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Renal Involvement in Preeclampsia: Similarities to VEGF Ablation Therapy

By Janina Müller-Deile and Mario Schiffer


Glomerular VEGF expression is critical for the maintenance and function of an intact filtration barrier. Alterations in glomerular VEGF bioavailability result in endothelial as well as in podocyte damage. Renal involvement in preeclampsia includes proteinuria, podocyturia, elevated blood pressure, edema, glomerular capillary endotheliosis, and thrombotic microangiopathy. At least the renal signs, symptoms, and other evidence can sufficiently be explained by reduced VEGF levels. The aim of this paper was to summarize our pathophysiological understanding of the renal involvement of preeclampsia and point out similarities to the renal side effects of VEGF-ablation therapy

Topics: Review Article
Publisher: Hindawi Publishing Corporation
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Provided by: PubMed Central

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  1. (2003). A randomized trial of bevacizumab, an anti-vascular endothelial growth factor antibody, for metastatic renal cancer,”
  2. (2009). Acute and transient podocyte loss and proteinuria in preeclampsia,”
  3. (2010). Anti-vascular endothelial growth factor (VEGF) therapy: a new cause of hypertension,”
  4. (2002). B.C.Kuenen,M.Levi,J.C.M.Meijersetal.,“Analysisofcoagulation cascade and endothelial cell activation during inhibition of vascular endothelial growth factor/vascular endothelial growthfactorreceptorpathwayincancerpatients,”Arteriosclerosis, Thrombosis,
  5. (1999). Eitner et al., “VEGf mediates glomerular endothelial repair,”
  6. (2002). Exaggerated hypotensive effect of vascular endothelial growth factor in spontaneously hypertensive rats,”
  7. (2003). Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction hypertension, and proteinuria in preeclampsia,”
  8. (2003). Functional evidence thatvascularendothelialgrowthfactormayactasanautocrine factoronhumanpodocytes,”AmericanJournalofPhysiology—
  9. (2010). G i l b e r t ,J .V e r z w y v e l t ,D .C o l s o n ,M .A r a n y
  10. (2010). Glomerular structure andfunctionrequireparacrine,notautocrine,VEGF-VEGFR2 signaling,”
  11. (2010). Gr¨ unwald et al., “Renal side effects of VEGF-blocking therapy,”
  12. (1998). Hypoxia and endothelin-1 induce VEGF production in human vascular smooth muscle cells,”
  13. (1995). i m o n ,H .J .G r o n e ,O .J o h r e ne ta l . ,“ E x p r e s s i o no f vascular endothelial growth factor and its receptors in human renal ontogenesis and in adult kidney,”
  14. Inhibition of tyrosine kinases by sunitinib associated with focal segmental glomerulosclerosis lesion in addition to thrombotic microangiopathy,”
  15. (2005). Investigation of vascular responses in endothelial nitric oxide synthase/cyclooxygenase-1 double-knockout mice: key role for endothelium-derived hyperpolarizing factor in the regulation of blood pressure in vivo,”
  16. (2002). KDR (VEGF receptor 2) is the major mediator for the hypotensive effect
  17. (2005). Managing patients treated with bevacizumab combination therapy,”
  18. (2004). Maternal serum sFlt1 concentration is an early and reliable predictive marker of preeclampsia,”
  19. Nephrotic syndrome after bevacizumab: case report and literature review,” AmericanJournalofKidneyDiseases,vol.49,no.2,pp.e23–e29,2007.
  20. (2003). Neutralization of circulating vascular endothelial growth factor (VEGF) by anti-VEGF antibodies and soluble VEGF receptor 1 (sFlt-1) induces proteinuria,”
  21. P at el,J .A.M o rgan,G.D .De metrietal.,“ Ap r eec lampsialike syndrome characterized by reversible hypertension and proteinuria induced by the multitargeted kinase inhibitors sunitinib and sorafenib,”
  22. (2006). P.L.Zhang,J.W.Prichard,F.Linetal.,“Chronicactivethrombotic microangiopathy in native and transplanted kidneys,”
  23. (2008). Parietal epithelia cells in the urine as a marker of disease activity in glomerular diseases,”
  24. (2007). Petrovic et al., “Glomerular expression of nephrin and synaptopodin, but not podocin, is decreased in kidney sections from women with preeclampsia,”
  25. (2008). PlGF and sFlt-1 as markers for predicting pre-eclampsia,”
  26. (2007). Possible molecular mechanisms involved in the toxicity of angiogenesis inhibition,”
  27. (2005). Preeclampsia: a renal perspective,”
  28. (2008). r e m i n a
  29. (2010). Rapid development of hypertension and proteinuria with cediranib, an oral vascular endothelial growth factor receptor inhibitor,”
  30. (2007). Recombinant vascular endothelial growth factor 121 attenuates hypertension and improves kidney damage in a rat model of preeclampsia,”
  31. (2009). Renal effects of antiangiogenesis therapy: update for the internist,”
  32. (2007). Renal thrombotic microangiopathy caused by anti-VEGF-antibody treatment for metastatic renal-cell carcinoma,”
  33. (2007). Role of the VEGF-A signaling pathway in the glomerulus: evidence for crosstalk between components of the glomerular filtration barrier,”
  34. (2006). Soluble endoglin contributes to the pathogenesis of preeclampsia,”
  35. (2009). The balance of autocrine
  36. (1990). The Hellp Syndrome: is this a clinical form of thrombotic angiopathy?”
  37. (2007). Thrombotic microangiopathy and anti-VEGF agents,”
  38. (2009). Thrombotic microangiopathy secondary to VEGF pathway inhibition by sunitinib,”
  39. (2009). Thrombotic thrombocytopenia purpura (TTP) and other thrombotic microangiopathies,” Best Practice and Research: Clinical Haematology,
  40. (2007). Toward a mouse model of diabetic nephropathy: is endothelial nitric oxide synthase the missing link?”
  41. (2007). Urinary podocyte excretion as a marker for preeclampsia,”
  42. (2005). Urinary podocyte loss is a more specific marker of ongoing glomerular damage than proteinuria,”
  43. (2000). Vascular endothelial growth factor accelerates renal recovery in experimental thrombotic microangiopathy,”
  44. (1999). Vascular endothelial growth factor signals endothelial cell production of nitric oxide and prostacyclin through Flk-1/KDR activation of c-Src,”