A 10-year-old boy with post-streptococcal glomerulonephritis has electron microscopy showing subepithelial 'hump-shaped' electron-dense deposits. Immunofluorescence shows coarse granular IgG and C3 deposits in a 'starry sky' pattern. Which complement pathway is primarily activated?
- A Alternative pathway via streptococcal products acting as properdin stabilizers ✓
- B Classical pathway via IgG immune complexes activating C1q
- C Mannose-binding lectin (MBL) pathway triggered by streptococcal mannose
- D Terminal complement pathway (C5b-9 MAC) exclusively, without early complement involvement
Explanation
Post-infectious GN (classically post-streptococcal GN) primarily activates the alternative complement pathway, evidenced by low C3 levels with normal C4 levels (C4 is consumed in classical and MBL pathways but not the alternative pathway). Streptococcal cationic proteins (nephritis-associated plasmin receptor NAPR, and SpeB/SPEB) plant in the glomerular basement membrane and directly activate the alternative pathway. The IgG in IF may reflect passive antibody trapping rather than primary immune complex deposition. This distinguishes it from lupus nephritis (classical pathway, low C3 and C4).
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.