From placenta to podocyte: Vascular and podocyte pathophysiology in preeclampsia

Steven J. Wagner, Iasmina M. Craici, Joseph P. Grande, Vesna D. Garovic

Research output: Contribution to journalArticle

18 Scopus citations

Abstract

Preeclampsia is a disorder of hypertension and proteinuria that affects 6-8% of normal pregnancies. Recent research has revealed many molecular mechanisms that may contribute to systemic endothelial dysfunction, glomerular capillary endotheliosis, dysregulation of the glomerular filtration apparatus, and podocyte loss. An ischemic placenta elaborates soluble FMS-like tyrosine kinase 1 (sFlt-1), a soluble receptor for vascular endothelial growth factor (VEGF). A variety of mediators, including nitric oxide, Angiotensin II receptor autoantibodies (AT1AA), and endothelin-1 may serve to maintain placental ischemia and systemic endothelial dysfunction. Endothelin-1 and decreased vascular endothelial growth factor may adversely affect overall expression and distribution of podocyte foot process proteins, leading to proteinuria. Podocyte derangements may lead to podocyte apoptosis and loss, as evidenced by the detection of live podocytes and podocyte products in the urine of preeclamptic women. In this review, we explore recent research elucidating the interactions of placenta, endothelium, and podocyte leading to the clinical syndrome of preeclampsia.

Original languageEnglish (US)
Pages (from-to)241-249
Number of pages9
JournalClinical nephrology
Volume78
Issue number3
DOIs
StatePublished - Sep 1 2012

Keywords

  • Endothelium
  • Placenta
  • Podocyte
  • Podocyturia
  • Preeclampsia

ASJC Scopus subject areas

  • Nephrology

Fingerprint Dive into the research topics of 'From placenta to podocyte: Vascular and podocyte pathophysiology in preeclampsia'. Together they form a unique fingerprint.

  • Cite this