Preeclampsia is a multisystem hypertensive disorder of pregnancy characterized by new-onset hypertension (systolic greater than or equal to 140 mmHg or diastolic greater than or equal to 90 mmHg on two occasions at least 4 hours apart) developing after 20 weeks gestation with proteinuria (greater than or equal to 300 mg/24 hours or protein/creatinine ratio greater than or equal to 0.3) or evidence of end-organ dysfunction. The pathophysiology originates from defective trophoblast invasion of the spiral arteries during placentation (weeks 8-18): normally, extravillous cytotrophoblasts remodel spiral arteries into low-resistance, high-capacity vessels by replacing the muscular and endothelial layers. In preeclampsia, this remodeling fails, leaving spiral arteries with intact muscular walls that maintain high resistance, reducing uteroplacental perfusion and creating a hypoxic placental environment. The ischemic placenta releases anti-angiogenic factors into the maternal circulation -- soluble fms-like tyrosine kinase 1 (sFlt-1) binds and neutralizes vascular endothelial growth factor (VEGF) and placental growth factor (PlGF), while soluble endoglin (sEng) impairs TGF-beta signaling in endothelial cells. The resulting systemic endothelial dysfunction causes widespread vasospasm (hypertension), increased vascular permeability (edema, proteinuria), platelet activation and...