Pathology of Kidney Disorders

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Pathology of Glomerulonephritis
Dr. Venkatesh Murthy Shashidhar Senior Lecturer
in Pathology
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Normal Kidney
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Normal Glomerulus (PAS)
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Anatomy
Cap. loops
J.G.App.
DCT
Afferent.A DCT Efferent.A
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Filtration Unit
1. Fenestrated Endothelium 2. Lamina Rara
Interna 3. Lamina Rara Densa 4. Lamina Rara
Externa 5. Podocytes Slit membrane
Capillary Lumen
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Glomerular Filtration
BLOOD Proteins 3.6nm/70,000MW
Glomerular Capillary Lumen
Plasma - Proteins FILTRATE
Bowmans Capsule Space
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Pathogenesis

• Immune mechanisms Most common
• Autoimmune
• Planted Antigen
• Immune complex.
• Toxins
• Metabolic

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Glomerular diseases
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Pathogenesis of Immune GN

• Ab, Ag/Ab or Immune complex deposition.
• Immune reaction
• Inflammation Activation of complement
• destruction of glomerular structure
• Renal dysfunction, Proteinuria, Hematuria

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Immune Glomerulonephritis
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Glomerular damage - patterns
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Immune Glomerulonephritis

• In-Situ immune complex formation
• Tissue antigens - Goodpasture anti GBM Ag
• Planted antigens - infections, toxins, drugs.
• Circulating immune complex deposition.
• Endogenous - DNA as in SLE
• Exogenous - infections.
• Cell mediated Immune injury

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Immune Glomerulonephritis
C.Immune Complex ANTI-GBM
HEYMANN
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Clinical Syndromes

• Nephritic syndrome.
• Oliguria, Haematuria, Proteinuria, Oedema.
• Nephrotic syndrome.
• Gross proteinuria, hyperlipidemia,
• Acute renal failure (RPGN).
• Oliguria, loss of Kidney function - within weeks
• Chronic renal failure.
• Over months and years - Uremia

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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.

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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)
• Humps in GBM on EM or IF Microscopy

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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)

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Progression of DPGN
Focal segmental glomerulo sclerosis

• Poststreptococcal DPGN

Complete Healing
Tubulo Interstitial Damage
CGN
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Clinical Features G.Nephritis

• Hypertension
• Skin Infections
• Congestive Cardiac Failure

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Laboratory Features G.Nephritis

• Inflammation
• Decreased filtration
• Damage to filtration unit

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Diffuse Proliferative GN

• Hyperplasia of epithelium endothelium.
• Cell Swelling.
• Inflammatory cells.
• Obstruction to flow.
• Enlarged hypercellular glomeruli.

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• Normal

• Proliferative
• Post strepto

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IF- Diffuse Proliferative GN
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Complications
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Glomerular diseases
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Chronic Glomerulonephritis
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Urine Microscopy

• Cells Casts Crystals.
• Casts are formed within nephron.
• Casts Suggest Kidney pathology.
• Casts can be made up of Protein, lipid, cells or
  mixed.
• Crystals suggest high concentration or altered
  solubility.

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Formation of Casts
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Red cell Casts in Urine
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The greatest test of courage is to bear defeat
without losing heart! Robert G. Ingersoll
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Glomerular diseases
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Minimal Change/Lipoid
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Minimal Change Disease
Loss of Foot processes
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Membranous GN
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Crescentic GN - (RPGN)
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Crescentic GN - (Trichrome Stain)
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Goodpasture Syndrome
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Membranous GN
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Focal Segmental Gl. Sclerosis
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Mesangiocapillary GN (MPGN)