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Urinary System Tutorial Glomerulonephritis

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Title: Urinary System Tutorial Glomerulonephritis Author: murphyaj Last modified by: amurphy Created Date: 1/31/2006 9:14:39 PM Document presentation format – PowerPoint PPT presentation

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Title: Urinary System Tutorial Glomerulonephritis


1
Urinary System Tutorial Glomerulonephritis
2
The renal biopsy
  • Glomeruli
  • Glomerulonephritis
  • Renal tubules and Interstitium
  • Acute tubular necrosis
  • Acute interstitial nephritis
  • Chronic tubulointerstitial nephritis
  • Vasculature
  • Nephrosclerosis
  • Renal artery sclerosis

3
Normal structure of the glomerulus
4
Presentation of glomerular disease
  • Nephrotic syndrome / Proteinuria
  • Proteinuria (gt 3.5g protein / day)
  • Hypoproteinaemia
  • Oedema
  • Hyperlipidaemia
  • Nephritic syndrome / Haematuria
  • Haematuria
  • Lesser amounts of proteinuria
  • Hypertension
  • Progressive renal failure

5
Pathogenesis of glomerular disease
  • Immune mediated
  • Immune complex formation/deposition
  • Intrinsic glomerular antigens (anti-GBM)
  • Circulating antigens deposited in glomerulus
    (Membranous)
  • Circulating immune complexes deposited in
    glomerulus
  • Activation of complement
  • Cytokine release
  • Neutrophil / macrophage recruitment and
    activation
  • Activation of coagulation system

6
Pathogenesis of glomerular disease
  • Immune mediated
  • Subepithelial immune complexes
  • less inflammation
  • BM alterations /- podocyte damage
  • Proteinuria
  • Subendothelial immune complexes inflammatory GN
  • more inflammation and cellular proliferation
  • Vessel damage
  • Haematuria
  • BM complexes
  • Either presentation, usually haematuria

7
Pathogenesis of glomerular disease
  • Non-immune mediated
  • Activation of complement
  • inflammatory GN like picture but no immune
    deposits
  • Epithelial cell injury
  • Toxins / cytokines / unknown factors
  • Loss of foot processes
  • Detachment from BM
  • Proteinuria

8
Glomerular response to injury
  • Increased cells (Hypercellularity)
  • Seen in inflammatory diseases
  • Proliferation of mesangial and endothelial cells
  • Inflammatory cells
  • Proliferation of epithelial cells /- crescent
    formation
  • Increased matrix / connective tissue
    (Hyalinization / Fibrosis)
  • Hyalinization accumulation of pink homogenous
    material
  • Plasma protein/BM/Mesangial matrix
  • Eventually leads to Fibrosis
  • Increased basement membrane
  • Thickened capillary loops
  • Increased BM / immune deposits

9
Investigation of glomerular disease
  • Histopathology / Light microscopy
  • Glomeruli
  • Hypercellularity
  • Increased matrix / Hyalinization / Fibrosis)
  • Thickened basement membrane
  • Secondary changes in tubules/interstitium
  • Amount of tubular atrophy and fibrosis is a
    sensitive indicator of prognosis
  • Associated large vessel disease

10
Investigation of glomerular disease
  • Immunofluorescence
  • Formation of immune complexes with deposition of
    antibodies in glomerulus
  • IgG, IgA, IgM
  • Basement membrane, mesangium
  • Linear or granular pattern
  • Electron microscopy
  • Changes in podocytes, basement membranes and
    mesangium
  • Location and presence of immune deposits
    (subepithelial, subendothelial, basement
    membrane)

11
Classification of glomerular disease
  • How many glomeruli?
  • Focal only some glomeruli
  • Diffuse all glomeruli affected
  • How much of a single glomerulus?
  • Segmental only part of the glomerulus
  • Global the entire glomerulus
  • Primary vs Secondary
  • primarily renal disease vs renal complication of
    systemic disease

12
Glomerular diseases associated with nephrotic
syndrome
  • Primary
  • Minimal change disease
  • Membranous GN
  • Focal segmental glomerulosclerosis (FSGS)
  • Secondary
  • Diabetic nephropathy
  • Amyloidosis

13
Glomerular diseases associated with nephritic
syndrome
  • Primary
  • Postinfectious / Diffuse proliferative GN
  • Membranoproliferative GN
  • IgA nephropathy (Mesangioproliferative GN)
  • Crescentic GN
  • Secondary
  • HSP
  • Systemic vasculitis
  • SLE
  • Systemic sclerosis

14
(Minimal change disease)
15
Minimal change disease
  • Commonest cause of nephrotic syndrome in children
  • Can occur in adults
  • Characterised by
  • Lack of glomerular changes on light microscopy
  • Lack of immune deposits
  • Good response to steroids
  • Pathogenesis
  • Circulating factor causing damage to podocytes
    (glomerular epithelial cells)

16
Minimal change disease
  • Light microscopy (LM) Normal
  • Immunofluorescence (IF) Normal (no immune
    deposits)
  • Electron microscopy (EM) Fusion of podocyte
    foot processes

