You are currently viewing Acute post-streptococcal glomerulonephritis: Pathogenesis, Morphology
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Acute post-streptococcal glomerulonephritis is developed after streptococcal bacterial infection in children and young adults. It is the most common disorder in developing countries in the world.

Age group: Most frequently present in children between 6-10 years of age, but may develop in adults.

Etiology and Pathogenesis of Acute post-streptococcal glomerulonephritis

  • Follows streptococcal infection (hence post-streptococcal infection) rather than direct primary infection of the kidney by bacteria streptococci.
  • Primary streptococcal infection generally involves the part of the pharynx (pharyngitis) or the skin area (impetigo/pyoderma).
  • Infections of Skin are usually associated with scarlet fever, overcrowding, and poor hygiene.
  • Certain strains of group Aβ -hemolytic streptococci are nephritogenic. More than 90% are due to types 12, 4, and 1.
  • The streptococcal antigenic component responsible for immune reaction in acute post-streptococcal glomerulonephritis is streptococcal pyogenic exotoxin B (SpeB) in most but not all cases.
  • The latent period of 1 to 4 weeks following primary streptococcal infection.
  • Immune-complex mediated disease.

Mechanism of Damage

  • Immune complexes are formed in the circulation and get deposited within glomeruli.
  • Immune complexes initiate inflammation via. activating complement & other humoral & cellular mediators of inflammation.
  • The inflammatory mediators attract and activate neutrophils and monocytes and stimulate the proliferation of the mesangial and endothelial cells.
  • The result is Hypercellular glomerulus.

Presentation (LAB FINDINGS)

  • Hematuria 1-3 weeks following group A streptococcal infection.
  • Periorbital edema.

Morphology of Acute post-streptococcal glomerulonephritis


  • The kidneys are enlarged and show a pale capsular surface and cortex.


Acute post-streptococcal glomerulonephritis

Light Microscopy (LM)

  • Glomeruli:
    • Increased cellularity  (Proliferation of mesangial, endothelial, and neutrophils).
    • The hypercellularity is due to;
      • Infiltration by leukocytes (neutrophils and monocytes).
      • Proliferation and swelling of endothelial and mesangial cells.
      • Rarely proliferation of parietal cells lining Bowman’s capsule.
    • Diffuse involvement.
    • Obliteration or eradication of glomerular capillary lumen:  Due to swelling and proliferation of endothelial cells & mesangial cells + infiltration by leukocytes.
  • Tubules:
    • Contains red cell casts in the lumen and the tubular epithelial cells may show degenerative changes.
  • Interstitium:
    • Edema and inflammatory cell infiltrate.
  • Blood vessels: Unremarkable.

Immunofluorescence Microscopy

  • Granular deposits of IgG, IgM, and C3 in the mesangium and along with the GBM →granular fluorescence.

Electron microscopy

  • Sub-epithelial“humps” (Immune complexes deposit).
  • Sub-epithelial deposits of discrete,  amorphous, electron-dense deposits are a characteristic feature.

Clinical Course

Acute proliferative glomerulonephritis:

  • Periorbital edema.
  • Mild to moderate hypertension.
  • An affected child develops
    • Malaise
    • Fever
    • Nausea
    • Oliguria
    • Hematuria (smoky or cola-colored urine) 1 to 2 weeks after sore throat recovery.
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