A 40-year-old HIV-positive patient develops nephrotic syndrome. Renal biopsy shows collapsing focal segmental glomerulosclerosis (FSGS) with microcystic tubular dilatation. Electron microscopy shows prominent tubuloreticular inclusions in endothelial cells. What is the pathogenesis of this lesion?
- A Direct HIV infection of podocytes causing dedifferentiation and proliferation ✓
- B Immune complex deposition triggering complement-mediated podocyte injury
- C Minimal change disease triggered by HIV-induced T-cell dysregulation
- D Membranous nephropathy from HBV co-infection
Correct answer: A. Direct HIV infection of podocytes causing dedifferentiation and proliferation
Explanation
HIV-associated nephropathy (HIVAN) features collapsing FSGS where HIV directly infects podocytes, causing their dedifferentiation, proliferation (podocytes re-enter cell cycle), and collapse of glomerular capillaries. Microcystic tubular dilatation is characteristic. Tubuloreticular inclusions (TRI) in endothelial cells result from interferon-alpha-mediated response and are a hallmark of HIV-related kidney disease. This differs from idiopathic FSGS which has tip lesion variant or NOS pattern without TRI.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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