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Burt's Renal Final > Renal Immuno > Flashcards

Renal Immuno Flashcards

(67 cards)

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1
Q

How do you define AKI

A

Rapid decrease in kidney function as measured by an increase in serum creatinine

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2
Q

Impairment of kidney filtration is activated by ______________ in vascular and tubular cells

A

ATP depletion

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3
Q

What are the causes of kidney hypoperfusion

A

Sepsis, medications, decreased effective circulating volume, hypotension, hepatorenal syndrome

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4
Q

Kidney injury that doesn’t heal correctly can lead to

A

Renal tissue fibrosis

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5
Q

Why is kidney damage hard to track

A

Often not identified until 60-70% of kidney has been damaged beyond repair

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6
Q

What is the main cause of kidney injury that we look at

A

Ischemia

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7
Q

What is the general inflammation cascade

A
  1. Ischemic event
  2. Cytokine release
  3. Expression of adhesion molecules
  4. Increased permeability
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8
Q

What happens to small arterioles in post-ischemic kidney disease

A

They vasoconstrict due to decreased production of NO

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9
Q

What are the inflammatory cytokines that we are looking at

A

TNFα, IL-1β, IL-6, IL-12, IL-15, IL-18

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10
Q

Besides inflammation, what else does small vessel occlusion lead to

A

Activation of the coagulation system

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11
Q

What are the main end-effects of ischemic AKI

A
  1. Reduced GFR
  2. High FE_Na
  3. Concentrating defects
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12
Q

What is the main signal of sterile inflammation

A

Release of DAMPs or ALARMINS

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13
Q

What are the main DAMPs released by parenchymal cells

A

HMGB1 (nucleolus), uric acid, HSPs (heat shock proteins from exosomes), Hyaluronans in ECM, S100 protein in cytoplasm

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14
Q

What are DAMPs recognized by? What does this activate

A

TLR; NF-κB

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15
Q

What TLR recognizes DAMPs

A

TLR-4

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16
Q

What cells in the inflammation process migrate to LN

A

Dendritic cells

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17
Q

What do dendritic cells function in

A

Acute kidney injury and infections

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18
Q

What is the function of macrophages in acute kidney injury

A

Continue to present signals to T cells to keep them active

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19
Q

What induces M1 macrophages

A

PAMPs/DAMPs, IFN-γ

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20
Q

What type of macrophages are in charge of the acute phase

A

M1

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21
Q

What do M1 macrophages primarily produce

A

ROS, NO, lysosomal enzymes, IL-1, IL-12, IL-23

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22
Q

What induces M2 macrophages

A

IL-13 and IL-4

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23
Q

What do M2 macrophages produce

A

TGFβ and IL-10

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24
Q

What does TGFβ do

A

Serves as a chemotractant for repair cells (fibroblasts)

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25
What cells predominate in the M1 response
Neutrophil, NK cell, Th1/17
26
What cells predominate in the M2 response
Th2 and Treg
27
What does the severity of the immune response depend on?
The ratio of M1:M2 cells that respond
28
What has shown the best results as a renal disease inhibitor
Complement inhibitors; anti-C5
29
Deficiency of what has protected mice from ischemic injuries? What worked the best
C3a receptor or C5a receptor; C5a receptor
30
How do we determine degree of complement activation
changes in level of C3 and C4 in blood (C3 being highest); C3a and C5a in the urine or plasma
31
What type of cells are rarely found in healthy kidney tissue
Mast cells
32
What are the main causes of fibrosis in kidneys
TGFβ and Ang II
33
What can also generate Ang II besides ACE
Chymase
34
What participate in tissue remodeling
Tryptase, chymase, and carboxypeptidase A
35
What influences T cells to become Th1
IL-12
36
What influences T cells to become Th2
IL-4
37
What influences T cells to become Treg
TGFβ
38
What influences T cells to become Th17
TGFβ and IL-6
39
What do Th1 cells produce
IFNγ and T-bet
40
What do Th2 cells produce
IL-4 and GATA3
41
What do Tregs produce
TGFβ and FoxP3
42
What do Th17 cells produce
IL-17 and RORγT
43
Early stages of the adaptive immune response are mediated by
Th17
44
At later stages of the adaptive immune response, what cells are prevailing
Th1
45
What do Th1 produce and what do they activate
IFNγ; resident macrophages
46
The outcome of the inflammatory disease depends on
The balance between pro- and anti-inflammatory immune cells
47
What recruits neutrophils
IL-17
48
What do Th17 produce that recruits monocytes and Th1 cells
CCL20
49
What switches M1 macrophages to M2
Treg
50
Type II hypersensitivity is what
Ab against tissue Ags and complement
51
What are type III hypersensitivities
Soluble Ag-Ab complexes
52
What can increase the likelihood of successful xenografts
Inserting human genes
53
When is ABO matching not important
Non-vascularized tissues - corneal transplants - heart valve transplantation - bone and tendon grafts
54
ABO incompatibility is/isn’t important in stem cell transplants
Isn’t
55
What is the universal recipient
AB; they have no AB in their blood
56
What is the universal donor
O; they don’t have an Ag present
57
Why are class 1 HLA so important for transplantation
All cells have type 1
58
What cells don’t express type 1 HLA
RBC and platelets
59
What makes it difficult for a mother to receive transplant from her kids
Pregnancy has induced HLA sensitization
60
How do we test HLA 1? 2?
Measure intracellular dye after exposing them to different ABs in serum; proliferation of cells
61
What causes direct allorecognition? Indirect?
Donor dendritic cells activate host T cells and you get direct CTL killing; recipient DC samples graft and activates response and you get Ab and inflammatory cytokines
62
Direct rejection v. Indirect
Direct - CTL | Indirect - CD4+ and Ab
63
What causes humoral rejection
Th2
64
What causes cellular rejection
Th1
65
What causes hyperacute rejection? Accelerated? Acute? Chronic?
Preformed Ab and complement; reactivation of sensitized T cells; primary activation of T cells; immunologic and non-immunologic factors alike
66
How are host v. graft carried out
FasL and Fas; binding of perforin and granzyme
67
What is graft v. host disease
Donor APC activate donor CD8

Burt's Renal Final (7 decks)

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