Focal segmental glomerulosclerosis (FSGS) secondary to HIV nephropathy (HIVAN) shows a characteristic histological variant. Which variant and which ultrastructural feature distinguish HIVAN-associated FSGS?

• A Tip variant with podocyte proliferation at the tubular pole
• B Collapsing variant with reticulotubular inclusions in endothelial cells ✓
• C Perihilar variant with hyalinosis at the vascular pole
• D Cellular variant with endocapillary hypercellularity and IgG deposits

Explanation

HIV-associated nephropathy (HIVAN) presents as the collapsing variant of FSGS, characterised by implosive collapse of the glomerular tuft with overlying podocyte hypertrophy and hyperplasia, plus microcystic tubular dilation with proteinaceous casts. On electron microscopy, tubuloreticular inclusions (interferon-induced structures) are seen within glomerular endothelial cells, reflecting sustained interferon signalling from HIV replication. The tip and perihilar variants have different clinical associations (primary vs. adaptive FSGS). Cellular variant lacks endocapillary deposits.

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

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