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Renal Test 2 > Immunological Aspects of the Renal System > Flashcards

Immunological Aspects of the Renal System Flashcards

1
Q

major cause of Acute Renal Failure

A

ischemic Acute Kidney Injury (AKI)

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2
Q

What activates kidney filtration impairment

A

ATP depletion

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3
Q

what % of total cardiac output do kidneys receive

A

20% (~1L/ml more than other organs in the body)

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4
Q

Normal GFR and SCr (serum creatinine) for NKD

A

GFR >= 60ml/min per 1.73 m2

Stable SCr

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5
Q

What criteria must be met for AKI

A
  1. Increase in SCr by 50% in 7 days
  2. SCR increase by 0.3 mg/dL in 2 days
  3. Oliguria (little urine output)
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6
Q

What criteria must be met for Chronic Kidney Disease (CKD)

A

Decreased GFR <60ml/min for >3 months

structural kidney damage for >3 months

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7
Q

another name for kidney failure

A

ESRD (end state renal disease)

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8
Q

6 causes of kidney hypoperfusion & AKI

A
  1. Intravascular volume depletion & hypotension
  2. Decreased effective intravascular volume
  3. medications
  4. hepatorenal syndrom
  5. sepsis
  6. renal vascular disease
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9
Q

what perfusion condition leads to AKI

A

hypoxia

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10
Q

body locations that contribute to intravascular volume depletion/hypotension

A
  1. GI tract
  2. dermal losses
  3. renal
  4. hemorrhage
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11
Q

conditions that contribute to decreased effective intravascular volume

A
  1. congestive heart failure
  2. cirrhosis
  3. nephrosis
  4. peritonitis
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12
Q

what contributes to large vessel renal vascular disease

A
  1. renal artery thrombosis
  2. arterial occlusion during surgery
  3. renal artery stenosis
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13
Q

what contributes to small vessel renal vascular disease

A
  1. vasculitis
  2. atheroembolism
  3. hemolytic uremic syndrome
  4. malignant HTN
  5. scleroderma
  6. pre-eclampsia
  7. sickle cell anemia
  8. hypercalcemia
  9. transplant rejection
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14
Q

Most times AKI is not caused by infection but rather…

A

sterile inflammation

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15
Q

How are DAMPs introduced to the blood stream

A
  1. released by dying parenchymal kidney cells

2. ECM degradation

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16
Q

compare C-Reactive protein (CRP) to IgM

A

both have 5 subunits

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17
Q

how do DAMPs activate complement

A

DAMPs bind CRP –>activate complement via classical pathway

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18
Q

what are DAMPs

A

Alarmins

endogenous molecular strucutures

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19
Q

How do DAMPs cause renal inflammation

A

TLRs recognize DAMPs–> TRLs activated –> innate immune response induced –> RENAL INFLAMMATION

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20
Q

HMGB1

A

nucleolus protein that’s a DAMP

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21
Q

uric acid

A

DAMP/alarmin

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22
Q

HSP

A

exosome that’s a DAMP

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23
Q

S100 protein

A

found in the cytoplasm

DAMP

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24
Q

Hyaluronans

A

fond in ECM

DAMP

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25
Q

What are Exogenous ligands and where are they found

A

PAMPs
found on pathogens: bacteria and viruses
Result: Innate Immunity

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26
Q

CPG and ds RNA

A

PAMP nucleic acids

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27
Q

lipid A

A

PAMP lipids

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28
Q

PGN

A

PAMP proteins

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29
Q

What are endogenous ligands and where are they found

A

stuff from ECM degradation

Result: homeostatic inflammation

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30
Q

ATP

A

DAMP nucleic acid

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31
Q

oxLDL and saturated fatty acids

A

DAMP lipids

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32
Q

SP and HMGB1

A

DAMP proteins

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33
Q

Inflammation sensors for DAMPS

A

TLRs

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34
Q

Inflammation sensors for PAMPs

A

NOD-like receptors

C-type Lectin

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35
Q

Mediators for DAMP and PAMP inflammation

A

TNF-alpha
IL-6
IL-1 beta

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36
Q 
What renal cell is involved with:
Type 1 IFNs
CXCL2
IL-1 beta
IL-12
antigen presentation
migration

What is the result?

