Preeclampsia is a frequent cause of maternal and fetal morbidity and mortality worldwide. The underlying causes of this hypertensive complication have remained elusive. The placenta seems to be at the origin of the disease, as its removal appears to be the only effective treatment available. Many organs can potentially be affected. Nonetheless, kidney alterations are always present: proteinuria is one of the hallmarks for a preeclampsia diagnosis. VEGF is pivotal for maintaining glomerular filtration barrier function; hence, the elevated concentrations of placental-derived VEGF inhibitors, such as sFlt-1, may largely explain the renal alterations observed. Classically, glomerular endothelial injury was considered responsible for the renal impairment present in preeclampsia. Recent findings, however, have shown that podocytes are crucial in explaining the loss of filtration capacity of the preeclamptic kidney. The aims of this manuscript are to detail the main findings that associate podocyte injury with proteinuria in preeclampsia, and discuss the eventual applications of podocyte damage biomarkers in clinical practice.