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CVPR > CVPR Week 8: Renal diseases Part A > Flashcards

CVPR Week 8: Renal diseases Part A Flashcards

1
Q

Glomerular diseases

A
  • Minimal change disease
  • Focal segmental glomerulosclerosis
  • Membranous nephropathy
  • Mesangio-proliferative GN
  • Membrano-proliferative GN (MPGN)
  • Proliferative GN
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2
Q

GN AKA

A

Glomerulonephritis

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3
Q

Renal biopsy for glomerular diseases is assessed by?

A
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4
Q

Stains for light microscopy renal biopsies

A
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5
Q

Patterns of glomerular injury as seen through PAS

A
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6
Q

What is the purpose of immunofluorescence microscopy in renal disease

A

To check for abnormal immune deposits in a patient’s glomerulus

Such as IgG, IgA, IgM, C3, C1q, kappa, lambda

and in what kind of pattern is it granular or linear

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7
Q

Identify

A
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8
Q

Features of nephrotic syndrome

A
  • Massive proteinuria - Loss of >=3.5 g of protein per day
  • Hypalbuminuria - plasma albumin levels <3 g/dL
  • Generalized edema
  • Hyperlipidemia and lipiduria
  • typically insidious onset
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9
Q

Nephrotic syndrome onset

A

insidious onset

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10
Q

Membranous nephropathy etiology

A
  • Primary - ~75% of cases are idiopathic
  • Secondary - associated with systemic diseases
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11
Q

Systemic diseases that can lead to membranous nephropathy

A
  • Systemic lupus erythematosus
  • Infections (chronic hepatitis B and C
  • Malignancies (lung, colon and melanoma)
  • Drugs (penicillamine, captopril, gold and NSAIDs
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12
Q

Membranous nephropathy onset

A

Insidious onset of nephrotic syndrome

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13
Q

Membranous nephropathy clinical course

A
  • proteinuria persists in >60% of cases
  • 10% progress to renal failure in 10 years
  • <40% develop severe chronic kidney disease
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14
Q

Membranous nephropathy considerations

A

Doesn’t respond well to steroids

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15
Q

Pathogenesis of autoimmune membranous nephropathy

A
  • Linked to certain HLA alleles (HLA DQA1)
  • Autoantigen is phospholipase A2 receptor (PA2R)
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16
Q

Pathogenesis of immune-complex-mediated disease of membranous nephropathy

A
  • Activation of complement
  • Production of proteases and oxidants
  • Causes capillary wall injury and protein leakage
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17
Q

Pathogenesis of secondary disease of membranous nephropathy

A
  • Antigens from infectious microbes (e.g. hepatitis B virus) from immune complexes
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18
Q

Identify

A
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19
Q

Identify

A
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20
Q

Identify

A
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21
Q

Identify

A
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22
Q

Membranous nephropathy features on light microscopy

A
  • Uniform thickening of glomerular capillary wall
  • Spikes on Jones silver stain (are basement membrane material)
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23
Q

Membranous nephropathy features on immunofluorescence microscopy

A

Granular deposits of immunoglobulins and complement

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24
Q

Membranous nephropathy features on electron microscopy

A
  • Subepithelial electron dense deposits (between GBM and podocytes)
  • Spikes
  • Podocyte foot process effacement
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25
Q

IgA nephropathy AKA

A

Mesangio-proliferative GN

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26
Q

Types of proliferative GN

A

Post streptococcal GN

Pauci-immune GN (ANCA disease)

Anti-GBM GN

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27
Q

What is hematuria?

A

red blood cellls in urine

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28
Q

Azotemia =

A
  • decreased GFR
  • but increased creatinine and BUN
29
Q

Nephritic syndrome features

A
  • Hematuria
  • Azotemia
  • Oliguria
  • Mild to moderate proteinuria
  • hypertension
  • acute onset
  • active urine sediment
30
Q

Active urine sediment signifies

A

acute glomerular inflammation

31
Q

What is active urine sediment?

A
  • red cells
  • dysmorphic red cells
  • red cell casts
  • leukocytes
32
Q

Membranoproliferative glomerulephritis AKA

33
Q

Membranoproliferative glomerulonephritis is common in?

A

Adolescents or young adults

34
Q

Membranoproliferative glomerulonephritis nephritic/nephrotic?

