preeclampsia pathophysiology is not completely understood, but relies on endothelial damage due to VEGF dysregulation and recent evidence shows an imbalance between pro-angiogenic and anti-angiogenic molecules: excess of fms-like tyrosine kinase 1 (sFlt-1), a soluble receptor of VEGF, leads to a reduced VEGF effect on glomeruli and damage to the podocytes, with reduced expression of nephrin and synaptopodin (proteins essential for the actin skeletal functions) [63,64,66]. Here, VEGFA is linked to preeclampsia.