Glomerulonephritis

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: