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

CVPR Week 8: Renal diseases Part A Flashcards

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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
IgA nephropathy AKA
Mesangio-proliferative GN
26
Types of proliferative GN
Post streptococcal GN Pauci-immune GN (ANCA disease) Anti-GBM GN
27
What is hematuria?
red blood cellls in urine
28
Azotemia =
* decreased GFR * but increased creatinine and BUN
29
Nephritic syndrome features
* Hematuria * Azotemia * Oliguria * Mild to moderate proteinuria * hypertension * acute onset * active urine sediment
30
Active urine sediment signifies
acute glomerular inflammation
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What is active urine sediment?
* red cells * dysmorphic red cells * red cell casts * leukocytes
32
Membranoproliferative glomerulephritis AKA
MPGN
33
Membranoproliferative glomerulonephritis is common in?
Adolescents or young adults
34
Membranoproliferative glomerulonephritis nephritic/nephrotic?
* Usually nephritic * sometimes nephrotic/nephritic
35
Membranoproliferative glomerulonephritis course of disease
* slowly progressive * ~50% develop chronic renal failure in 10 years
36
Membranoproliferative glomerulonephritis treatment considerations
steroids or other immunosuppressant usually aren't beneficial
37
MPGN AKA
Membranoproliferative glomerulonephritis
38
Type 1: Membranoproliferative glomerulonephritis pathogenesis 5 listed
* 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
Type 1 Membranoproliferative glomerulonephritis light microscopy features
* 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
Membranoproliferative glomerulonephritis Immunofluoresence microscopy
Deposits of IgG and C3 in granular pattern
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Type 1 Membranoproliferative glomerulonephritis electron microscopy features
subendothelial electron-dense deposits
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Identify
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Identify
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Identify
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Identify
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Identify
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Identify
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Type 1 MPGN light microscopy
* 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
Type 1 MPGN immunofluorescence microscopy
Deposits of IgG and C3 in a granular pattern
50
Type 1 MPGN electron microscopy
subendothelial electron-dense deposits
51
Type 2 MPGN AKA
Dense deposit disease
52
Type 2 MPGN prevalence
Very rare
53
Type 2 MPGN pathology
* circulating autoantibody termed C3 nephritic factor (C3NeF) * electron dense deposits are intramembranous
54
Pauci-Immune GN (ANCA Disease) most common in?
* adults but it also occur in children
55
ANCA disease AKA
Pauci-Immune GN
56
Pauci-Immune GN clinical features
* 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
ANCA =
Anti-Neutrophil Cytoplasmic Antibodies
58
What do ANCAs do?
* ANCAs bind to proteins in the cytoplasm of neutrophils * ANCAs activate neutrophils * Activated neutrophils incite inflammation in the glomeruli
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Pauci-immune GN pathology
* ANCAs bind to proteins in the cytoplasm of neutrophils * ANCAs activate neutrophils * Activated neutrophils incite inflammation in the glomeruli
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Types of ANCAs
* P-ANCA - perinuclear staining against myeloperoxidase (MPO-ANCA) * C-ANCA -cytoplasmic staining against proteinase 3 (PR3-ANCA)
61
P-ANCA =
Perinuclear staining against myeloperoxidase (MPO-ANCA)
62
C-ANCA =
Cytoplasmic staining against proteinase 3 (PR3-ANCA)
63
Identify
64
Pauci-immune GN light microscopy features
* breaks in glomerular capillaries * cellular crescents * often neutrophils in glomerular tuft
65
Pauci-immune GN immunofluorescence microscopy
* no specific staining (or focal weak non-specific staining) * That's why it's called PAUCI-immune GN
66
Pauci-immune GN electron microscopy
lack of deposits (or scant small deposits present)
67
Clinical Lab test for ANCA
* 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
Perinuclear vs cytoplasmic staining

CVPR (93 decks)

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