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CPR Exam 2 > 13. Immunological Aspects of the Renal System > Flashcards

13. Immunological Aspects of the Renal System Flashcards

1
Q

what is the fxnal criteria for acute kidney injury (AKI)

A

increased SCr by 50% w/i 7 days

increases in SCr by 0.3 mg/dL in 2 days

oliguria

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2
Q

what is the fxnal criteria for CKD

A

GFR <60 mL/min per 1.73 m2 for > 3 months

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3
Q

what does ischemic AKI lead to that is a major cause of acute renal failure

A

metabolic acidosis

ATP depletion

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4
Q

what are the factors that lead to hypoxia & AKI

A

renal vascular disease

sepsis

medications

decreased effective intravascular vol

intravascular vol depletion & hypotension

hepatorenal syndrome

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5
Q

Most cases of AKI is caused by

A

sterile inflammation

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6
Q

what are the DAMPs that initiate inflam via TLRs in the kidneys

A

=endogenous intracell molecules

  1. HMGB1
  2. uric acid
  3. HSP
  4. S100 protein
  5. Hyaluronans in ECM
  6. oxLDL
  7. nucleic acids
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7
Q

what complement pathway is activated when DAMPs bind C reactive proteins

A

classical path

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8
Q

what is HMGB1 recognized by & what does it cause the release of

A

receptor of advanced glycation end products

activate NF-kB and release inflam cytokines

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9
Q

what is uric acid recognized by & what does it cause the release of

A

NLRP3

activate NF-kB –> release inflam cytokines

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10
Q

what are the HSPs recognized by & what do they cause the release of

A

scavenger receptor class A

activate NF-kB –> inflam cytokines

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11
Q

at early stages, what cells mediate immune responses

A

Th17 cells

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12
Q

at later stages, what cells mediate immune responses

A

Th1 cells

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13
Q

what type of macrophages does AKI activate

A

M1 (induced by DAMPs binding TLRs & PRRs)

–> increase TNF-alpha & IL-6

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14
Q

what is the job of M2 macrophages & how are they activated

A

tissue repair

IL-4 & IL-13

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15
Q

what promotes differentiation of M1

A

INF-gamma & proinflam cytokines

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16
Q

which cytokines are imp in renal tissue repair & fibrosis

A

(made by M2)

IL-10

TGF-beta

–> anti-inflam effects

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17
Q

what are the proinflam cytokines

A

IL-1

IL-12

IL-23

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18
Q

what is the role of CCL20

A

aka MIP-3

activated by IL-17

to recruit neutrophils & infiltration of monocytes, Th1, Th17 cells

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19
Q

what are the cytokines that activate Th1, Th2 & Th17 cells

& what is the result

A

Th1- activated by IL-12 –> Ag presentation & cellular immunity

Th2 - activated by IL-4 –>humoral immunity & allergy

Th17 - activated by IL-6 & TGF-beta –> tissue inflam

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20
Q

What is the role of the complement pathway in AKI

A

for MAC complex for cell death

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21
Q

What is the reason for kidney’s unique susceptibility to complement induced damage

A

filtration favors tissue deposition of imm complex

***

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22
Q

RBC destruction after transfusion w/ mismatched blood is what type of hypersensitivity? & what is its mechanism

A

Type II - form cell bound Ag

IgG or IgM antibody bind to cellular antigen –> activate complement –> cell lysis

IgG mediate ADCC w/ cytotoxic T cells, NK cells, macrophages & neutrophils

23
Q

what type of hypersensitivity is post-streptococcal glomerulonephritis, RA & systemic lupus

& what is its mechanism of action

A

Type III - form soluble Ag

Ag-Ab complex deposit in tissue; complement activation provide inflam mediates & recruit neutrophils –> release enzymes that damage tissues

