Paper II
Question
Discuss the etiopathogenesis and urinary findings in poststreptococcal glomerulonephritis
Answer
Etiopathogenesis
- Follows infection (typically pharyngitis or skin infection/impetigo) with specific “nephritogenic” strains of group A beta-haemolytic Streptococcus
- Immune-complex mediated (Type III hypersensitivity) injury — streptococcal antigens (e.g., streptococcal exotoxin B, NAPlr) trigger antibody formation; immune complexes deposit in the glomerulus (either forming in situ or depositing after circulating), activating complement and causing neutrophil-mediated glomerular injury
- Occurs typically 1–4 weeks after the preceding streptococcal infection (the latent period corresponding to the time needed for antibody formation)
- Diffuse proliferative glomerulonephritis results — hypercellular glomeruli due to endothelial/mesangial proliferation and neutrophil infiltration, with characteristic subepithelial “hump-shaped” electron-dense deposits and granular (“lumpy-bumpy”) IgG/C3 deposits on immunofluorescence
Urinary findings
- Haematuria — classically producing “smoky” or “cola-coloured” urine
- Red cell casts (indicating glomerular origin of bleeding)
- Mild to moderate proteinuria (usually sub-nephrotic range)
- Oliguria in more severe cases
- Low serum complement (C3) levels during the acute phase, typically normalizing within weeks