A

Dendritic Cells

Result: AKI + infections

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37
Q 
What renal cell is involved with: 
IL-1 beta
TNF
IL-6
chemokines
ROS

What is the result?

A

macrophages

Result: most kidney disease

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38
Q

What renal cell is involved with:
TNF
IL-6
IFN-alpha

What is the result?

A

endothelial cells

Result: IC-GN (immune complex glomerulonephritis)

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39
Q

What processes are triggered by inflammation

A
  1. leukocyte activation
  2. cytokine release
  3. margination
  4. tissue migration (DCs)
  5. reduced flow
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40
Q

what is margination

A

free flowing leukocytes exit central blood stream and initiate leukocyte and endothelial cell reactions

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41
Q

what cells mediate early immune response causing renal tissue injury

A

Th17 cells

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42
Q

what cells mediate late immune response

A

Th1 cells

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43
Q

AKI macrophages

A

M1 macrophages

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44
Q

tissue repair macrophages

A

M2 macrophages

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45
Q

which cells differentiate into Th1 and Th17

A

dendritic cells

PRO-inflammatory

46
Q

pro or anti-inflammatory:

increase TNF-alpha

A

pro inflammatory

M1

47
Q

pro or anti-inflammatory:

increase IL-6

A

pro inflammatory

M1

48
Q

pro or anti-inflammatory:

increase arginase-1

A

anti-inflammatory

M2

49
Q

pro or anti-inflammatory:

increase IL-10

A

anti-inflammatory

M2

50
Q

pro or anti-inflammatory:

increase CD4 Th1 response

A

pro inflammatory

51
Q

pro or anti-inflammatory:

increase IFN-gamma

A

pro-inflammatory

**promotes differentiation of M1 macrophages

52
Q

pro or anti-inflammatory:

decrease IL-4

A

pro-inflammatory

53
Q

pro or anti-inflammatory:

decrease antigen specific T-cell expansion

A

anti-inflammatory

54
Q

Of DCs, macrophages, and T-cells, which is NOT involved in anti-inflammation

A

DCs

DCs, Macrophages, and T-cells are all involved in pro-inflammation BUT
ONLY macrophages and T-cells are involved in anti-inflammation (tissue repair)

55
Q

characteristics of M1 machrophages

A
  • classical activation (Th1)
  • make NO
  • induced by PAMPs and DAMPs (TLR binding + PRRs)
  • cytokines made by M1 macs cause the acute phase of kidney inflammation
56
Q

what induces the monocyte to differentiate to an M2 macrophage

A

IL-13 and IL-4

57
Q

functions of M2 macs

A
  • anti-inflammation
  • would repair
  • RENAL FIBROSIS
58
Q

what induces the monocyte to differentiate to an M1 macrophage

A
  • microbial TLR-ligands

- IFN-gamma

59
Q

functions of M1 macs

A
  • phagocytosis
  • bacteria/fungi killing
  • INFLAMMATION
60
Q

what releases IL-1, IL-12, IL-23, chemokines

A

M1 macs

-result: inflammation (IL-12 & IL-23) via antigen presentation

61
Q

what releases ROS, NO, lysosomal enzymes

A

M1 macs

-result: phagocytosis + killing

62
Q

what releases IL-10, TGF-beta

A

M2 macs

-anti inflammatory

63
Q

what releases proline, polyamines, TGF-beta

A

M2 macs

  • wound repair
  • renal fibrosis
64
Q

characteristics of M2 macs

A
  • alternative activation (Th2)
  • induced by IL-4 and IL-13
  • controlled by IL-10 and TGF-beta
  • key for tissue repair (build ECM)
  • none of these: Ag presentation, NO
65
Q

what increases adhesion and proinflammatory activators for M1 differentation

A

ICAM-1

osteopontin

66
Q

what reprograms M1 macs to turn into M2 macs

A

CSF-1 (M-CSF)

IL-10

67
Q

what cell is produced by macs that stimulate ECM production

A

pericytes (–> myofibroblasts–>matrix deposition)

