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Flashcards

Glomerular disease

roatf1 nephrology University English 59 cards

Cards in this deck (59)

  1. 1what are the general consequences of GN?inflammation of the glomeruli and nephrons:
    1) glomerular damage -> restricted blood flow -> compensatory HTN
    2) filtration mechanism damaged -> protein + blood in the urine
    3) loss of filtration capacity -> AKI
  2. 2what is the general spectrum of disease encountered with GN?depends on degree of inflammation and cause but:
    1) BP - normal to malignant
    2) urine dipstick - proteinuria (mild to nephrotic) and haematuria (mild to macroscopic)
    3) renal function - normal to severe impairment
  3. 3what syndromes might someone with a GN present with?nephrotic
    nephritic
  4. 4what is the gist of nephrotic syndrome?normal BP to mild HTN
    proteinuria >3.5g/day
    normal GFR to mild impairment
  5. 5describe the gist of the nephritic syndrome?moderate to severe HTN
    mild - macro haematuria
    moderate to severe GFR impairment
  6. 6what are the 1y causes of nephrotic syndrome?membranous GN
    minimal change dz
    FSGS
    mesangiocapillary GN
  7. 7what are the 2y causes of nephrotic syndrome?DM
    SLE (class V nephritis)
    amyloid
    hep B/C
  8. 8what are the 1y causes of nephritic syndrome?IgA nephropathy
    mesangiocapillary GN
  9. 9what are the 2y causes of nephritic syndrome?post strep GN
    vasculitis
    SLE
    anti -GBM dz (goodpastures)
    cryoglobulinaemia
  10. 10what investigation categories are appropriate for the GN?bloods
    Urine
    Imaging
    renal bx
  11. 11bloods in GN?FBC
    U+E
    ESR
    CRP
    Ig
    electrophoresis
    complement (C3,4)
    autoab: ANA, ANCA, anti-dsDNA, anti-GBM
    blood culture
    ASOT
    HBsAg, anti-HCV
  12. 12urine tests in GN?RBC casts
    MC+S
    Bence jones protein
    ACR
  13. 13what imaging is appropriate in GN?CXR
    renal USS
  14. 14why renal bx in GN?gives most information
    can classify the GN
    1) what? (mesangial cells, capillaries, BM, endothelium)
    2) extent? (focal vs diffuse)
    3) glomerular extent? (segmental vs global)
    4) IF (Ig deposition, complement, immune complexes, pauci immune)
    5) EM
  15. 15general mangt in GN?refer to nephrologist
    keep BP <130/80 or <125/75 if proteinuria >1g/d
    ACEI or ARB - no benefit from dual therapy
  16. 16what is IgA nephropathy?commonest GN in developed world
    macro/micro haematuria
    sometimes nephritic syndrome
  17. 17who is the typical IgA nephropathy patient?young male
    episodic macroscopic haematuria
    elevated IgA possibly from infection which forms immune complexes and deposits in mesangial cells
  18. 18renal bx in IgA nephropathy?mesangial proliferation
    IF - deposits of IgA + C3
  19. 19Tx of IgA nephropathy?BP control w/ ACEi
    if nephritic then IS can slow decline of renal fxn
    px worse if HTN, male, proteinuria or renal failure at presentation, 20% develop ESRF over 20 yrs
  20. 20what is henoch schonlein purpura?systemic variant of IgA nephropathy
    small vessel vasculitis
  21. 21what are the features of HSP?purpuric rash on extensor surfaces esp legs
    flitting polyarthritis
    abdo pain (GI bleeding)
    nephritis
  22. 22dx HSP?clinical
    confirm w/ IF +ve for IgA + C3 in skin or renal bx (same as IgA nephropathy)
  23. 23tx for HSP?same as for IgA nephropathy
    15% nephritic go to ESRF
    if nephritic + nephrotic 50% go to ESRF
  24. 24what is anti-GBM dz?anti glomerular basement membrane
    also called goodpastures
    auto ab to type 4 collagen
    pulmonary haemorrhage can also occur as type 4 collagen also in BM in lung
  25. 25presentation and tx for anti-GBM dz?haematuria/nephritic syndrome
    AKI
    tx - plasma exchange, steroids +/- cytotoxics- start early and can have full recovery w/ relapses rare
    px poor if dialysis dependent at presentation
  26. 26what is post strep GN?diffuse, proliferative
    1-12 wks post sore throat/skin infxn
    strep ag deposited on glomerulus - host reaction + immune complex formation
  27. 27how does post strep GN present?nephritic syndrome
  28. 28how is post strep GN dx?clinical - history
    bx usually not done unless atypical presentation - inflammation of mesangial and endothelial cells, IF: IgG + C3
    serology - ASOT elevated + elevated C3
  29. 29tx post strep GN?supportive - 95% regain fxn
  30. 30what is rapidly progressive GN?most aggressive
    can cause ESRF in days
    3 categories - all have crescents affecting the glomeruli on bx
  31. 31what are the categories of RPGN?immune complex dz- 45%
    pauci-immune dz - 50%, most ANCA +ve
    anti-GBM dz - 3%
  32. 32what immune complex dz cause RPGN?post infectious
