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Renal I Final > Renal Immunology > Flashcards

Renal Immunology Flashcards

1
Q

No Kidney Disease

A

GFR greater than 60

Stable serum creatinine

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2
Q

Acute Kidney Injury

A

No structural changes
Increase in serum creatinine levels by 50%
Oliguria

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3
Q

Chronic Kidney Injury

A

GFR less than 60 for more than 3 months

Structural changes

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4
Q

Risk factors for Kidney disease

A 
GARD HM
Genetics
Age
Race
Diabetes
Hypertension
Metabolic syndrom
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5
Q

What two things can an ischemic acute kidney injury lead to? What is it the major cause of?

A

Lead to metabolic acidosis and ATP depletion

Major cause of acute renal failure.(ARF)

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6
Q

What is usually the cause of AKI (Acute Kidney injury)

A

Sterile Inflammation

causes hypoxic state in the kidney

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7
Q

Steps that lead to Sterile Inflammation

A
  1. Cells recodnize DAMPS
  2. CRP protein binds DAMPs
  3. Complement pathway activated
  4. Immune cells recognize DAMPs via Toll-like receptors
  5. Inflammation
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8
Q

5 Types of Alarmins

A 
HMGB1
Uric acid
HSPs
S100 protein
Hyaluronans in ECM
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9
Q

What cell type is responsible for mediating immune response to AKI in early stages?

A

Th17 cells

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10
Q

What cell type is responsible for mediating immune response against AKI in later stages?

A

Th1

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11
Q

M1/M2 polarization

A 
M1 = Acute Kidney Injury
M2 = Tissue repair
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12
Q

How are M1 macrophages activated?

A
  • PAMPs and DAMPs bind TLRs and PRRs

- IFN-y promotes differentiation

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13
Q

How are M2 macrophages activated?

A
  • IL-4 and IL-13
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14
Q

What causes Chronic AKI?

A

Persistent activation of M2 –> leads to constant production of myofibroblasts —> they keep making connective tissue and this can lead to fibrosis/stenosis!

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15
Q

Effects of Th1 cells

A

Produce IFN-y

- Antigen presentation and cellular immunity

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16
Q

Effects of Th2 cells

A

Produce IL-4, IL-5, IL-13

- Humoral immunity and allergy

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17
Q

Effects of Th17 cells

A

Produce IL-17

- Tissue inflammation

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18
Q

How does Th17 contribute to the progression of damage in AKI?

A

Th17 cells produce IL-17, which will recruit neutrophils and induce a specific chemokine pattern that ultimately secrete CCL20 (MIP-3), which will promote infiltration of monocytes.

This recruitment will lead to the progression of damage.

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19
Q

What types of hypersensitivity are associated with AKI?

A

Hypersensitivity II and III

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20
Q

Type II Hypersensitivity rxns

A

Anti-glomerular basement membrane AB-mediated GN

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21
Q

Type II Hypersensitivity rxns

A

Post-strepp GN
RA
SLE

22
Q

Types of HVG responses

A 
Hyperacute = immediate, caused by Antibodies
Acute = days to weeks, caused by T-cells
Chronic = months to years, caused by vascular trauma
23
Q

GVH responses

A

Donor lymphocytes attack the host.

  • Seen in bone marrow or parenchymal tissue grafts
  • Perfusion pressure also causes damage
24
Q

Autografts

A

graft taken from body and put somewhere else on same body

25
Q

Isograft

A

between identical twins (same genetic makeup)

26
Q

Allografts

A

members of same species

27
Q

Xenografts

A

members of different species

28
Q

What are the 4 key concepts on Transplantation?

A
  1. Condition of the allograft
  2. Donor-host antigenic disparity
  3. Strength of host anti-donor response
  4. Immunosuppressive regiment
29
Q

What type of transplants don’t require ABO matching?

