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Renal pathology CRRABII > 10.30 > Flashcards

10.30 Flashcards

1
Q

In glomerular talk, what does “diffuse” mean?

A

All glomeruli are involved

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2
Q

In glomerular talk, what does “focal” mean?

A

A proportion of glomeruli are involved

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3
Q

In glomerular talk, what does “global” mean?

A

Entire single glomerulus is involved

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4
Q

In glomerular talk, what does “segmental” mean?

A

Portion of single glomerulus is involved

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5
Q

What is Goodpasture disease?

A

Autoimmune disease with Ab’s against components of the GBM (NC1 of the alpha3 chain of type IV collagen)

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6
Q

How does Goodpasture disease present on IF?

A

Linear pattern…the GBM is continuous

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7
Q

Besides the GBM what else can the Goodpasture antibody affect?

A

Alveolar basement membrane

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8
Q

What does the Heymann antigen bind to?

A

The membrane of the basal surface of visceral epithelial cells (podocytes)

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9
Q

What does IF of Heymann affected people look like?

A

Granular

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10
Q

What does EM of Heymann affected people look like?

A

Electron dense deposits along the subepi aspect of the GBM

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11
Q

What causes nephritic syndromes?

A

Inflammatory and Proliferative diseases

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12
Q

What causes nephrotic syndromes?

A

Damage to Podocytes

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13
Q

What are examples of nephritic syndromes?

A 
Acute Post-streptococcal GN
Rapidly Progressive (Crescentic) GN
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14
Q

What are examples of nephrotic syndromes?

A

Membranous GN [MGN]
Minimal Change Disease (Lipoid Nephrosis) [MCD]
Focal Segmental Glomerulosclerosis [FSGS]
Membranoproliferative GN [MPGN]

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15
Q

Who is affected by MGN?

A

Adults

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16
Q

What causes MGN?

A

85% idiopathic (unknown cause)

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17
Q

What are some drugs associated with MGN?

A

Penicillamine
Captopril
Gold
NSAIDS

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18
Q

What type of malignancies are associated with MGN?

A

Lung
Colon
Melanoma

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19
Q

What other conditions are associated with MGN?

A

SLE
Various infections
Diabetes Mellitus
Thyroiditis

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20
Q

What causes the symptoms of MGN?

A

Ag-Ab mediated disease (exo or endo)

Complement mediates GBM damage

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21
Q

Micro features of MGN?

A

Normocellular glomeruli
Uniform, diffuse thickening of capillary wall

Later features: mesangial sclerosis and glomerular hyalinization

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22
Q

What is seen on a silver stain of MGN?

A

Spikes…correspond to BM material laid down b/w deposits

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23
Q

What is seen on IF of MGN?

A

Granular deposits (IgG and C3) along GBM

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24
Q

What is seen on EM of MGN?

A

Subepithelial deposits
Later, spike of BM b/w deposits
Eventually thickened BM with lucent defects–because deposits are resorbed
Effacement of foot processes

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25
Q

What is the end effect of MGN?

A

Chronic proteinuria and slow deterioration

40% will develop CRI
10% will die or have CRF

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26
Q

What are the treatment options for MGN?

A

Possibly corticosteroids…but they may be harmful

If secondary, treat the the cause

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27
Q

What is the most common cause of nephrotic syndrome in children?

A

MCD

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28
Q

What are associated with MCD?

A

Atopy (eczema, rhinitis)
Post respiratory infection or routine immunization
Hodgkin lymphoma

29
Q

How is MCD treated?

A

Corticosteroids…reverses podocyte damage

30
Q

What causes the symptoms of MCD?

A

Visceral epithelial injury:
Possible T cell dysfunction and release of cytokines that damage the podocytes
Loss of charge barrier or adhesion defects b/w epithelial cells

31
Q

What are the micro features of MCD?

A

Normal glomeruli

Proximal tubules may be filled with lipid

32
Q

What is seen on IF of MCD?

A

No staining

33
Q

What is seen on EM of MCD?

A

Diffuse effacement of foot processes of the podocytes

No deposits

34
Q

What are the symptoms of MCD?

A

Massive proteinuria (mostly albumin)

NO renal failure or HTN

35
Q

What is the most common cause of nephrotic syndrome in adults?

A

FSGS

35% in adults
10% in kids

36
Q

What are associated with FSGS?

A

HIV
Heroin addiction
Sickle cell disease
Morbid obesity

37
Q

What is thought to be the cause of FSGS symptoms?