68
Q

Steps leading to activation of naive CD4+ T-cell and ultimately tissue inflammation

A

naive CD4+–> activated Tcell–> +IL-6 & TFG beta–> Th17 cell –> +IL-17–> TISSUE INFLAMMATION

69
Q

what 2 substances are secreted by Th17 cells

A

IL-17

CCL20/Macrophage Inflammatory Protein-3 (MIP-3)

70
Q

result of CCL20 secretion

A
  1. recruit monocytes
  2. recruit Th1 cells (later stages of inflammation)
  3. recruit Th17 cells (early stages of inflammation)
71
Q

What cells have receptors for IL-17 that’s secreted by Th17 cells

A
  • tubular epithelial cells
  • mesangial cells

**both of these renal cells release chemokines and other inflammatory mediators

72
Q

role of Treg cells in AKI

A

Treg cells inhibit inflammatory signals such as:
TGF-beta, IL-10, B & T lymphocytes

Goal: prevent inflammation (ANTI-INFLAMMATION)

73
Q

Immunoglobulins for Type II hypersensitivity

A

IgG or IGM

74
Q

Immunoglobulins for Type III hypersensitivity

A

IgG AND IGM

75
Q

components of Type II hypersensitivity mechanisms

A
  • IgG or IgM binds to cellular Ag
  • complement activation + cell lysis
  • ADCC (Ab dependent cellular cytotoxicity)
  • ACCC w/T cells, NK cells, Macs, & neutrophils
76
Q

Type II hypersensitivity Reactions

A

RBC destruction post-transfusion (bc of mismatched blood types)

hemolytic disease of the newborn

77
Q

components of Type III hypersensitivity mechanisms

A
  • Ag-Ab complexes
  • complement activation –> inflammatory mediators
  • recruit neutrophils and release enzymes from damaged tissues
78
Q

Type III hypersensitivity Reactions

A

-post-strep glomerulonephritis

RA

SLE (systemic lups erythematosus)

79
Q

What methods are used to prevent graft (transplant) rejection

A

HLA matching

immunosuppression

80
Q

types of host vs graft responses

A

4 types that cause transplant rejection:

  1. histocompatibility Ags
  2. hyper-acute rejection
  3. acute rejection
  4. chronic rejection
81
Q

histocompatibility Ags

A

Host vs graft rejection

-targets for rejection

82
Q

hyper-acute rejection

A 
host vs graft rejection
Time: immediately post-Transplant
Cause: pre-formed antibody &amp; complement (classical)
hypersensitivity: type II
major probs: occlusion &amp; thrombosis
83
Q

acute rejection

A

host vs graft rejection
Time: days to weeks post-Transplant
Cause: T-cell mediated (Th1 cells & CTLs), CD4+, CD8+ T-cells
hypersensitivity: type IV
major probs: inflammation & leukocytes infiltrate graft vessels
other: donor DCs (passenger leukocytes) are key

84
Q

chronic rejection

A

host vs graft rejection
time: months to years post-Transplant
cause: vascular trauma, inflammatory T cell products, Antibodies, (DTH)
cells: M2 macs, T-cells
hypersensitivity: type IV
probs: intimal thickening & fibrosis of graft vessels
NOTE: does NOT respond to immunosuppressive therapy

85
Q

graft vs host reactions (GVHD)

A

when the donor lymphocytes attack the graft recipient

  • acute or chronic
    cause: Donor T-cells proliferate & attack recipient tissues
    hypersensitivity: type IV
    probs: diarrhea, rash, jaundice
  • *common in bone marrow transplants
  • *common in immunocompromised patients
86
Q

what’s required post-transplant to minimize rejection

A

immunosuppressive drugs

***Note: cannot be used for chronic rejection

87
Q

autograft

A

graft exchanged from one part of the body to another (same person)

88
Q

isograft

A

exchanged btwn different ppl (twins)

89
Q

allograft

A

exchanged btwn different ppl (non-twins)

-same species

90
Q

xenograft

A

exchanged btwn diff members of DIFF species

  • rapid attack
  • increase chance of survival by inserting human genes into genome
91
Q

