Figure 4.

Schematic overview of the putative mechanism underlying podocyte replacement in preeclampsia. Hypertension, dysregulation of VEGF, and other factors cause damage and loss of podocytes during preeclampsia, resulting in increased shedding of podocytes into the urine. In preeclampsia, an increase in turnover of podocytes results from increased proliferation of parietal epithelial cells and higher numbers of activated parietal epithelial cells on a podocyte location. As a result of this increased turnover, the absolute number of glomerular podocytes is stable during preeclampsia. The replacement of lost podocytes by activated parietal epithelial cells is a compensatory mechanism that, if sufficient, leads to the resolution of clinical symptoms, including proteinuria. However, if compensation is not sufficient, this mechanism can trigger persistent podocytopathy, with progressive proteinuria and renal function loss later in life, histologically characterized by FSGS. VEGF, vascular endothelial growth factor.