A

Adaptive response to loss of renal tissue–scarring in area of previous necrotizing lesions (like IgA nephropathy)

38
Q

What are the micro features of FSGS?

A

Collapse of GBM
Increased mesangial matrix
Hyalinization
Possibly foam cells

39
Q

What is seen on EM of FSGS?

A

Diffuse effacement of foot processes

Focal detachment of epithelial cells from GBM

40
Q

What is seen on IF of FSGS?

A

Mesangial deposits of IgM and C3 in sclerotic area

41
Q

What are the symptoms of FSGS?

A 
Nephrotic sydrome
HTN
Reduced GFR
50% have ESRD w/in 10 years
20% have CRF w/in 2 years
42
Q

Is FSGS easy to treat?

A

NO

Poor response to corticosteroids
Recurs post transplantation

43
Q

What are general characteristics of MPGN?

A

Proliferation of glomerular cells
Leukocyte infiltration
Changes in GBM

44
Q

Is MPGN nephrotic or nephritic?

A

Primarily nephrotic…but also can present as nephritic

45
Q

What are associated with MPGN?

A

Chronic immune complex diseases
Partial Lipodystrophy (type II)
Alpha-1 antitrypsin defeciency
Malignancy (CLL, lymphoma, melanoma)

46
Q

What are the micro features of MPGN?

A

Similar for type I and type II

Large, hypercellular glomeruli with lobular architecture
Thickened GBM…silver stains as tram track–mesangial cell interposition into the GBM

47
Q

What is seen on IF of MPGN?

A

Depends on type…
Type I: Granular (C3, IgG, C1q, C4)
Type II: Granular (C3 only)

48
Q

What is seen on EM of MPGN?

A

Depends on type…
Type I: subendo deposits +/- subepi and mesangial deposits
Type II: Dense deposit disease–lamina densa is ribbon-like and extremely electron dense due to deposits of unknown material

49
Q

What are the symptoms of MPGN?

A

50% develop CRF w/in 10 years

50
Q

Which type of MPGN is more common?

A

Type I

51
Q

Is MPGN easy to treat?

A

NO

Steroids and immunosuppressive drugs don’t help
Commonly recurs post transplant (especially Type II)

52
Q

What is the most common type of glomerulonephritis worldwide?

A

IgA nephropathy (Berger Disease)

53
Q

What are the symptoms of IgA nephropathy?

A

Recurrent hematuria

Possibly proteinuria

54
Q

What vascular disease has similar symptoms to IgA nephropathy?

A

Henoch-Schonlein purpura

55
Q

What are associated with Berger Disease?

A

Gluten enteropathy

Liver disease…cannot clear IgA

56
Q

What causes the symptoms of IgA nephropathy?

A

Accumulation of IgA–> IgA gets trapped in glomerulus–> complement pathway attacks

57
Q

What type of disease is Alport Syndrome?

A

Hereditary nephritis

58
Q

What are the symptoms of Alport Syndrome?

A

Nephritis
Nerve deafness
Eye disorders (lens dislocation, cataracts, corneal dystrophy)

59
Q

What is the inheritance of Alport Syndrome?

A

Mostly X-linked dominant…but also some cases of auto recessive and auto dominant

60
Q

What are the micro features to Alport Syndrome?

A

Glomeruli with segmental proliferation or sclerosis
Mesangial matrix increase
Persistence of fetal-like glomeruli
Foam cells

61
Q

How does Alport Syndrome cause the symptoms?

A

Defective GBM synthesis…mutation on COL4A5

62
Q

What is another hereditary glomerular disease that presents with hematuria?

A

Thin membrane disease

63
Q

What is often the end result of GN’s?

A

Chronic glomerulonephritis

64
Q

Does chronic glomerulonephritis always present with another GN first?

A

NO

65
Q

What is the most significant finding microscopically of chronic GN?

A

Globally hyalinized glomeruli

66
Q

What type of nephritis stains with everything and has thickened capillary walls because of subendothelial deposits?

A

Lupus nephritis

67
Q

What are the 5 patterns of lupus nephritis?

A 
Normal
Mesangial lupus GN
Focal proliferative GN
Diffuse proliferative GN
Membranous GN
68
Q

Which is the most severe pattern of lupus nephritis? Which is the most common pattern of lupus nephritis?

A

Diffuse proliferative for both

69
Q

Who most commonly gets Henoch-Schonlein Purpura?

A

3-8yo kids after a URI

Renal pathology CRRABII (4 decks)

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