A 32-year-old primigravida at 34 weeks gestation presents with BP 158/106 mmHg, proteinuria 3+, and serum uric acid of 7.8 mg/dL. She complains of epigastric pain and visual disturbances. Her platelet count is 88,000/mm³ and LDH is 780 IU/L. Which component of the sFlt-1/PlGF pathophysiology best explains the development of proteinuria in her condition?

• A Angiotensin II type-1 receptor autoantibodies directly damage the tubular epithelium
• B Elevated TNF-α increases glomerular basement membrane permeability via complement activation
• C Reduced prostacyclin synthesis impairs the glomerular capillary blood flow leading to proteinuria
• D Excess sFlt-1 neutralizes circulating VEGF and PlGF, causing podocyte injury and loss of glomerular endotheliosis ✓

Explanation

In pre-eclampsia, excess anti-angiogenic sFlt-1 (soluble fms-like tyrosine kinase-1) scavenges free VEGF and PlGF (placental growth factor), leading to endothelial dysfunction. In the kidney this manifests as glomerular endotheliosis — swelling of endothelial cells with loss of fenestrae and podocyte damage — producing proteinuria. The other options describe mechanisms with minor or no primary role in proteinuria pathogenesis.

Reference: Williams Obstetrics, 26th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.