In pre-eclampsia, the imbalance between sFlt-1 (soluble FMS-like tyrosine kinase-1) and PlGF (placental growth factor) leads to endothelial dysfunction primarily through which mechanism?

• A PlGF excess drives trophoblastic invasion beyond the decidua, triggering maternal immune activation
• B sFlt-1 activates complement cascade causing glomerular endotheliosis directly
• C Elevated PlGF/sFlt-1 ratio indicates placental insufficiency and predicts IUGR
• D sFlt-1 sequesters free VEGF and PlGF, preventing their endothelial-protective signaling ✓

Explanation

sFlt-1 is an anti-angiogenic protein elevated in pre-eclampsia that acts as a decoy receptor, binding free VEGF and PlGF in the circulation and preventing them from interacting with their endothelial receptors. This impairs endothelial NO production and causes widespread endothelial dysfunction. PlGF is reduced (not elevated) in pre-eclampsia; a low PlGF/sFlt-1 ratio predicts pre-eclampsia. Complement activation is secondary to endothelial injury.

Reference: Williams Obstetrics, 26th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.