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NDT Advance Access published online on July 7, 2007
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfm429
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Angiogenic factors in preeclampsia: so complex, so simple?

Nadia Berkane1, Guillaume Lefevre2 and Alexandre Hertig3,4,5

1AP-HP, Hôpital Tenon, Service de Gynécologie Obstétrique, 2AP-HP, Hôpital Tenon, Service de Biologie et Hormonologie, 3AP-HP, Hôpital Tenon, Urgences Néphrologiques & Transplantation Rénale, 4INSERM, U702 and 5Université Pierre et Marie Curie-Paris 6, UMR S 702, France

Correspondence and offprint requests to: Nadia Berkane, MD, Service de Gynécologie Obstétrique et Médecine de la Reproduction, Hôpital Tenon, AP-HP, 4 rue de la Chine, 75020 Paris, France. Email: nadia.berkane@tnn.aphp.fr

Keywords: glomerular endotheliosis; HELLP preeclampsia; PlGF; sFlt-1; TGFß; VEGF

The first 150 words of the full text of this article appear below.



   Introduction
 
Preeclampsia is a common cause of fetal and maternal morbidity and mortality, that affects ~2–7% of all healthy nulliparous women [1]. Until recently, the pathophysiology of preeclampsia was not well understood. Successive hypotheses have been proposed, each being challenged by subsequent publications. The current most plausible hypothesis involves abnormal placentation leading to placenta ischaemia [2]. Recently, ischaemic trophoblast cells [3] were shown to synthesize anti-angiogenic factors, notably the soluble form of fms-like tyrosine kinase-1 (sFlt-1), which is a receptor for vascular endothelial growth factor (VEGF). In addition, sFlt-1 mRNA is highly expressed in the placenta from preeclamptic patients, and administration of sFlt-1 induces a preeclampsia-like syndrome in pregnant rats [4]. Therefore, sFlt-1 could be the link between implantation disorders and maternal symptoms of preeclampsia.



   Angiogenic factors
 
A major advance in the understanding of the pathophysiology of preeclampsia was made in 2003, when Karumanchi and . . . [Full Text of this Article]



   Conclusion
 

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