Preeclampsia (PE) is a unique pathophysiologic situation that physiologic interests of mother, fetus, and placenta diverge. PE is related to the increased circulating antiangiogenic factors originated from hypoxic placenta. It is simply defined by the new onset of hypertension (≥140/90 mmHg) and proteinuria (≥0.3 g/day) after 20 weeks of gestation. PE is associated with kidney dysfunction due to deficiency in podocyte specific vascular endothelial growth factor (VEGF). Hypoxic placenta in PE patients produces increased levels of fms-like tyrosine kinase 1(sFlt-1), a soluble receptor of VEGF. sFlt-1 abrogates binding of VEGF to its receptor on endothelial cells and podocytes, and ultimately damages the filtration barrier. Glomerular endotheliosis and thrombotic microangiopathy (TMA) are the main features of kidney involvement in PE and can induce clotting and vessel occlusion. This complex pathophysiology is ameliorated after delivery; however, permanent kidney damages may remain and is intensified thereafter. This review aims to highlight the biochemical, genetic, and immunological-involved factors in the initiation of PE and explores the relationship between the kidney and PE. This work mainly discusses the pathologic mechanisms of kidney involvement in PE through the lens of the imbalanced VEGF-VEGF receptor signaling pathway.