A 6-year-old boy presents with periorbital oedema and heavy proteinuria. Renal biopsy shows normal glomeruli on light microscopy, negative immunofluorescence, and fusion (effacement) of podocyte foot processes on electron microscopy. What is the underlying pathophysiological mechanism of proteinuria?

• A Immune complex deposition activates complement causing GBM disruption
• B Anti-GBM antibodies cause linear IgG deposits and GBM fragmentation
• C Mesangial proliferation narrows glomerular capillaries reducing filtration
• D Loss of podocyte slit diaphragm integrity disrupts the filtration barrier, allowing albumin loss ✓

Explanation

Minimal change disease (MCD) is characterised by effacement of podocyte foot processes on EM without immune deposits. Injury to the podocyte slit diaphragm proteins (nephrin, podocin) disrupts the charge and size barrier, leading to massive selective proteinuria of albumin. It is the most common cause of nephrotic syndrome in children and responds to steroids. Anti-GBM disease (Goodpasture) shows linear IgG.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.