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Acute Glomerulonephritis

Glomerulonephritis acuta

For medical students2 min readUpdated 2026-10-10

Acute glomerulonephritis is an acute, immunologically mediated inflammation and injury of the renal glomeruli. The disease is clinically characterized by hematuria, azotemia, oliguria, and hypertension.

LocationRenal glomeruli
MechanismImmune complex-mediated with granular deposits
EtiologyNephritogenic strains of group A beta-hemolytic streptococci
MorphologyDiffuse glomerular hypercellularity
Latency period1–4 weeks post-infection

Etiology and Latent Period

Classic acute poststreptococcal glomerulonephritis typically develops 1–4 weeks following a streptococcal infection of the skin (impetigo) or pharynx (strep throat). It most commonly affects children aged 6–10 years, although patients of any age can be affected.

The causative agents are specific strains of group A $eta$-hemolytic streptococcus possessing nephritogenic properties. In addition to streptococcal infections, sporadic forms of non-streptococcal acute glomerulonephritis occur secondary to other infections:

Pathogenesis and Clinical Presentation

The pathological process is immunological in nature and operates via an immune complex mechanism. The antigens involved include components of the streptococcus itself, as well as endogenous host tissues (glomerular basement membrane and immunoglobulins) modified by bacterial enzymes to act as autoantigens.

The resulting immune response drives the characteristic clinical presentation, including:

Pathology and Microscopy

On gross and microscopic examination, the renal glomeruli are enlarged, hypercellular, and relatively ischemic. The increased cellularity is driven by four factors:

  1. Proliferation and swelling of endothelial cells.
  2. Proliferation of mesangial cells.
  3. Leukocyte infiltration (neutrophils within capillary lumens).
  4. Deposition of immune complexes on the epithelial side of the basement membrane.

The injury is diffuse, involving all lobules of all glomeruli. The combination of cell proliferation, swelling, and inflammatory infiltration leads to the obliteration of capillary lumens. The renal interstitium shows edema and inflammation, while renal tubules exhibit epithelial degeneration and red blood cell casts.

Special Diagnostic Methods

High-precision visualization methods are used for definitive diagnosis:

Mnemonic

Glomerulonephritis means HUMPS on electron microscopy (subepithelial electron-dense deposits), GLOMERULAR HYPERCELLULARITY, and HEMATURIA on urinalysis.

Frequently asked questions

What are the main differences between acute poststreptococcal glomerulonephritis and rapidly progressive glomerulonephritis?

The primary differences lie in the location of the proliferative process, characteristic morphological features, and the rate at which renal failure develops.

FeatureAcute Poststreptococcal GlomerulonephritisRapidly Progressive Glomerulonephritis
Site of ProliferationWithin capillary loops (endocapillary)Outside capillary loops (extracapillary)
MorphologySubepithelial deposits ("humps"), glomerular hypercellularityFormation of glomerular "crescents", foci of necrosis
Course and OutcomeDevelops 1–4 weeks post-infectionRapid progression to end-stage renal failure
What is the primary pathogenic mechanism of acute glomerulonephritis?

The disease is immunologically mediated and develops via an immune complex mechanism, which is confirmed by the detection of granular immune deposits within the glomeruli.

Which cells cause glomerular hypercellularity in this condition?

Hypercellularity results from the proliferation of endothelial and mesangial cells, infiltration by neutrophils, and the accumulation of immune complexes.

What are the characteristic electron microscopy findings in acute poststreptococcal glomerulonephritis?

The identification of electron-dense subepithelial deposits along the basement membrane, frequently shaped like characteristic "humps".

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