In the pathophysiology of pre-eclampsia, the imbalance between sFlt-1 (soluble FMS-like tyrosine kinase-1) and PlGF (placental growth factor) leads to which primary vascular effect?

• A Direct activation of the renin-angiotensin system independent of endothelial injury
• B Platelet activation via thromboxane A2 upregulation independent of endothelial damage
• C Selective inhibition of nitric oxide synthase in the myometrial spiral arteries
• D Antagonism of VEGF and PlGF at their endothelial receptors, causing endothelial dysfunction ✓

Explanation

sFlt-1, produced in excess by the ischemic placenta, is a decoy receptor that binds free VEGF and PlGF, preventing their interaction with endothelial receptors. This leads to widespread endothelial dysfunction, increased permeability, and the clinical features of pre-eclampsia. The sFlt-1/PlGF ratio >38 (Elecsys assay) is now used clinically to rule out pre-eclampsia within 1 week if negative. Platelet and RAS activation are downstream consequences, not the primary mechanism.

Reference: Williams Obstetrics, 26th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.