UPSC MainsMEDICAL-SCIENCE-PAPER-I201710 Marks
Q25.

Describe the gross and microscopic features of acute proliferative glomerulonephritis.

How to Approach

This question requires a detailed understanding of the pathological features of acute proliferative glomerulonephritis (APGN). The answer should be structured to first define APGN, then describe its gross features (what the kidney looks like macroscopically), followed by a comprehensive description of the microscopic features observed under light, immunofluorescence, and electron microscopy. Emphasis should be placed on the characteristic findings in each examination. A clear and organized presentation is crucial for a good score.

Model Answer

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Introduction

Acute proliferative glomerulonephritis (APGN), historically often following streptococcal infections (post-streptococcal glomerulonephritis), is a form of acute nephritic syndrome characterized by inflammation and proliferation of glomerular cells. It’s an immune-mediated disease resulting from the deposition of immune complexes within the glomeruli. While the incidence has decreased in developed countries due to improved antibiotic treatment of streptococcal infections, it remains a significant cause of acute kidney injury globally. Understanding its pathological features is crucial for diagnosis and management. This answer will detail the gross and microscopic characteristics of APGN.

Gross Features

The kidneys in APGN typically exhibit characteristic gross changes. Initially, the kidneys may appear normal in size or slightly enlarged. However, as the disease progresses, the following features become apparent:

  • Size: Kidneys are often enlarged and heavier than normal, reflecting edema and inflammation.
  • Color: The cortical surface appears pale and mottled due to congestion and edema.
  • Capsule: The renal capsule is easily stripped off.
  • Cut Surface: On cut section, the cortex shows prominent, diffuse swelling and congestion. Subcapsular fat is often prominent.

Microscopic Features

Light Microscopy

Light microscopy reveals several key features:

  • Glomerular Hypercellularity: This is the hallmark of APGN. The glomeruli show a marked increase in cellularity due to proliferation of mesangial, endothelial, and inflammatory cells (neutrophils, monocytes).
  • Capillary Luminal Occlusion: The glomerular capillary lumens are often narrowed or occluded by inflammatory cells and thrombi.
  • Inflammatory Cell Infiltration: Neutrophils and monocytes infiltrate the glomeruli and the surrounding interstitium.
  • Crescent Formation: In severe cases, crescent-shaped structures may form, representing proliferation of parietal epithelial cells and accumulation of fibrin and inflammatory cells within Bowman's space.
  • Tubular Changes: Tubular epithelial cells may show swelling, flattening, and even necrosis.

Immunofluorescence Microscopy

Immunofluorescence microscopy is critical for identifying the immune deposits characteristic of APGN:

  • Granular Deposits: A characteristic granular pattern of IgG and C3 deposition is seen along the glomerular basement membrane (GBM) and in the mesangium. IgA is typically absent, differentiating it from IgA nephropathy.
  • Distribution: The deposits are typically diffuse and circumferential, affecting all glomeruli.
  • Intensity: The intensity of staining can vary depending on the stage of the disease.

Electron Microscopy

Electron microscopy provides the highest resolution view of the glomerular pathology:

  • Subepithelial Humps: Dense, electron-dense deposits (immune complexes) are seen as “humps” located on the epithelial side of the GBM. These are characteristic, though not always present, in post-streptococcal APGN.
  • Mesangial Deposits: Electron-dense deposits are also found within the mesangium.
  • GBM Thickening: The GBM may show mild thickening.
  • Podocyte Foot Process Effacement: The foot processes of podocytes may be effaced, contributing to proteinuria.

Differential Diagnosis: It’s important to differentiate APGN from other forms of glomerulonephritis, such as membranoproliferative glomerulonephritis (MPGN) and rapidly progressive glomerulonephritis (RPGN). MPGN shows thickening of the GBM and mesangial interposition, while RPGN is characterized by extensive crescent formation.

Microscopic Feature Light Microscopy Immunofluorescence Electron Microscopy
Immune Deposits Not directly visible Granular IgG and C3 Subepithelial "humps", mesangial deposits
Glomerular Cellularity Increased (hypercellularity) Not directly assessed Proliferation of cells
GBM Normal or mildly thickened Not directly assessed Mild thickening

Conclusion

Acute proliferative glomerulonephritis presents with distinct gross and microscopic features. The hallmark findings include glomerular hypercellularity on light microscopy, granular IgG and C3 deposits on immunofluorescence, and subepithelial “humps” on electron microscopy. Accurate identification of these features is essential for diagnosis, differentiation from other glomerulonephritides, and appropriate management. Early diagnosis and treatment are crucial to prevent progression to chronic kidney disease.

Answer Length

This is a comprehensive model answer for learning purposes and may exceed the word limit. In the exam, always adhere to the prescribed word count.

Additional Resources

Key Definitions

Glomerulonephritis
Inflammation of the glomeruli, the filtering units of the kidneys, leading to kidney damage.
Mesangium
The central supporting structure of the glomerulus, composed of mesangial cells and extracellular matrix.

Key Statistics

Globally, glomerulonephritis affects an estimated 3-10 per million people annually. (Data as of 2022, based on various epidemiological studies)

Source: National Kidney Foundation

Approximately 10% of patients with post-streptococcal glomerulonephritis progress to end-stage renal disease within 20 years. (Based on long-term follow-up studies, knowledge cutoff 2023)

Source: Journal of the American Society of Nephrology

Examples

Post-Streptococcal Glomerulonephritis

A classic example of APGN, occurring 1-3 weeks after a streptococcal infection (e.g., strep throat or skin infection). It’s more common in children.

Frequently Asked Questions

What is the role of complement in APGN?

Complement activation plays a crucial role in the pathogenesis of APGN. C3 deposition is a key feature, and complement activation contributes to glomerular inflammation and injury.

Topics Covered

PathologyNephrologyKidney DiseaseGlomerulonephritisHistology