A 30-year-old woman presents with gross hematuria, fever, flank pain, and arthralgia 2 weeks after a streptococcal pharyngitis. Urinalysis shows red cell casts and proteinuria. Serum complement C3 is markedly reduced with normal C4. Anti-streptolysin O (ASO) titre is elevated. What is the MOST likely underlying mechanism of glomerular injury?
- A Subepithelial immune complex deposition activating classical complement pathway ✓
- B Anti-GBM antibody-mediated linear IgG deposition
- C ANCA-mediated pauci-immune necrotizing glomerulonephritis
- D Mesangial IgA deposition with alternative complement pathway activation
Explanation
Post-streptococcal glomerulonephritis (PSGN) classically presents 1–3 weeks after pharyngitis (or 3–6 weeks after skin infection) with nephritic syndrome. The hallmark is subepithelial 'hump-shaped' immune complex deposits seen on EM, containing IgG and C3, which activate the classical complement pathway, consuming C3 while leaving C4 relatively normal (alternative pathway activation also contributes). Reduced C3 with normal C4 is a key serological pointer to PSGN and MPGN. Anti-GBM disease (Goodpasture's) shows linear IgG on IF. ANCA-associated GN is pauci-immune (no/minimal deposits on IF) and has no infectious link. IgA nephropathy typically follows mucosal infections with only days between infection and hematuria, with mesangial IgA deposits.
Reference: Harrison's Principles of Internal Medicine, 21st ed.
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Written and medically reviewed by the StethoPrep medical team.