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Renal Final > Immunological Aspects of the Renal System > Flashcards

Immunological Aspects of the Renal System Flashcards

1
Q

What is the functional criteria and structural criteria for no kidney disease (NKD)?

A

Functional criteria:
GFR>=60 mL/min per 1.73 m^2
Stable SCr (serum creatinine)

Structural criteria:
No damage

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2
Q

What is the functional criteria and structural criteria for acute kidney injury (AKI)?

A

functional criteria:
increase in SCr (serum creatinine) by 50% within 7 days, or increase in SCr by 0.3 mg/dL within 2 days, or Oliguria

structural criteria:
no criteria

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3
Q

What is the functional criteria and structural criteria for chronic kidney disease (CKD)?

A

functional criteria:
GFR<60 ml/min per 1.73 m^2 for >3 months

structural criteria:
kidney damage for > 3 months

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4
Q

Risk factors for kidney disease

A 
age
race or ethnic groups
genetic factors
hypertension
diabetes melliuts
metabolic syndrome
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5
Q

kidney disease modifiers

A 
severity of acute kidney injury
stage of chronic kidney disease
number of episodes
duration of acute kidney injury
proteinuria
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6
Q

outcomes of kidney injury/disease

A 
cardiovascular events
kidney events
ESRD (end stage renal disease)
disability
diminished quality of life
death
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7
Q

What is the major filtering organ?

A

kidneys

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8
Q

How much human body mass are the kidneys?

A

0.5%

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9
Q

How much CO do the kidneys receive?

A

20% of total CO
about 1L/ml
more than any other organ in the body

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10
Q

What is the high oxygen demand in the kidneys associated with?

A

tubular oxygen consumption necessary for solute reabsorption

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11
Q

What does AKI stand for?

A

ischemic acute kidney injury

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12
Q

What does AKI lead to?

A

metabolic acidosis and ATP depletion

major cause of acute renal failure (ARF)

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13
Q

What does ARF stand for?

A

acute renal failure

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14
Q

What is ARF?

A

abrupt decrease in kidney function

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15
Q

What is the incidence of AKI?

A

5% of hospitalized patients

30% of critically ill patients

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16
Q

What are the causes of kidney hypoperfusion and AKI?

A
  • intravascular volume depletion and hypotension
  • hepatorenal syndrome
  • renal vascular disease
  • sepsis
  • medications
  • decreased effective intravascular volume

All lead to hypoxia and acute kidney injury

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17
Q

How can intravascular volume deplesion and hypotension occur?

A

GI tract losses
renal losses
dermal losses
hemorrhage

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18
Q

What are causes of renal vascular disease?

A

Large vessel

  • renal artery thrombosis
  • arterial occlusion during surgery
  • renal artery stenosis

Small vessel

  • vasculitis
  • arthroembolism
  • hemolytic uremic syndrome/thrombotic thrombocytopenic purpura
  • malignant hypertension
  • scleroderma
  • preeclampsia
  • sickle cell anemia
  • hypercalcemia
  • transplant rejection
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19
Q

What are medications that cause AKI?

A
  • cyclosproin A
  • tacrolimus
  • angiotensin-converting enzyme inhibitors
  • nonsteroidal antiinflammatory drugs
  • radiocontrast agents
  • amphotericin
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20
Q

What causes decreased effective intravascular volume?

A
  • congestive heart failure
  • cirrhosis
  • nephrosis
  • peritonitis
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21
Q

What is the cause of AKI in most cases?

A

STERILE INFLAMMATION;

not infection

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22
Q

What is sterile inflammation induced by?

A

intrinsic damage-associated molecular patterns (DAMPs)

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23
Q

Where are DAMPs released?

A

dying parenchymal kidney cells

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24
Q

When are DAMPs generated?

A

during ECM degredation and remodeling

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25
Q

What are DAMPs?

A

molecular patterns (alarmins) are endogenous intracellular molecular structures:

  • HMGB1 (nucleolus protein)
  • uric acid
  • HSPs (exosomes)
  • S100 protein (cytoplasm)
  • hyaluronans in ECM
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26
Q

What is the function of C reactive protein (CRP)?

A
  • has 5 subunits

- can bind to DAMPs and activate complement via classical pathway

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27
Q

How do immune cells recognize DAMPs?

A

toll-like receptors

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28
Q

Once DAMPs bind to TLRs and become activated, what do they induce?

