Uteroplacental ischemia results in proteinuric hypertension and elevated sFLT-1

Kidney Int. 2007 May;71(10):977-84. doi: 10.1038/sj.ki.5002175. Epub 2007 Mar 21.


Preeclampsia is a complication of pregnancy with significant morbidity and mortality for the mother and the fetus. Presumptions are made that placental hypoxia has a causative role in the clinical syndrome. Furthermore, soluble fms-like tyrosine kinase 1 (sFLT-1) has been shown to have a role in the maternal syndrome of preeclampsia. We investigated the relationship between uteroplacental ischemia (UPI), the maternal clinical syndrome of preeclampsia and sFLT-1 in non-human primates. The induction of UPI in a pregnant non-human primate resulted in the development of a clinical entity analogous to human preeclampsia. This was illustrated by the increase in blood pressure, development of proteinuria, and renal histological changes identical to human preeclampsia. A significant elevation in the placental and peripheral blood mononuclear cell sFLT-1 mRNA expression was noted, translating to a significant elevation in circulating sFLT-1. Thus, this sequence suggests that a pathogenic reduction in placental perfusion results in the development of the maternal syndrome of preeclampsia and an increase in circulating sFLT-1, which is derived both from placental and extra-placental sources.

MeSH terms

  • Animals
  • Female
  • Hypertension / etiology*
  • Ischemia / blood*
  • Ischemia / complications*
  • Kidney / metabolism
  • Kidney / pathology
  • Monocytes / metabolism
  • Papio
  • Placenta / blood supply*
  • Placenta / metabolism
  • Pre-Eclampsia / etiology*
  • Pre-Eclampsia / pathology
  • Pregnancy
  • Proteinuria / etiology*
  • RNA, Messenger / metabolism
  • Uterus / blood supply*
  • Vascular Endothelial Growth Factor Receptor-1 / blood
  • Vascular Endothelial Growth Factor Receptor-1 / genetics
  • Vascular Endothelial Growth Factor Receptor-1 / metabolism*


  • RNA, Messenger
  • Vascular Endothelial Growth Factor Receptor-1