Glomerulonephritis
Dr. Isbandiyah, SpPD
Anatomy of the glomerulus
Schematic Representation of a Glomerular Lobe
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Nomenclature • Glomerulonephritis = glomerulopathy →
glomerular injury• Glomerulonephritis: injury with evidence of
inflammation such as leukocyte infiltration, antibody deposition, and or complement activation
• Primary or secundary• Acute (days or weeks), subacute or rapidly
progressive (weeks or few months) and chronic (many months or years)
• Focal (<50%) or diffuse (> 50%) of glomeruli
Nomenclature (cont)
• Proliferative: ↑ glomerular cell number due to infiltration or proliferation
• Sclerosis: ↑ extracellular material of the same ultrastructur and chemical composition as GBM and mesangial matrix.
• Fibrosis: consequence of healing of crescents• Membranous: dominated by expansion of the
GBM by immune deposits.• RPGN: cresentic glomerulonephritis
Glomerular damage - patterns:
Glomerular diseases:
Pathogenesis:
• Immune mechanisms – Most common– Autoimmune– Planted Antigen– Immune complex.
• Toxins• Metabolic
Pathogenesis of Immune GN:
1. Ab, Ag/Ab or Immune complex deposition.2. Immune reaction3. Inflammation Activation of complement4. destruction of glomerular structure5. Renal dysfunction, Proteinuria, Hematuria
Immune Glomerulonephritis:
Interrelation of pathologic and clinical manifestation of glomerular injury
• Minimal change glomerulopathy• Membranous glomerulopathy• Focal segmental glomerulosclerosis• Mesangioploriferative
glomerulopathy• Membranoploriferative
glomerulonephritis• Proliferative glomerulonephritis• Acute diffuse proliferative
glomerulonephritis• Cresentic glomerulonephritis
Nephrotic syndrome
Nephritic syndrome
Clinical Syndromes:• Asymptomatic– Proteinuria, hematuria
• Nephritic syndrome.– Oliguria, Haematuria, mild proteinuria, mild oedema, HT.
• Nephrotic syndrome.– Gross proteinuria, hyperlipidemia, severe oedema,
hypoalbuminemia• Acute renal failure (RPGN).- Oliguria, loss of Kidney function - within weeks
• Glomerulonephritis chronic (CKD)– HT, renal insuf, proteinuria,
Nephritic Syndromes :
• Diffuse Proliferative GNDiffuse Proliferative GN– Post Streptococcal.
• Rapidly Progressive GN (or Crescentic)Rapidly Progressive GN (or Crescentic)– Post Streptococcal, Goodpasture’s,
• Focal GlomerulonephritisFocal Glomerulonephritis– Primary: Bergers disease (IgA Nephritis)– Secondary IgA nephritis, Henoch Schonlein
purpura, SBE, Coeliac Disease etc.
Post Streptococcal GN (Prol.GN):
• 1-4 weeks following streptococcal infection (nephritogenic strains)
• Immune mediated (time for Ab formation)• Granular deposits of IgG,IgM & C3 in GBM,
(subepithelial location common)
Pathogenesis of Diffuse PGN:• Streptococcal infection - Immune complex Streptococcal infection - Immune complex
deposition, inflammation & proliferation.deposition, inflammation & proliferation.• Glomerular capillary obstruction:Glomerular capillary obstruction:– J.G.A stimulation – Renin – high blood pressure– Reduced filtration – raised blood urea– Fluid retention – Oedema
• Damage to GBM:Damage to GBM:– Unselective proteinuria (form Pr. casts in tubule)– Haematuria (form RBC casts in tubule)
Diffuse Proliferative GN:
• Hyperplasia of epithelium & endothelium.
• Cell Swelling.• Inflammatory cells.• Obstruction to flow.• Enlarged hypercellular
glomeruli.
Normal
ProliferativePost strepto
Complications:
Chronic Glomerulonephritis:
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