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Acute Renal Failure

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Acute Renal Failure Terry Cook Imperial College London – PowerPoint PPT presentation

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Date added: 10 June 2020
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Title: Acute Renal Failure


1
Acute Renal Failure
  • Terry Cook
  • Imperial College London

2
Acute Renal Failure
  • Rapid loss of glomerular filtration and tubular
    function leading to abnormal water, electrolyte
    and solute balance
  • Occurs over hours to days
  • Usually associated with oliguria. Some patients
    develop non-oliguric ARF eg. After radiocontrast
    media
  • Acute-on chronic renal failure

3
Aetiology of ARF
  • Pre-renal
  • Renal
  • Glomerular
  • Tubulointerstitial
  • Vascular
  • Post-renal

4
Aetiology of ARF
  • Glomerular
  • RPGN
  • Tubulointerstitial
  • Acute tubular necrosis
  • Acute tubulointerstitial nephritis
  • Infection
  • Cast nephropathy
  • Vascular
  • Thrombotic microangiopathy
  • Cholesterol emboli
  • Vasculitis

5
Rapidly Progressive Glomerulonephritis (RPGN)
  • RPGN is a clinical term for clinical
    manifestations that suggest severe crescentic
    glomerulonephritis
  • Crescentic glomerulonephritis may be used for
    glomerulonephritis with any crescents but WHO
    suggests gt50

6
Crescentic glomerulonephritis
  • Crescents are an indication of severity of
    glomerulonephritis rather than its cause
  • Complete pathological diagnosis requires analysis
    of immunofluorescence, electron microscopy and
    serology

7
Natural history of crescents
Breach in integrity of GBM ROS, proteases etc
from inflammatory cells
Cells and fibrin in Bowmans space
Accumulation of macrophages and proliferating
epithelial cells
Apoptosis of cells and laying down of
collagen Fibrocellular crescents and fibrous
crescents
8
Causes of crescentic glomerulonephritis
  • Anti-GBM disease
  • Immune complex disease
  • Pauci-immune

9
Frequency of types of crescentic GN
Any Crescents gt50 crescents Arteritis in Biopsy
Anti-GBM 5 11 3
Immune complex 49 29 14
Pauci-immune 47 61 84
After Jenette and Falk
10
Frequency of types of crescentic GN
Age (years) Age (years) Age (years) Age (years)
10-19 20-39 40-64 gt65
Anti-GBM 15 24 2 11
Immune complex 50 48 30 8
Pauci-immune 35 28 69 82
11
Crescent formation in different glomerular
diseases
Patients with any crescents Patients with gt50 crescents
Anti-GBM disease 95 81
Pauci-immune (ANCA-associated) 90 48
Lupus GN (class III and IV) 40 11
Henoch-Schonlein purpura 53 5
IgA nephropathy 27 5
Postinfectious GN 25 3
Fibrillary GN 20 7
Type I membranoproliferative GN 20 3
12
Crescentic GN Differential diagnosis
Light microscopy Immuno-fluorescence Other
Anti-GBM Synchronous crescents Linear IgG and C3 Circulating anti-GBM antibody
Pauci-immune Focal and segmental necrosis /- vasculitis Scanty ANCA
Immune complex Focal and segmental or global hypercellularity Various Various e.g lupus serology, cryoglobulins etc
13
Anti-GBM disease
  • Presents with RPGN often accompanied by lung
    haemorrhage
  • Rare disorder (1 pmp) predominantly in Caucasian
    populations
  • Characterised by circulating and deposited
    anti-GBM antibodies

14
Immune complex crescentic GN
Immunofluorescence Electron microscopy Clinical
Lupus WHO Class III or IV Full House Deposits at all sites Tubulo-reticular bodies Serology, anti-C1q etc
Henoch Schonlein purpura IgA, C3 Mesangial /- capillary wall deposits Rash, arthralgia, abdominal pain
IgA nephropathy IgA, C3 Mesangial /- capillary wall deposits History of sore throat
Membranoproliferative GN Type I Capillary wall C3 /- others Subendothelial deposits Double contours Infections eg. Hep C Cryoglobulins
Post-infectious GN Capillary wall C3 /- IgG humps ASOT
Fibrillary GN Mesangial IgG, C3 Fibrils
15
Pauci-immune crescentic GN
  • Basic lesion is focal and segmental necrosis
  • Often associated with vasculitis either in kidney
    or elsewhere

