Minimal change disease in adults shows no abnormality on light microscopy and immunofluorescence, but electron microscopy reveals diffuse podocyte foot process effacement. The primary immunological driver is thought to be:

• A Deposition of IgA immune complexes in the mesangium
• B Anti-GBM antibodies targeting type IV collagen alpha-3 chain
• C In-situ immune complex formation with planted antigens
• D Circulating permeability factor (possibly CD80-mediated T-cell cytokine) ✓

Explanation

Minimal change disease is thought to be mediated by a circulating T-cell derived factor — a proposed 'glomerular permeability factor' possibly related to CD80 (B7-1) overexpression on podocytes — which disrupts the charge barrier of the glomerular filtration membrane. This explains the dramatic response to corticosteroids. Anti-GBM antibodies cause Goodpasture syndrome (nephritic). IgA mesangial deposits are seen in IgA nephropathy.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.