A

innate immune responses and renal inflammation

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29
Q

What are the inducers for innate immunity and homeostatic inflammation?

A 
innate:
pathogens (bacteria and virus)
-PAMPs (exogenous ligands)
-nucleic acid (CpG and dsRNA)
-lipid (lipid A)
-protein (PGN)
homeostatic inflammation:
cell/ECM derived molecules
-DAMPs (endogenous ligands)
-nucleic acid (ATP)
-lipid (oxLDL and saturated fatty acids)
-protein (HSP and HMGB1)
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30
Q

What are the sensors for PAMPs and DAMPs?

A

toll-like receptors
NOD-like receptors
C-type lectin

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31
Q

What are the mediators for PAMPs and DAMPs?

A

TNF alpha
IL-6
IL-1 beta

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32
Q

What are the functions of dendritic cells? What disease are they present in?

A

functions:

  • antigen presentation
  • migration
  • Type 1 IFNs, CXCL2, IL-1beta and IL-12

Acute kidney injury and infections

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33
Q

What do resident renal cells activate when they sense DAMPs?

A

dendritic cells
macrophages
endothelial cells

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34
Q

What are macrophages associated with? Disease?

A

ROS, IL-1beta, TNF, IL-6 and chemokines

most kidney diseases

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35
Q

What are endothelial cells associated with? diseases?

A

TNF, IL-6, chemokines, and IFNalpha

IC-GN (ischemia induced glomerulonephritis)
diabetes
sepsis

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36
Q

What cells are activated during inflammation? What happens next?

A 
WBC recruitment
neutrophils
macrophages
lymphocytes
dendritic cell activation
leukocyte activation
cytokine release
margination
tissue migration
reduced flow
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37
Q

What are the pro inflammatory responses in the development of acute kidney injury?

A

DC –> increase Th1 and Th17 differentiation
macrophage –> M1 increased TNF alpha, increased IL-6
T cell –> increased CD4 Th1 response, increased IFN-gamma, increased IL-6, decreased IL-4

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38
Q

What are the anti inflammatory responses and tissue repair for macrophages and T cells?

A

macrophage –> M2 increased clearance of early apoptotic cells, increased arginase-1, increased IL-10
T cell –> decreased antigen specific T cell expansion

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39
Q

What are immune responses mediated by in early stages? late stages?

A 
early = Th17 cells
late = Th1 cells
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40
Q

What macrophages play a key role in AKI?

A

M1

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41
Q

What macrophages play a key role in tissue repair?

A

M2

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42
Q

Describe the classically activated M1 macrophage pathway

A
  • induced by PAMPs and DAMPs through binding to TRLs and other PRRs
  • IFN-gamma and proinflammatory cytokines promote differentiation of M1 macrophages
  • cytokines produced by M1 macrophages perpetuate the acute phase of inflammation in kidney
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43
Q

Describe the alternatively activated M2 macrophage pathway

A
  • induced by IL-4 and IL-13 produced by T cells

- M2 macrophages are important in tissue repair and renal fibrosis which both are controlled by IL-10 and TGF-beta

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44
Q

Which macrophage is involved in presentation of antigens to T cells?

A

M1

using IL-12 and IL-23

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45
Q

What initiates macrophage reprogramming?

A

CSF-1, IL-10

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46
Q

What cytokine(s) promote Th1 cells?

A

IL-12

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47
Q

What cytokine(s) are secreted by Th1 cells?

A

IFN gamma

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48
Q

What is the function of Th1 cells?

A

antigen presentation and cellular immunity

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49
Q

What cytokine(s) promote Th2 cells?

A

IL-4

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50
Q

What cytokine(s) are secreted by Th2 cells?

A

IL-4
IL-5
IL-13

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51
Q

What is the function of Th2 cells?

A

humoral immunity and allergy

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52
Q

What cytokine(s) promote Th17 cells?

A

IL-6

TGF beta

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53
Q

What cytokine(s) do Th17 cells secrete?

A

IL-17

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54
Q

What is the function of Th17 cells?

A

tissue inflammation

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55
Q

What does IL-17 stimulate?

A

stimulates resident renal cells to produce chemokines and other inflammatory mediators

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56
Q

What do the chemokines initiated by IL-17 recruit?

A

recruitment of neutrophils

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57
Q

What do Th17 cells secrete besides IL-17? What might be its function?