16
Pauci-immune crescentic GN - syndromes
  • Limited to kidney
  • Microscopic polyangiitis necrotizing vasculitis
    in other systems including skin, mucous
    membranes, lungs, brain, gastrointestinal tract
    and muscle
  • Wegeners granulomatosis similar lesions to
    microscopic polyangiitis together with
    necrotizing granulomas of the upper and lower
    respiratory tract
  • Churg-Strauss syndrome history of asthma or
    allergic rhinitis and blood eosinophilia
  • N.B. These syndromes cannot be distinguished on
    the basis of renal histology

17
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18
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19
ANCA in small vessel vasculitis
IIF pattern C-ANCA P-ANCA Antigen Proteinase
3 Myeloperoxidase Syndromes WG,MP MP,
renal-limited vasculitis
20
Clinical studies of ANCA
  • Specific and sensitive marker for systemic
    vasculitis
  • ANCA pattern and specificity correlate with
    clinical features
  • Levels correlate with disease activity and extent
  • Rising levels predict relapse

21
European Vasculitis Study Group biopsy findings
  • Biopsies from 96 patients with ANCA-associated
    vasculitis and creatinine lt500 mmol/l
  • Studied
  • GFR0 GFR at presentation
  • GFR18 GFR at 18 months
  • CORGFR18 GFR at 18 months corrected for GFR0

22
European Vasculitis Study Group biopsy findings
  • Predictors for GFR0
  • normal glomeruli
  • glomeruli with crescents
  • Extent of tubular atrophy and interstitial
    fibrosis

23
European Vasculitis Study Group biopsy findings
  • Predictors for CORGFR18
  • glomeruli with fibrinoid necrosis
  • glomeruli with cellular crescents
  • Tubulointerstitial inflammation
  • Tubular atrophy and interstitial fibrosis did not
    predict CORGFR18 even though they correlated with
    GFR18 implying that this was dependent on GFR0

24
European Vasculitis Study Group biopsy findings
  • In ANCA GN the best histological predictors of
    long-term renal function are
  • Normal glomeruli, glomerulosclerosis,
    interstitial fibrosis and tubular atrophy
  • The best predictors of the improvement in renal
    function from 0 to 18 months are
  • Crescents, fibrinoid necrosis and interstitial
    inflammation

25
Acute tubular necrosis
  • Prolonged hypoperfusion
  • Drugs NSAIDs, ACE inhibitors
  • Direct toxicity
  • Drugs eg. Aminoglycosides, cisplatin
  • Radiocontrast agents
  • Haem pigments
  • Snake venom
  • Heavy metals lead , mercury
  • Associated with nephrotic syndrome

26
Acute tubular necrosis
Tubular dilatation Loss of brush
border Epithelial cell vacuolation Detachment of
epithelial cells Granular casts Hyperchromasia
of tubular nuclei Mitoses Calcification
Interstitial oedema Interstitial
inflammation Nucleated rbcs in vasa recta
27
Acute tubulointerstitial nephritis
  • Infectious eg. HIV, BKV, fungi, TB
  • Drugs
  • Post infectious
  • SLE
  • ANCA associated
  • With uveitis (TINU)

28
Acute tubulointerstitial nephritis
  • Interstitial infiltrate of mononuclear cells
  • Mainly T cells and macrophages
  • Tubulitis
  • /- eosinophils
  • May rarely be anti-TBM antibodies

29
Granulomatous tubulointerstitial nephritis
  • Infectious
  • Sarcoidosis
  • Drugs
  • Idiopathic

30
Myeloma Cast Nephropathy
  • Light chains precipitate in tubules
  • Casts are large and eosinophilic may be
    fractured or fragemented
  • Multinucleate giant cells my be found adjacent to
    casts
  • In some cases the casts may stain for amyloid
  • Interstitium typically shows an infiltrate of
    lymphocytes and macrophages

31
Thrombotic microangiopathy
  • Haemolytic-uraemic syndrome
  • Infection particularly verotoxin-producing E.
    coli
  • Drugs CNIs, mitomycin
  • Transplant rejection
  • Antiphospholipid antibodies
  • Post-partum
  • Factor H deficiency
  • Bone marrow transplantation
  • Thrombotic thrombocytopenic pupura
  • Malignant Hypertension
  • Scleroderma

32
Thrombotic microangiopathy
  • Glomeruli
  • Thrombosis
  • Trapped fragmented rbc
  • Thickened capillary walls with subendothelial
    fibrin
  • Ischaemic changes
  • Arterioles fibrinoid
  • Interlobular arteries loose intimal thickening

33
Cholesterol emboli
  • Common cause of unexplained renal failure in
    elderly
  • Predisposing factors
  • Trauma eg catheterisation, surgery
  • Anticoagulation
  • Spontaneous
  • May be slowly progressive
  • May involve glomeruli
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