24
Q

what are autografts

A

self, graft transplanted from one site on the body to another in the same person

25
Q

what are isografts

A

tissue graft btn identical twins

26
Q

what are allografts

A

grafts from non-identical members of the same species

27
Q

what are xenografts

A

grafts btn members of different species

28
Q

which non-immunological factors can contribute to hyperacute allograft rejection

A

mechanical damage

ischemia-rejection

  • clotting cascade generate fibrin & fibrinopeptides –> increase vascular permeability & accumulation of chemoattractants for neutrophils & macrophages
  • kinin cascade make bradykinin –> vasodilate, Sm M contraction, increased vascular permeability
29
Q

what blood type

= universal donor

=universal acceptor

A

=donor = type O

=acceptor = AB+

30
Q

what happens if you get blood from an imcompatible donor

A

complement activation –> MAC complexes –> cell death

31
Q

when is no ABO testing required

A

cornea

heart valve

bone & tendon

32
Q

how do you test for pre-existing non-ABO Abs

A

recipient serum w/ Ab added to donor cells

complement is added

MAC makes pores in cell

add Dye

if dye builds up then Ab for the donor cells are present

33
Q

how many HLA alleles are there

A

12

6 class I & 6 class II

34
Q

which HLA alleles are the strongest barrier for transplantation

A

HLA-A, B, C

all nucleated cells express them

HLA II expressed by professional APCs only

35
Q

what are sources of lymphocytes for HLA typing from donor

A

spleen/LN

peripheral blood (remove RBC & platelets)

36
Q

what complement pathway is activated by HLA typing

A

classical

37
Q

if donor & recipient both take up dye during HLA-I testing –

A

both have the Ag & are compatible for that HLA test

38
Q

if the donor cell takes up dye from HLA-1 testing and recipient does not –

A

only donor has Ag

=not compatible

39
Q

how do you test for class II HLA compatability

A

mixed lymphocyte response test

-if recipient cells proliferate = not compatible

if NO proliferation = compatibile

40
Q

what is a host-vs-graft disease

A

recipient’s immune system detroy donor tissure bc of adaptive immune response

41
Q

what is direct allorecognition

A

T-cells of recipient recognise allognic MHC in graft w/o being processed by APCs

42
Q

what is indirect allorecognition

A

T-cell recognize processed peptide of allogeneic MHC molecules bound to self MHC molecule on host APC

43
Q

which cytokines are released in humoral rejection

A

Th2 release IL-4, 5 & 10

44
Q

which cytokines are released in cellular rejection

A

Th1 releases IL-2 and IFN-gamma

45
Q

what is activated in hyperacute rejection

A

preexisting Ab & complement system

= type II hypersensitivity

recipient has been sensitized to donor MHC from previous transplants, blood transfusion, or pregnance

46
Q

what is activated in chronic rejection

A

M2 macrophages & T cells

type IV hypersensitivity

47
Q

what cells play an imp role in acute rejection

A

Donor DCs (aka passenger leukocytes)

migrate to LN that is draining the organ & stimulate primary recipient response

48
Q

what cells contribute to acute graft rejection

A

donor DC cells

Th1 cells; cytotoxic T cells –> delayed type hypersensitivity (type IV)

CD4+ or CD8+

-leukocytes infliltration of graft vessel

*most common

49
Q

what may be the non-immunologic factors in chronic rejection

A

ischemia- reperfusion

recurrence of disease

nephrotoxic drugs

50
Q

when does GVHD occur

A

allogeneic stem cell transplants

often in bone marrow

transplants in small bowl, lungs or liver

51
Q

what are the results of acute GVHD

A

epithelial cell death in skin, liver & GI

rash, jaundice, diarrhea & GI hemorrhage

52
Q

what are the results of chronic GVHD

A

fibrosis & atrophy of affected organ

may cause complete dysfxn of affected organ or produce obliteration of small airways

53
Q

what type of hypersensitivity is GVHD

& what is its mechanism

A

type IV

Donor APCs activate donor CD8+ T cells by cross presenting on MHC class 1

Fas-FasL –> apoptosis

-perforin/granzyme

CPR Exam 2 (20 decks)

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