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. 2. 3. 4. 5. Ab, Ag/Ab or Immune complex deposition. Immune reaction Inflammation Activation of complement destruction of glomerular structure 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 GN
Post Streptococcal.

Rapidly Progressive GN (or Crescentic)

Post Streptococcal, Goodpastures,

Focal 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 deposition, inflammation & proliferation. Glomerular capillary obstruction:
J.G.A stimulation Renin high blood pressure Reduced filtration raised blood urea Fluid retention Oedema

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

Proliferative Post strepto

Complications:

Chronic Glomerulonephritis: