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Renal dysfunction and podocyturia in pre-eclampsia may be explained by increased urinary VEGF.

Luca Valsecchi1, Alessandro Galdini1, Daniela Gabellini2

  • 1Department of Obstetrics and Gynecology, IRCCS San Raffaele Scientific Institute, Milan, Italy.

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association
|May 5, 2021
PubMed
Summary

Pre-eclampsia causes kidney dysfunction by inhibiting vascular endothelial growth factor (VEGF). The kidneys may compensate by increasing VEGF production, leading to podocyturia and further renal damage.

Keywords:
VEGF inhibitionhypoxiapodocyturiapre-eclampsiapregnancy

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Area of Science:

  • Nephrology
  • Obstetrics
  • Vascular Biology

Background:

  • Pre-eclampsia significantly impacts renal function, manifesting as proteinuria and podocyturia.
  • The precise mechanism by which soluble Fms-like tyrosine kinase-1 (sFlt-1) inhibits vascular endothelial growth factor (VEGF) activity in pre-eclampsia and affects renal function is not fully understood.

Purpose of the Study:

  • To investigate whether a localized renal response to VEGF inhibition in pre-eclampsia directly influences kidney function.
  • To explore the role of renal-centered VEGF escape mechanisms in pre-eclamptic pregnancies.

Main Methods:

  • Evaluated plasma and urinary VEGF, placental growth factor (PlGF), plasma sFlt-1, carbonic anhydrase IX (CAIX), albuminuria, and podocyturia.
  • Compared 21 women with pre-eclampsia, 18 with uncomplicated pregnancies, and 18 non-pregnant controls, matched for age and gestational age.

Main Results:

  • Plasma VEGF was reduced in both uncomplicated and pre-eclamptic pregnancies compared to controls.
  • Pre-eclampsia showed increased plasma CAIX, indicating hypoxia, and a paradoxical increase in urinary VEGF excretion.
  • Urinary VEGF and podocyte concentrations correlated with each other and with plasma sFlt-1 levels.

Conclusions:

  • Systemic VEGF inhibition in pre-eclampsia may trigger increased VEGF synthesis in the kidney, potentially in podocytes.
  • Local VEGF overproduction is implicated in the pathogenesis of podocyturia and subsequent renal dysfunction in pre-eclampsia.