4 variables that determine successful transplant

A
  1. allograft condition
  2. donor-host antigenic disparity
  3. strength donor-host response
  4. immunosuppressive regimen
92
Q

immune events that cause rejection

A
  1. APCs trigger CD4+ and CD8+ T cells
  2. local AND systemic immune response
  3. cytokines recruit and activate immune cells
  4. develop specific T-cells, NK cells, macs = CYTOTOXICITY
  5. Rejection!!
93
Q

what non-immuno factors cause rejection

A

mechanical trauma + ischemia-reperfusion injury

94
Q

how does the clotting cascade impact rejection

A

makes: fibrinopeptides

result 1: increased local vascular permeability (same as bradykinin)

result 2: chemoattractant for neutrophils & macs

if not controlled: HYPER-ACUTE REJECTION!

95
Q

how does the kinin cascade impact rejection

A

makes: bradykinin

result 1: vasodilation

result 2: smooth muscle contraction

result 3: increased vascular permeability (same as clotting cascade)

if not controlled: HYPER-ACUTE REJECTION!

96
Q

why is ABO matching NOT important for corneal, heart valve and bone/tendon grafts

A

non-vascularized tissues

anti-class I/II HLA abs not important here

97
Q

chromosomal arm with HLA region

A

short arm

98
Q

how are HLA Ags expressed

A

co-dominantly expressed

99
Q

most important HLA Ags for successful transplantation

A

class II HLA

  • HLA-DR
  • HLA-DP
  • HLA-DQ
100
Q

HLA Ags that are the strongest barriers to transplantation

A

class I HLA
HLA-A
HLA-B (most number of alleles –>polymorphism)

101
Q

Steps for: microcytotoxicity test for preformed Abs

A

step1: recipient serum + donor cells
step2: add complement
step 3: add dye
step 4: PREFORMED ANTIBODIES PRESENT

102
Q

steps for: serological Class I HLA typing for HLA-A3

A

step1: Abs are added to donor and recipient cell
step2: complement added to both
step 3: pores formed
step 4: dye added
result: HLA ag are identical

Note: classical complement cascade

103
Q

Microtoxicity test (Class I MHC) for HLA-A7

A

step1: Abs are added to donor and recipient cell
step2: complement added to both
step 3: pores formed (donor only)
step 4: dye added
result: HLA ag are identical

104
Q

How do you know if recipient cells DON’T share class II MHC donor

A

There is proliferation of the recipient cells!

step1: add radiation to donor cells
step2: donor + recipient cells mixed
step3: add 3H-thymidine
step 4: if radioactivity see in cells = recipient cells proliferation

*recipient cells DO NOT share class II MHC donor

105
Q

How do you know if recipient cells share class II MHC donor

A

NO proliferation- means that recipient cells SHARE class II MHC of donor

step1: add radiation to donor cells
step2: donor + recipient cells mixed
step3: add 3H-thymidine
step 4: radioactivity NOT incorporated = no proliferation

106
Q

direct recognition

A

T-cell recognizes unprocessed MHC

-on graft APcs

107
Q

indirect allorecognition

A

T cell recognizes processed MHC bound to self MHC

-on host APC

108
Q

Host vs Graft Response

A
  • non-immune injury of the graft (Danger signals, DAMPs)
  • humoral rejection Th2 (IL-4, IL-5, IL-10)
  • cellular rejection Th1 (IL-2, INF-gamma)
109
Q

non-immunologic factors for chronic graft rejection

A
  1. ischemia-reperfusion damage
  2. recurrence of disease
  3. nephrotoxic drugs (cyclosporine A)
110
Q

Acute GVHD causes and Sx

A

epithelial cell death in skin, liver, GI

Sx: rash, jaundice, diarrhea, GI hemorrhage

111
Q

Chronic GVHD causes and Sx

A

fibrosis and atrophy of affected organ

Sx: complete dysfunction of the organ, obliteration of small airways

112
Q

2 effector mechanisms of GVHD

A
  1. Fas-FasLigand (result: apoptosis)

2. perforin/granzyme (result: apoptosis)

Renal Test 2 (9 decks)

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