Soluble fms-like tyrosine kinase-1 (sFlt-1) is elevated in pre-eclampsia. What is its primary pathogenic mechanism?

• A It activates neutrophil extracellular traps (NETs), causing systemic inflammation
• B It directly activates thrombin generation in the maternal circulation
• C It inhibits prostacyclin synthesis, shifting the thromboxane/prostacyclin balance toward vasoconstriction
• D It binds and sequesters circulating VEGF and PlGF, reducing their angiogenic signaling to endothelium ✓

Explanation

sFlt-1 is a truncated, soluble form of the VEGF receptor that lacks the transmembrane and intracellular domains; it circulates freely and antagonizes VEGF and PlGF by binding them before they can reach their endothelial receptors. This anti-angiogenic state impairs endothelial repair, promoting hypertension, proteinuria, and end-organ damage. NET formation and thrombin activation are downstream effects, not the primary sFlt-1 mechanism.

Reference: Williams Obstetrics, 26th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.