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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
what are isografts
tissue graft btn identical twins
26
what are allografts
grafts from non-identical members of the same species
27
what are xenografts
grafts btn members of different species
28
which non-immunological factors can contribute to hyperacute allograft rejection
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
what blood type = universal donor =universal acceptor
=donor = type O =acceptor = AB+
30
what happens if you get blood from an imcompatible donor
complement activation --\> MAC complexes --\> cell death
31
when is no ABO testing required
cornea heart valve bone & tendon
32
how do you test for pre-existing non-ABO Abs
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
how many HLA alleles are there
12 6 class I & 6 class II
34
which HLA alleles are the strongest barrier for transplantation
HLA-A, B, C all nucleated cells express them HLA II expressed by professional APCs only
35
what are sources of lymphocytes for HLA typing from donor
spleen/LN peripheral blood (remove RBC & platelets)
36
what complement pathway is activated by HLA typing
classical
37
if donor & recipient both take up dye during HLA-I testing --
both have the Ag & are compatible for that HLA test
38
if the donor cell takes up dye from HLA-1 testing and recipient does not --
only donor has Ag =not compatible
39
how do you test for class II HLA compatability
mixed lymphocyte response test -if recipient cells proliferate = not compatible if NO proliferation = compatibile
40
what is a host-vs-graft disease
recipient's immune system detroy donor tissure bc of adaptive immune response
41
what is direct allorecognition
T-cells of recipient recognise allognic MHC in graft w/o being processed by APCs
42
what is indirect allorecognition
T-cell recognize processed peptide of allogeneic MHC molecules bound to self MHC molecule on host APC
43
which cytokines are released in humoral rejection
Th2 release IL-4, 5 & 10
44
which cytokines are released in cellular rejection
Th1 releases IL-2 and IFN-gamma
45
what is activated in hyperacute rejection
preexisting Ab & complement system = type II hypersensitivity recipient has been sensitized to donor MHC from previous transplants, blood transfusion, or pregnance
46
what is activated in chronic rejection
M2 macrophages & T cells type IV hypersensitivity
47
what cells play an imp role in acute rejection
Donor DCs (aka passenger leukocytes) migrate to LN that is draining the organ & stimulate _primary recipient response_
48
what cells contribute to acute graft rejection
donor DC cells Th1 cells; cytotoxic T cells --\> delayed type hypersensitivity (type IV) CD4+ or CD8+ -leukocytes infliltration of graft vessel \*most common
49
what may be the non-immunologic factors in chronic rejection
ischemia- reperfusion recurrence of disease nephrotoxic drugs
50
when does GVHD occur
allogeneic stem cell transplants often in bone marrow transplants in small bowl, lungs or liver
51
what are the results of acute GVHD
epithelial cell death in skin, liver & GI rash, jaundice, diarrhea & GI hemorrhage
52
what are the results of chronic GVHD
fibrosis & atrophy of affected organ may cause complete dysfxn of affected organ or produce obliteration of small airways
53
what type of hypersensitivity is GVHD & what is its mechanism
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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