Etiology and timeline
Classic acute poststreptococcal glomerulonephritis typically develops 1–4 weeks after a skin or pharyngeal streptococcal infection. This condition is most common in 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 streptococcus, sporadic forms of non-streptococcal acute glomerulonephritis occur in association with other infections:
- Bacterial: staphylococcal endocarditis, pneumococcal pneumonia, meningococcemia.
- Viral: viral hepatitis B, chickenpox, mumps, infectious mononucleosis.
- Parasitic: malaria, toxoplasmosis.
Pathogenesis and clinical presentation
The pathological process has an immunological basis and is mediated through an immune-complex mechanism. The antigens include components of the streptococcus itself, as well as the body's own tissues (glomerular basement membrane and immunoglobulins) damaged by pathogen enzymes and converted into autoantigens.
The immune response leads to a specific clinical presentation comprising:
- Hematuria and red blood cell casts in the urine.
- Oliguria.
- Azotemia.
- Mild to moderate arterial hypertension.
Pathological anatomy and microscopy
On macro- and microscopic examination, the renal glomeruli are enlarged, hypercellular, and relatively ischemic. The increased cellularity is due to four factors:
- Proliferation and swelling of endothelial cells.
- Proliferation of mesangial cells.
- Leukocytic infiltration (neutrophils within capillary lumens).
- Deposition of immune complexes on the epithelial side of the basement membrane.
The involvement is diffuse—affecting all lobules of all glomeruli. The combination of proliferation, swelling, and inflammatory infiltration leads to the obliteration of capillary lumens. Edema and inflammation are observed in the stroma (interstitial tissue), while the tubules exhibit signs of epithelial degeneration and red blood cell casts.
Special diagnostic methods
High-precision imaging and diagnostic methods are used for definitive verification:
- Immunofluorescence microscopy: reveals granular deposits consisting of IgG, IgM immunoglobulins, and C3 complement located in the mesangium and along the glomerular basement membrane.
- Electron microscopy: detects electron-dense deposits on the epithelial side of the membrane (beneath podocytes), which frequently appear as characteristic «humps».
Briefly: answers to topical questions
What are the main differences between acute poststreptococcal glomerulonephritis and rapidly progressive glomerulonephritis?
The main differences lie in the localization of the proliferative process, characteristic morphological features, and the rate of progression of renal failure.
| Sign | Acute poststreptococcal glomerulonephritis | Rapidly progressive glomerulonephritis |
|---|---|---|
| Localization of proliferation | Within capillary loops (intracapillary) | Outside capillary loops (extracapillary) |
| Morphology | Subepithelial deposits ("humps"), glomerular hypercellularity | Formation of "crescents" in Bowman's capsule, foci of necrosis |
| Course and outcome | Develops 1–4 weeks post-infection | Rapid progression of renal failure to end-stage uremia |
Glomerulonephritis features HUMPS under the microscope (electron-dense subepithelial deposits), glomerular HYPERCELLULARITY, and HEMATURIA in lab tests.
Class and exam questions
What is the primary mechanism of development of acute glomerulonephritis?
The disease is immunologically mediated and develops via an immune-complex mechanism, as confirmed by the detection of granular immune deposits in the glomeruli.
Which cells cause glomerular hypercellularity in this pathology?
Hypercellularity develops due to the proliferation of endothelial and mesangial cells, neutrophil infiltration, and the deposition of immune complexes.
What are the characteristic findings of electron microscopy in acute poststreptococcal glomerulonephritis?
Detection of electron-dense subepithelial deposits on the basement membrane, which frequently take the shape of characteristic "humps".
What else to study on this topic
- Intracapillary proliferative glomerulonephritis on histological specimens
- Differential diagnosis of streptococcal and non-streptococcal glomerulonephritis
- The role of complement C3 and immunoglobulins IgG and IgM in immunofluorescence
- Morphological changes in the renal interstitium and tubules during oliguria
- Pathogenetic significance of glomerular basement membrane autoantigens
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