    SLE
    IgA/HSP
  33. 33what pauci immune dz cause RPGN?granulomatosis w/ polyangiitis (wegener's)
    microscopic polyangitis
    churg strauss
  34. 34what are the clinical features of RPGN?AKI +/- systemic features (fever, myalgia, wt loss, haemoptysis)
    pulm haemorrhage commonest COD in anca+ve
  35. 35tx for RPGN?high dose IV steroids + cyclophosphamide +/- plasma exchange
    5 yrs @80%
  36. 36what is the nephrotic syndrome?proteinuria >3.5g/d
    hypoalbuminaemia (<25g/L)
    oedema - always dipstick when oedema so don't miss renal dz
    also often severe hyperlipidaemia - total chol >10
  37. 37what is the pathophysiology of the nephrotic syndrome?podocyte injury - usually wrap around glomerular capillaries and maintain filtration barrier - breakdown = heavy protein loss
  38. 38what kind of oedema do nephrotic syndrome patients have?pitting
  39. 39what is the ddx for nephrotic syndrome?CCF - check JVP, pulm oedema, usually mild proteinuria
    liver dx - would be low albumin
  40. 40what to suspect in children w/ nephrotic syndrome?minimal change dz
    trial of steroids will resolve most - avoid bx unless no steroid response or if likely another cause EG: <1yr, family hx, extrarenal dz eg arthritis, rash, anaemia; renal failure, haematuria.
  41. 41assessment of nephrotic syndrome in adults?renal bx + full Gn assessment
  42. 42why might renal bx be difficult in pt w/ nephrotic syndrome?hypercoagulable state
    gross oedema
  43. 43what are the complications of nephrotic syndrome?infection - cellulitis, strep, SBP - due to low serum IgG, low complement and low T cell fxn (IS tx)
    thromboembolism - DVT/PE, renal vein thrombosis. hypercoagulable - increased clotting factors + plt abnormalities
    hyperlipidaemia - high chol + triglycerides - from hepatic lipoprotein synthesis in response to low oncotic pressure
  44. 44how is nephrotic syndrome tx-ed?1) reduce oedema - loop diuretics (IV as gut oedema can prevent oral absorption) Fluid and salt restrict, monitor wt.
    2) reduce proteinuria - ACEi/ARB
    3) reduce complications - anticoagulate, start statin, tx infections and vax (pneumovax II, flu)
    4) tx underlying cause - infxn, malignancy, systemic dz, stop drugs.
  45. 45what can cause MCD in adults?idiopathic
    NSAIDs
    hodgkin's lymphoma
  46. 46what is MCD on bx?normal on LM
    EM - effaced podocyte foot processes
  47. 47tx for MCD?most remiss w/ steroids but ALSO relapse
    frequent relapses - cyclophophamide/tacromilus/ciclosporin
    px - <1% go to ESRF
  48. 48what is membranous nephropathy?most idiopathic
    malignancy/ hep B, gold/penicillamine/NSAIDs
    AI - thyroid, SLE
    dx - diffusely thick GBM + IgG + C3 deposits on IF
  49. 49tx for membranous nephropathy?tx underlying cause
    idiopathic - ACEi/ARB, diuretics
    complete spontaneous remission 30%
    partial spontaneous remission 24-40% @ 5yrs
    future - IS tx as phospholipase A2 receptor ab in 80%
  50. 50what is mesangiocapillary GN?two types
    IC mediated
    complement mediated
  51. 51what is IC mediated MCGN?immune complexes deposit in kidney + activate complement
    usually underlying cause eg hep C, SLE, monoclonal gammopathy
  52. 52what is complement mediated MCGN?less common type
    persistent activation of alternative complement pathway (unlike IC - classical)
    can have extra-renal probs eg drusen
  53. 53bx in MCGN?mesangial and endocapillary proliferation
    thick capillary BM
    double countouring (tramline) capillary walls
    IF - Ig staining, complement or light chains
    EM - electron dense deposits
  54. 54what is the tx for MCGN?underlying cause
    ACEi/ARB for all
    IS if rapid progression - steroids/cyclophos
    px - poor where no underlying cause, ESRF can recur in transplants
  55. 55what is FSGS?focal segmental glomerular sclerosis
    idiopathic/secondary
    presents as nephrotic syndrome or proteinuria
  56. 56what are the 2y causes of FSGS?vesicoureteric reflux
    IgA nephropathy
    Alport's syndrome
    vasculitis
    sickle cell
    heroin
    HIV - associated with the collapsing subtype - poor px
  57. 57bx findings in FSGS?segmental scarring of some glomeruli
    IF - IgM + C3 deposits
  58. 58what is the tx for FSGS?corticosteroids in 30%
    cyclophosphamide/ciclosporin
  59. 59what is the px for FSGS?untx - ESRF
    spontaneous remission <10%
    if present w/ abnormal renal fxn - poorer px - 30-50% to ESRF
    recurs in 20% transplanted kidneys - may respond to plasma exchange

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University nephrology Flashcards on Glomerular disease, created by roatf1 on 27/10/2014.
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