A

Nonvascularized tissues

  • Cornea
  • Heart valve transplantation
  • Bone and tendon grafts
  • Stem cell transplant
30
Q

Who is a better donor and why? mother or father

A

Father- mom can have antibodies against the baby during pregnancy, so if she were to donate to her kid, there’s a possibility that the graft has antibodies against the recipient.

31
Q

What are the steps of Microcytotoxicity Test for Preformed Abs?

What is it testing for?

A

Testing for the presence of preformed HLA Ab

  1. Add recipient’s serum with Ab to the donor cells
  2. Add complement proteins
  3. Complement makes holes
  4. If cell takes up the dye –> There are preformed Abs present on the cell
32
Q

What are two sources of lymphocytes for HLA typing?

A
  1. Spleen and lymph nodes (from cadaver)

2. Peripheral blood

33
Q

Where is HLA antisera usually obtained from?

A

Multiparous women

Planned immunization of volunteers

34
Q

Steps of Class I HLA Typing

A
  1. Add antibodies
  2. Add complement proteins
  3. Add dye
35
Q

What is an indication of donor-recipient matching in a Class I HLA Typing?

A

Dye is present inside both the donor and recipient cells.

(Antibodies that are against a specific Ag are added to the cells –> If the cells have that Ag, then the Ab will recognize it and bind, allowing complement to be activated. If dye is in both cells that means that both the donor and recipient have the same Ag, so it’s a match.)

  • Can also do this with 9 different Abs in a grid, look for the highest number of matches
36
Q

What are the steps of Class II HLA typing? (a.k.a. Mixed Lymphocyte Response)

A
  1. Apply radiation treatment to donor cells.
  2. Add recipient cells to the mix.
  3. Add H-thymidine
  4. If you have proliferation –> NOT a match
37
Q

What dyes are used in Class I HLA typing?

A

Acridine Orange
Ethidium bromide
Hematoxylin stain

38
Q

What are the steps of events in Allograft Rejection?

A
  1. APCs trigger CD4 and CD8 T cells
  2. Develop local immune response
  3. Cytokines recruit immune cells
  4. Develop of specific T cell, NK cells, or MO-mediated cytotoxicity
  5. Allograft rejection
39
Q

What happens in direct Allorecognition?

A

T cells recognize MHC complex on APCs of the donor cell itself.

40
Q

What happens in indirect allorecognition?

A

T cells recognize APCs of the recipient that are presenting the donor cells as their pathogen.

41
Q

What are the effector mechanisms of a a Humoral graft rejection?

A

Th2 rejection via IL-5, IL-5, IL-10

42
Q

What is the effector mechanism of a cellular graft rejection?

A

Th1 rejection via IL-2, IFN-y

43
Q

What mechanism is involved in a hyperacute rejection? How long does this typically take?

A

Classical complement activation + preexisting antibodies

  • Immediate
44
Q

What mechanism is involved in an acute rejection?

A

Cytotoxic T-cells, Th1 cells

Weeks

45
Q

What mechanism is involved in a chronic rejection?

A

M2 macrophages, T cells
- occlusion of vessels and ischemia of the organ

1-2 years

46
Q

What type of hypersensitivity is a hyperacute rejection?

A

Type II

47
Q

What type of hypersensitivity is an acute rejection?

A

Type IV

48
Q

What type of hypersensitivity is a chronic rejection?

A

Type IV

49
Q

What are three non-immunologic factors involved in a chronic rejection>

A

Ischemia-perfusion
Recurrence of a disease
Effects of a nephrotoxic drug

50
Q

What happens in Acute GVHD?

A

Epithelial cell damage in skin, liver, GI

Rash, jaundice, diarrhea, GI hemorrhage

51
Q

What happens in Chronic GVHD?

A

Fibrosis and atrophy of the affected organ

Complete dysfunction of the affected organ
Obliteration of small airways

52
Q

What are the two effector mechanisms of GVHD?

A

Fas-FasL pathway

Perforin-Granzyme pathway

Renal I Final (7 decks)

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