A

CCL20 also called macrophage inflammatory protein-3 (MIP-3)

facilitate the infiltration of monocytes, Th1 cells, and Th17 cells

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58
Q

What does recruitment of pro-inflammatory leukocyte subsets lead to in the kidney?

A

immune-mediated kidney damage

59
Q

What is the function of Treg cells in AKI?

A 
antiinflammatory
inhibits B lymphocytes
inhibits T lymphocytes
promote TGF beta and IL-10
inhibits neutrophils and monocytes
60
Q

Who is likely to have complement proteins in biopsies of the kidney?

A
  • glomerulonephritis

- various kidney disease

61
Q

Where does complement activation occur in acute kidney injury?

A

downstream of immune complex deposition (type III)

downstream of antibody-mediated injury (type II)

62
Q

What are the immune reactant of type II hypersensistivity?

A

immune reactant: IgG or IgM

63
Q

immune reactant of type III hypersensistivity?

A

immune reactant: IgG and IgM

64
Q

type II hypersensitivity antigen form

A

antigen form: cell-bound antigen

65
Q

type II hypersensitivity mechanism of activation

A

mechanism of activation: IgG or IgM antibody binds to cellular antigen, leading to complement activation and cell lysis

66
Q

type II hypersensitivity example

A

example: patients with anti-glomerular basement membrane (GBM) antibody mediated GN

67
Q

antigen form type III hypersensitivity

A

antigen form: soluble antigen

68
Q

mechanism of activation of type III hypersensitivity

A

mechanism of activation: antigen-antibody complexes are deposited in tissues. complement activation provides inflammatory mediators and recruits neutrophils. enzymes released from neutrophils damage tissue.

69
Q

examples of type III hypersensitivity

A

post-streptococcal glomerulonephritis, rheumatoid arthritis, systemic lupus erythematosus

70
Q

What is the treatment for end stage renal disease?

A

kidney transplantation

71
Q

What is the barrier to transplantation?

A

genetic incompatibility of the donor and recipient

72
Q

What are the methods used for preventing graft rejection?

A

HLA matching

immunosuppression

73
Q

What causes transplant rejection?

A

host versus graft responses

74
Q

What are the targets of rejection?

A

histocompatibility antigens

75
Q

What is a hyperacute rejection?

A

immediate reaction caused by antibody

76
Q

What is acute rejection?

A

occurs days to weeks after transplantation and caused by T cells

77
Q

What is chronic rejection?

A

seen months or years after transplantation and caused by vascular trauma, inflammatory products of T cells

78
Q

What are graft versus host rejections?

A

donor lymphocytes attack the graft recipient

mechanism of GVHD can be acute or chronic

79
Q

What does successful organ transplantation depend on?

A

immunosuppressive drugs

80
Q

What are autografts?

A

grafts exchanged from one part to another part of the same individual

81
Q

What are isografts?

A

grafts exchanged between different individuals of identical genetic constitutions (identical twins)

82
Q

What are allografts?

A

grafts exchanged between nonidentical members of the same species

83
Q

What are xenografts?

A

graft exchanged between members of different species

84
Q

What classification of grafts are particularly susceptible to rapid attack by naturally occurring antibodies and complement?

A

xenografts

85
Q

What increases the chances of successful survival in xenografts?

A

insertion of human genes into the genomes of the donor animals (miniature swine)

86
Q

What variables determine transplant outcome?

A
  1. condition of the allograft
  2. donor-host antigenic disparity
  3. strength of host anti-donor response
  4. immunosuppressive regimen
87
Q

What are non-immunological factors?

A
  • mechanical trauma and ischemia-reperfusion injury to the graft tissues
  • mediators are released which trigger several biochemical cascades leading to immediate tissue damage
88
Q

What does the clotting cascade generate?

A

fibrin and fibrinopeptides

89
Q

What do fibrinopeptides do?

A

increase local vascular permeability and serve as chemoattractant for neutrophils and macrophages

90
Q

What does the kinin cascade produce? what does it cause?

A

bradykinin causes vasodilation, smooth muscle contraction, increased vascular permeability

91
Q

What results from uncontrolled early proinflammatory responses?

A

hyperacute allograft rejection

92
Q

What does intensified immunosuppression and immunological understanding prevent?

A

hyperacute rejection related to ABO incompatible kidney transplantation (ABOi-KT) for patients with end-stage kidney disease

93
Q

What is the major blood group system?

A

ABO

94
Q

Are ABO antigens expressed on other tissues?