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19
Membranous GN
  • Commonest cause of nephrotic syndrome in adults
  • Idiopathic (85) or secondary (15) to
  • Neoplasms (lung, colon, melanoma)
  • Autoimmune disease (SLE, thyroiditis)
  • Infections (Hep B, syphilis, malaria)
  • Drugs (Penicillamine, gold)
  • 40 progress to chronic renal failure (CRF)
  • Pathogenesis
  • Subepithelial immune deposits
  • Thickening of BM between deposits eventually
    envelopes and covers the deposits

20
Membranous GN
  • Light microscopy (LM)
  • Thickened capillary BM
  • BM spikes on silver stain
  • Immunofluorescence (IF) diffuse granular GBM
    staining
  • Electron microscopy (EM) subepithelial deposits

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25
FSGS
  • Idiopathic or secondary to
  • Other glomerular disease (IgA)
  • Other renal disease (chronic reflux /
    pyelonephritis / interstitial nephritis)
  • Systemic disorder (HIV)
  • Drugs (Heroin)
  • Characterised by
  • Sclerosis of portions of some, not all glomeruli
  • Often progresses to chronic renal failure (CRF)
  • Recurs in 25-50 renal transplants

26
FSGS
  • Light microscopy (LM)
  • Focal segmental sclerosis
  • Some normal glomeruli
  • Immunofluorescence (IF)
  • IgM and C3 deposition in sclerotic areas
  • Electron microscopy (EM)
  • Fusion of podocyte foot processes

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Postinfectious / Diffuse proliferative GN
  • Characterised by
  • Onset 1 4 weeks after upper respiratory /
    cutaneous infection with Group A ?-haemolytic
    streptococci
  • Can occur after a number of other bacterial,
    viral and parasitic infections
  • Elevated antistreptococcal antibody and decreased
    C3
  • Secondary to anti-strep antibodies binding to
    glomerular components
  • Usually resolves within 6 weeks

29
Postinfectious / Diffuse proliferative GN
  • Light microscopy (LM)
  • Diffuse glomerular proliferation
  • Immunofluorescence (IF)
  • Granular BM IgG, IgM, C3
  • Electron microscopy (EM)
  • Subepithelial deposits

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32
Membranoproliferative GN
  • Type I
  • Immune complex disease
  • Idiopathic or secondary to Neoplasm, Autoimmune
    disease, Infections, Drugs
  • Subendothelial immune complexes
  • Type II
  • Complement activation
  • BM deposits (dense deposit disease)
  • 50 progress to chronic renal failure (CRF)
  • High recurrence rate in renal transplants
  • Characterised by
  • Thickened capillary loops
  • Glomerular hypercellularity due to mesangial
    proliferation
  • Mesangial interposition double GBMs (Type I)

33
Membranoproliferative GN
  • Light microscopy (LM)
  • Mesangial proliferation
  • Thickened capillary BM
  • Double BMs on silver stain (Type I)
  • Immunofluorescence (IF)
  • Type I Granular BM and mesangial IgG, IgM, C3
  • Type II Granular BM C3
  • Electron microscopy (EM)
  • Type I Subendothelial deposits and mesangial
    interposition
  • Type II Dense deposits in GBM

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37
IgA Nephropathy Mesangioproliferative GN
  • Pathogenesis
  • Increased mucosal IgA secretion in response to
    inhaled/ingested antigens
  • Glomerular (mesangial) deposition of IgA
  • Characterised by episodic haematuria following
    respiratory tract infections
  • 50 progress to chronic renal failure (CRF)
  • Recurs in 20-60 of transplants
  • Varying histology

38
Mesangioproliferative GN
  • Light microscopy (LM)
  • Increased mesangial matrix
  • Mesangial proliferation
  • Focal sclerosis (FSGS)
  • Immunofluorescence (IF) mesangial IgA
  • Electron microscopy (EM) mesangial deposits

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41
Crescentic GN Rapidly progressive GN
  • Characterised by
  • Glomerular crescents
  • Accumulation of cells in Bowmans space
  • Inflammatory cells, fibrin and epithelial cell
    proliferation
  • Compression of glomerulus
  • Rapidly progressive clinical course
  • Pathogenesis
  • Damage to glomerular vessels
  • Egress of inflammatory cells and fibrin into
    Bowmans space
  • Proliferation of epithelial cells

42
Crescentic GN Rapidly progressive GN
  • Pathogenesis
  • Type I anti-GBM antibodies
  • linear deposition of IgG
  • May bind to alveolar BM in lung Goodpastures
    disease
  • Type II immune complexes
  • Idiopathic or secondary to autoimmune disease or
    other GN
  • SLE
  • HSP
  • IgA nephropathy
  • Postinfectious GN
  • Type III pauci-immune
  • Idiopathic or secondary to systemic vasculitis
  • Wegeners
  • PAN

43
Crescentic GN
  • Light microscopy (LM)
  • Cellular crescents of epithelium and inflammatory
    cells
  • Fibrotic crescents
  • Immunofluorescence (IF)
  • Type I linear IgG
  • Type II granular IgG
  • Type III no deposits
  • Electron microscopy (EM)
  • Type II subendo, mesangial and subepi deposits

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