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Excessive salt intake does not cause preeclampsia. Although salt can influence blood pressure, preeclampsia is not a salt-sensitive condition. The disorder arises from placental malperfusion, not dietary sodium. Studies show no consistent link between sodium intake and preeclampsia incidence.

Increased cardiac output and plasma volume are normal physiological adaptations in pregnancy. These changes support fetal growth and do not cause preeclampsia. In fact, preeclampsia often presents with reduced plasma volume and vasoconstriction, not hypervolemia. The pathology is vascular, not volume-driven.

Overproduction of placental prostacyclin is not implicated in preeclampsia. Prostacyclin is a vasodilator and platelet inhibitor. In preeclampsia, there is a relative deficiency of prostacyclin and excess thromboxane A2, leading to vasoconstriction and platelet aggregation. The imbalance favors hypertension and endothelial damage.

Increased production of nitric oxide does not occur in preeclampsia. In fact, nitric oxide synthesis is reduced due to endothelial damage. This contributes to vasoconstriction and impaired uteroplacental perfusion. The imbalance favors vasoconstrictors like endothelin-1 and thromboxane A2.

Decreased vascular sensitivity to angiotensin II is incorrect. In preeclampsia, there is increased sensitivity to angiotensin II, contributing to hypertension. The vasculature responds excessively to circulating vasoconstrictors due to endothelial dysfunction and reduced nitric oxide.

Reduced platelet activation and aggregation is inaccurate. Preeclampsia is associated with increased platelet activation, leading to microthrombi formation and consumption of platelets. This contributes to thrombocytopenia and disseminated intravascular coagulation in severe cases.

Hepatic microvascular thrombosis is associated with HELLP syndrome, not the renal findings described. It causes elevated liver enzymes and right upper quadrant pain, not oliguria or creatinine rise. The renal pathology in preeclampsia is glomerular, not hepatic.

Increased glomerular filtration rate is a normal pregnancy adaptation, not a feature of preeclampsia. In preeclampsia, GFR is reduced due to glomerular endotheliosis and vasoconstriction. Elevated creatinine and oliguria reflect decreased filtration, not enhancement.

Immune complex deposition is characteristic of glomerulonephritis, not preeclampsia. Preeclampsia lacks immune-mediated inflammation or complement activation. The renal lesion is non-inflammatory, with endothelial swelling and capillary narrowing

Excessive prostacyclin production and vasodilation are not features of HELLP syndrome. In preeclampsia and HELLP, prostacyclin is reduced, favoring vasoconstriction and platelet aggregation. Vasodilation would oppose thrombosis and organ ischemia, which are central to HELLP pathology.

Autoimmune destruction of red blood cells is characteristic of autoimmune hemolytic anemia, not HELLP. HELLP involves mechanical fragmentation of red cells due to microvascular thrombi, not antibody-mediated lysis. Coombs test is negative in HELLP.

Decreased fibrin deposition is incorrect. HELLP involves increased fibrin deposition in microvasculature, contributing to thrombotic microangiopathy. This leads to platelet consumption, hemolysis, and organ damage. Reduced fibrin would not explain thrombocytopenia or liver injury.