A 40-year-old man with HIV infection develops nephrotic syndrome. Renal biopsy shows collapsing focal segmental glomerulosclerosis (FSGS) with microcystic tubular dilatation and no immune deposits on immunofluorescence. What is the underlying pathogenetic mechanism?
- A Direct HIV infection of podocytes causing dysregulated proliferation and collapse of the glomerular tuft ✓
- B Circulating permeability factor (soluble urokinase receptor) causing podocyte foot process effacement
- C Immune complex deposition of HIV antigens with IgA in the mesangium
- D T-cell mediated cytokine injury identical to primary FSGS not otherwise specified
Explanation
HIV-associated nephropathy (HIVAN) presents as collapsing FSGS and is caused by direct HIV infection of podocytes and tubular epithelial cells, driving dedifferentiation, hypertrophic proliferation, and collapse of the capillary tuft. The absence of immune deposits on immunofluorescence and the specific collapsing morphology with microcystic tubules distinguishes HIVAN from immune complex-mediated nephropathies. It occurs predominantly in individuals of African descent.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
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Written and medically reviewed by the StethoPrep medical team.