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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
What is the end effect of MGN?
Chronic proteinuria and slow deterioration 40% will develop CRI 10% will die or have CRF
26
What are the treatment options for MGN?
Possibly corticosteroids...but they may be harmful | If secondary, treat the the cause
27
What is the most common cause of nephrotic syndrome in children?
MCD
28
What are associated with MCD?
Atopy (eczema, rhinitis) Post respiratory infection or routine immunization Hodgkin lymphoma
29
How is MCD treated?
Corticosteroids...reverses podocyte damage
30
What causes the symptoms of MCD?
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
What are the micro features of MCD?
Normal glomeruli | Proximal tubules may be filled with lipid
32
What is seen on IF of MCD?
No staining
33
What is seen on EM of MCD?
Diffuse effacement of foot processes of the podocytes | No deposits
34
What are the symptoms of MCD?
Massive proteinuria (mostly albumin) NO renal failure or HTN
35
What is the most common cause of nephrotic syndrome in adults?
FSGS 35% in adults 10% in kids
36
What are associated with FSGS?
HIV Heroin addiction Sickle cell disease Morbid obesity
37
What is thought to be the cause of FSGS symptoms?
Adaptive response to loss of renal tissue--scarring in area of previous necrotizing lesions (like IgA nephropathy)
38
What are the micro features of FSGS?
Collapse of GBM Increased mesangial matrix Hyalinization Possibly foam cells
39
What is seen on EM of FSGS?
Diffuse effacement of foot processes | Focal detachment of epithelial cells from GBM
40
What is seen on IF of FSGS?
Mesangial deposits of IgM and C3 in sclerotic area
41
What are the symptoms of FSGS?
``` Nephrotic sydrome HTN Reduced GFR 50% have ESRD w/in 10 years 20% have CRF w/in 2 years ```
42
Is FSGS easy to treat?
NO Poor response to corticosteroids Recurs post transplantation
43
What are general characteristics of MPGN?
Proliferation of glomerular cells Leukocyte infiltration Changes in GBM
44
Is MPGN nephrotic or nephritic?
Primarily nephrotic...but also can present as nephritic
45
What are associated with MPGN?
Chronic immune complex diseases Partial Lipodystrophy (type II) Alpha-1 antitrypsin defeciency Malignancy (CLL, lymphoma, melanoma)
46
What are the micro features of MPGN?
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
What is seen on IF of MPGN?
Depends on type... Type I: Granular (C3, IgG, C1q, C4) Type II: Granular (C3 only)
48
What is seen on EM of MPGN?
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
What are the symptoms of MPGN?
50% develop CRF w/in 10 years
50
Which type of MPGN is more common?
Type I
51
Is MPGN easy to treat?
NO Steroids and immunosuppressive drugs don't help Commonly recurs post transplant (especially Type II)
52
What is the most common type of glomerulonephritis worldwide?
IgA nephropathy (Berger Disease)
53
What are the symptoms of IgA nephropathy?
Recurrent hematuria | Possibly proteinuria
54
What vascular disease has similar symptoms to IgA nephropathy?
Henoch-Schonlein purpura
55
What are associated with Berger Disease?
Gluten enteropathy | Liver disease...cannot clear IgA
56
What causes the symptoms of IgA nephropathy?
Accumulation of IgA--> IgA gets trapped in glomerulus--> complement pathway attacks
57
What type of disease is Alport Syndrome?
Hereditary nephritis
58
What are the symptoms of Alport Syndrome?
Nephritis Nerve deafness Eye disorders (lens dislocation, cataracts, corneal dystrophy)
59
What is the inheritance of Alport Syndrome?
Mostly X-linked dominant...but also some cases of auto recessive and auto dominant
60
What are the micro features to Alport Syndrome?
Glomeruli with segmental proliferation or sclerosis Mesangial matrix increase Persistence of fetal-like glomeruli Foam cells
61
How does Alport Syndrome cause the symptoms?
Defective GBM synthesis...mutation on COL4A5
62
What is another hereditary glomerular disease that presents with hematuria?
Thin membrane disease
63
What is often the end result of GN's?
Chronic glomerulonephritis
64
Does chronic glomerulonephritis always present with another GN first?
NO
65
What is the most significant finding microscopically of chronic GN?
Globally hyalinized glomeruli
66
What type of nephritis stains with everything and has thickened capillary walls because of subendothelial deposits?
Lupus nephritis
67
What are the 5 patterns of lupus nephritis?
``` Normal Mesangial lupus GN Focal proliferative GN Diffuse proliferative GN Membranous GN ```
68
Which is the most severe pattern of lupus nephritis? Which is the most common pattern of lupus nephritis?
Diffuse proliferative for both
69
Who most commonly gets Henoch-Schonlein Purpura?
3-8yo kids after a URI

Renal pathology CRRABII (4 decks)

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