A
  • Usually nephritic
  • sometimes nephrotic/nephritic
35
Q

Membranoproliferative glomerulonephritis course of disease

A
  • slowly progressive
  • ~50% develop chronic renal failure in 10 years
36
Q

Membranoproliferative glomerulonephritis treatment considerations

A

steroids or other immunosuppressant usually aren’t beneficial

37
Q

MPGN AKA

A

Membranoproliferative glomerulonephritis

38
Q

Type 1: Membranoproliferative glomerulonephritis pathogenesis

5 listed

A
  • immune complexes (IgG, C3) deposited in glomerulus
  • complement activation
  • alterations of GBM
  • Influx of inflammatory cells
  • Proliferation of glomerular cells (mesangial cells and endothelial cells = endocapillary proliferation)
39
Q

Type 1 Membranoproliferative glomerulonephritis light microscopy features

A
  • glomeruli are hypercellular
  • due to the proliferation of mesangial cells and endothelial cells (endocapillary proliferation) infiltrating leukocytes
  • GBM thickened, double-contours or tram-tracks (duplication of basement membrane)
  • Obstruction of capillary loops
40
Q

Membranoproliferative glomerulonephritis Immunofluoresence microscopy

A

Deposits of IgG and C3 in granular pattern

41
Q

Type 1 Membranoproliferative glomerulonephritis electron microscopy features

A

subendothelial electron-dense deposits

42
Q

Identify

43
Q

Identify

44
Q

Identify

45
Q

Identify

46
Q

Identify

47
Q

Identify

48
Q

Type 1 MPGN light microscopy

A
  • glomeruli are hypercellular
  • Due to the proliferation of mesangial cells and endothelial cells (endocapillary proliferation), infiltrating leukocytes
  • Obstruction of capillary loops
  • GBM thickened, double-contours or “tram-tracks” (duplication of basement membrane)
49
Q

Type 1 MPGN immunofluorescence microscopy

A

Deposits of IgG and C3 in a granular pattern

50
Q

Type 1 MPGN electron microscopy

A

subendothelial electron-dense deposits

51
Q

Type 2 MPGN AKA

A

Dense deposit disease

52
Q

Type 2 MPGN prevalence

53
Q

Type 2 MPGN pathology

A
  • circulating autoantibody termed C3 nephritic factor (C3NeF)
  • electron dense deposits are intramembranous
54
Q

Pauci-Immune GN (ANCA Disease) most common in?

A
  • adults but it also occur in children
55
Q

ANCA disease AKA

A

Pauci-Immune GN

56
Q

Pauci-Immune GN clinical features

A
  • Presents with nephritic syndrome
  • Can present with acute renal failure (medical emergency as it is potentially life-threatening)
  • Treatment: high dose steroids and cyclophosphamide (plasmapheresis is controversial)
57
Q

ANCA =

A

Anti-Neutrophil Cytoplasmic Antibodies

58
Q

What do ANCAs do?

A
  • ANCAs bind to proteins in the cytoplasm of neutrophils
  • ANCAs activate neutrophils
  • Activated neutrophils incite inflammation in the glomeruli
59
Q

Pauci-immune GN pathology

A
  • ANCAs bind to proteins in the cytoplasm of neutrophils
  • ANCAs activate neutrophils
  • Activated neutrophils incite inflammation in the glomeruli
60
Q

Types of ANCAs

A
  • P-ANCA - perinuclear staining against myeloperoxidase (MPO-ANCA)
  • C-ANCA -cytoplasmic staining against proteinase 3 (PR3-ANCA)
61
Q

P-ANCA =

A

Perinuclear staining against myeloperoxidase (MPO-ANCA)

62
Q

C-ANCA =

A

Cytoplasmic staining against proteinase 3 (PR3-ANCA)

63
Q

Identify

64
Q

Pauci-immune GN light microscopy features

A
  • breaks in glomerular capillaries
  • cellular crescents
  • often neutrophils in glomerular tuft
65
Q

Pauci-immune GN immunofluorescence microscopy

A
  • no specific staining (or focal weak non-specific staining)
  • That’s why it’s called PAUCI-immune GN
66
Q

Pauci-immune GN electron microscopy

A

lack of deposits (or scant small deposits present)

67
Q

Clinical Lab test for ANCA

A
  • nutrophils on glass slide are incubated with patient serum
  • ANCA in patient serum bind to neutrophils
  • ANCA are detected with fluorescent anti-human Ig
  • ***Positive staining is abnormal -> ANCA disease***
68
Q

Perinuclear vs cytoplasmic staining

CVPR (93 decks)

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