Medicine, Charité University Hospital, Campus Virchow Clinic, Berlin, Germany

Duska Dragun, Clinic for Nephrology and Intensive Care Medicine, Charité CVK, Augustenburger Platz 1, 13353 Berlin, Germany. Tel: +49-30450653485; Fax: +49-3045055916; E-mail: duska.dragun@charite.de

Keywords: angiogenesis; catecholestradiols; maternal syndrome; preeclampsia

The first 10% of the full text of this article appears below.

Preeclampsia is a systemic disorder of pregnancy characterized by widespread maternal endothelial dysfunction. Clinical manifestations of preeclampsia include placental hypoxia, hypertension, proteinuria and fluid retention. The condition is common and affects over 5% of all pregnancies, thus remaining a leading cause of maternal and fetal morbidity and mortality worldwide [1]. Pregnancies complicated by preeclampsia are associated with greater risk and earlier onset of cardiovascular disease in both mother and infant [2,3]. Preeclampsia originates in the placenta, as it may occur only in the presence of placenta or a hydatiform mole and resolves dramatically postpartum after the delivery of the placenta. Generalized endothelial dysfunction resulting in vasoconstriction and end-organ ischaemia is attributed in all of the clinical aspects of the maternal syndrome . . . [Full Text of this Article]


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