A

yes

95
Q

What is ABO matching NOT important for?

A

corneal transplantation, heart valve transplantation, bone and tendon grafts (nonvascularized tissues)

96
Q

Is ABO incompatibility a contraindication to stem cell transplantation?

A

No

97
Q

Blood type A
antibodies?
antigens?
donor?

A

antibodies: B
antigens: A
donor: A or O

98
Q

Blood type B
antibodies?
antigens?
donor?

A

antibodies: A
antigens: B
donor: B or O

99
Q

Blood type AB
antibodies?
antigens?
donor?

A

antibodies: none
antigens: A/B
donor: A, B, AB, O

100
Q

Blood type O
antibodies?
antigens?
donor?

A

antibodies: A/B
antigens: none
donor: O

101
Q

What are the steps for testing for pre-existing anti-class I/II HLA abs? What is the test called?

A

“Microcytotoxicity Test for Preformed Abs”

  1. recipient serum is added to donor cells
  2. complement is added
  3. dye is added
  4. preformed antibodies are present
102
Q

What is the success of transplantation dependent on?

A

HLA Ags

103
Q

What are HLA Ags encoded by?

A

major histocompatibility complex: HLA class-I and class-II

104
Q

Why is HLA compatibility between donor and recipient required?

A

extreme polymorphism of HLA

105
Q

How many allelic forms are there of HLA molecules?

A

hundreds

106
Q

How many HLA alleles per person?

A

10-12

107
Q

How are HLA Ags expressed?

A

co-dominantly

108
Q

What are strong barriers to transplantation?

A

class I HLA Ags (HLA-A and HLA-B)

109
Q

What are the 3 most important pairs of the class II HLA Ags for transplantation?

A

HLA-DR
HLA-DP
HLA-DQ

110
Q

What are convenient sources of lymphocytes for HLA typing?

A
  • spleen and lymph node (cadaver)

- peripheral blood (RBCs and platelets removed)

111
Q

Where are HLA antisera obtained?

A

multiparous women or from planned immunization of volunteers

112
Q

What does antisera contain? How does antisera work?

A

antibodies to HLA Ags;
Abs bind to HLA Ag on the surface of lymphocytes, Ag-Ab complex formed activate classical complement cascade resulting in lymphocyte lysis. lymphocyte lysis can be detected by staining the cells with acridine orange, ethidium bromide, or hematoxylin stain

113
Q

What are the steps in testing for class I HLA compatibility?

A
  1. Abs are added
  2. Complement is added
  3. Dye is added
    Result in recipient: complement forms pores in the cells, dye is accumulated in cells if HLA Ag are identical
114
Q

What are the steps for testing for class II HLA compatibility? What is this test called?

A

“Mixed lymphocyte response”

  1. donor cells don’t proliferate due to the radiation treatment, but can serve as APCs
  2. mix with recipient cells + 3H-thymidine
  3. proliferation of recipient cells occur, radioactivity is incorporated in DNA that allows quantify cell proliferation
    result: recipient cells do not share class II MHC of donor
  4. radioactivity is NOT incorporated in DNA, no reaction/no radioactivity
    result: recipient cells share class II MHC of donor
115
Q

What are two types of immune responses in transplantation?

A

host versus-graft disease: kidney is transplanted the recipient’s T cells attack the transplant

graft versus host disease: bone marrow is transplanted the T cells in the transplant attack the recipient’s tissues

116
Q

What are the immune events in allograft rejection?

A
  1. APCs trigger CD4+ and CD8+ T cells
  2. both a local and systemic immune response develop
  3. cytokines recruit and activate immune cells
  4. development of specific T cells, NK cells, or macrophages mediated cytotoxicity
  5. allograft rejection
117
Q

What is host versus graft response?

A
  • host immune system attacks the donor tissue
  • adaptive immune response against the graft
  • immune response is more vigorous and strong than against a pathogen
  • higher frequency of T cells that recognize the graft as foreign
  • if a second graft is perfomed from the same donor, it is rejected more rapidly
118
Q

What is direct allorecognition?

A

T cell recognizes unprocessed (intact) allogenic MHC molecules on the surface of donor antigen-presenting cells (APCs) in the graft

119
Q

What is indirect allorecognition?

A

T cell recognizes processed peptide of allogenic MHC molecule bound to self MHC molecule on host APC

120
Q

What is host versus graft response?

A
  • up to 2% of the host T cells are capable of recognizing and responding to single foreign MHC
  • nonimmune injury of the graft (DangerSignals, DAMPs) activates endothelial cells and T cells enter the allograft
  • Ag specific T cells interact with APC and become stimulated
  • inflammatory cytokine/chemokine field is created and causes further activation of APC, endothelium and leukocyte traffic
121
Q

What are the effector mechanisms of graft rejection?

A

humoral rejection Th2 (IL-4, IL-5, IL-10)

cellular rejection Th1 (IL-2, IFN-gamma)

122
Q

What does hyperacute rejection trigger?

A

complement activation, endothelial damage, inflammation, and thrombosis (preexisting antibodies and complement)

123
Q

What does acute rejection trigger?

A

parenchymal cell damage, interstitial inflammation (primary activation of T cells Th1 cells and CTLs)

124
Q

What does chronic rejection trigger?

A

chronic DTH reaction in vessel wall, intimal smooth muscle cell proliferation, vessel occlusion (M2 macrophages and T cells)

125
Q

What type of hypersensitivities are hyperacute, acute, and chronic rejections? When is the onset?

A

hyperacute: II, immediate
acute: IV, days to weeks
chronic: IV, months to years

126
Q

What is the mechanism and vessel histology of hyperacute rejection?

A

preformed antibodies directed against the donor tissue caused by accidental ABO blood type incompatibility (very rare).
presents while still in surgery with thrombosis and occlusion of graft vessels.

127
Q

What is the mechanism and vessel histology of acute rejection?

A

T cell mediated immune response directed against the foreign MHC.
inflammation and leukocyte infiltration of graft vessels results. MOST COMMON type.

128
Q

What is the mechanism and vessel histology of chronic rejection?

A

T cell mediated process resulting from the foreign MHC “looking like” a self MHC carrying an antigen.
results in intimal thickening and fibrosis of graft vessels as well as graft atrophy.

129
Q

When is hyperacute graft rejection more likely to occur?

A
  • ABO blood group incompatibility

- recipient sensitized to donor MHC by previous transplants, multiple blood transfusions, or pregnancy

130
Q

What does classical complement activation lead to?

A

death of the endothelium

131
Q

What cells play an important role in triggering acute rejection?

A

donor DCs, also called passenger leukocytes

  • donor DCs migrate to the lymph nodes draining the organ and stimulate a primary recipient response
  • activated T cells migrate to the organ and lead to tissue damage by generation of cytotoxic T cells and induction of delayed-type hypersensitivity reactions
132
Q

What T cells can cause graft rejection: CD4+ or CD8+?

A

Both

133
Q

What are non-immunologic factors in chronic rejection?

A
  • ischemia-reperfusion damage
  • recurrence of the disease
  • nephrotoxic drugs
134
Q

What type of rejection does not respond to immunosuppressive therapy?

A

chronic rejection

135
Q

What is graft versus host disease (GVHD)?

A
  • caused by reaction of grafted mature T cells in the marrow inoculums with allo-Ags of the host.
  • reaction directed against minor H Ags of the recipient
136
Q

Who gets GVHD?

A

immunocompromised recipients because their immune system is unable to reject the allogenic cells in the graft;
transplants of small bowel, lung, or liver (naturally contain lots of T cells)

137
Q

How is GVHD classified?

A

acute or chronic

138
Q

What is acute GVHD?

A

epithelial cell death in the skin, liver, and GI

symptoms: rash, jaundice, diarrhea, and GI hemorrhage

139
Q

What is chronic GVHD?

A

fibrosis and atrophy of affected organ
clinically: may lead to complete dysfunction of the affected organ (or two of the same)
may produce obliteration of small airways

140
Q

What type of hypersensitivity is GVHD?

A

type IV

141
Q

What is the mechanism of GVHD?

A

donor APCs activate donor CD8+ T cells by cross presenting recipient antigens on MHC class I molecules

142
Q

What are the two effector mechanism of GVHD?

A

Fas-FasL

Perforin/granzyme

143
Q

What cytokines signal myocytes to become M1 or M2?

A

M1: microbial TLR ligands, IFN gamma
M2: IL-13, IL-4

144
Q

What are the functions of M1 macrophages? M2?

A

M1: microbicidial actions: phagocytosis and killing of bacteria and fungi; inflammation

M2: antiinflammatory effects; wound repair, fibrosis

Renal Final (7 decks)

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