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

Immunological Aspects of the Renal System Flashcards

1
Q
  • Functional and structural criteria of NKD (no kidney disease)
A
  • GFR > 60 mL/min per 1.73 m2
  • Stable Serum Creatinine
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2
Q
  • Functional and structural criteria of AKI
A
  • Increase in serum creatinine by 50% within 7 days or increase in Serum Creatinine by 0.3 mg/dL within 2 days
  • or Oligouria
  • No structural changes
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3
Q
  • Functional and structural criteria of CKD
A
  • GFR < 60 mL/min for > 3 months
  • Structural criteria: Kidney damage for > 3 months
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4
Q
  • Causes of Kidney Hypoperfusion and AKI
A
  • Intravascular volume depletion and hypotension
  • Decreased effective intravascular volume
  • Medications
  • Hepatorenal syndrome
  • Sepsis
  • Renal Vascular Disease
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5
Q
  • In most cases AKI is not caused by infection, it is caused by a _
A
  • Sterile Inflammation
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6
Q
  • Sterile renal inflammation is induced by intrinsic _
    • When are DAMPS released and generated?
  • _ protein has IgM like subunits that bind DAMPs and activate compliment via the _ pathway
A
  • DAMPs
  • Released from dying parenchymal kidney cells
  • Generated during ECM degradation and remodeling
  • CRP has IGM like subunits and can bind DAMPs
  • Classical
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7
Q
  • Immune cells can recognize DAMPs via _
  • Binding induces
A
  • Toll Like Receptors (TLRs)
  • Binding of TLRs on immune cells to DAMPs induces immune responses and renal inflammation
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8
Q
  • DAMPs
  • What are they?
  • What are some examples?
A
  • alarmins-endogenous intracellular molecular structures
  • HMGB1 (nucleolus protein)
  • Uric Acid
  • HSPs (exosomes)
  • S100 protein (cytoplasm)
  • Hyaluronans in ECM
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9
Q
  • Inflammation is caused by _ and _
  • PAMPs are part of _ immunity
  • DAMPs are part of _ immmunity
A
  • PAMPs and DAMPs
  • Innate
  • Adaptive (D in Damp and Adaptive)
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10
Q
  • Sensors for PAMPs and DAMPs
A
  • TLRs
  • NOD like receptors
  • C type lectin
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11
Q
  • Inflammation mediators
A
  • TNF-alpha
  • IL=6
  • IL-1Beta
    *
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12
Q
  • What role do dendritic cells play in immune cell mechanisms of kidney injury?
A
  • Antigen presentation
  • Migration-travel to lymph to activate B and T Cells
  • Release Type I IFNs, CXCL2, IL-1Beta and IL-12

Important in acute kidney injury and infections

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13
Q
  • What types of macrophages are classically activated?
  • What types of macrophages are alternatively activated?
A
  • M1
  • M2
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14
Q
  • How are M1 macrophages activated?
  • What is their function?
A
  • Induced by PAMPs and DAMPs thru binding to TLRs and PRRs
  • IFN-gamma

Function:

-Secrete ROS, lysosomal enzymes that phagocytose and kill bacteria and fungi

-Secrete IL-12. Il-2, IL-23: INFLAMMATION

IMPORTANT FOR EARLY IMMUNE RESPONSE

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15
Q
  • How are M2 Macrophages Activated?
  • What is their function?
A
  • Activated by IL-4 and IL-13
  • Functions
    • ​Secrete: IL-10 and TGF beta which are ANTI-INFLAMMATORY
    • Secrete proline, polyamines, TGF B for wound repair and fibrosis
    • Overall work to mediate effects of M1s
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16
Q
  • By default, a T cell will differentiate into a _ cell
A
  • Th2
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17
Q
  • _ are T cells that play an important role in tissue inflammation by secreting IL-17
  • Which cytokine activates differentiation into this type of T cell?
A
  • Th17
  • IL-6, TGF Beta
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18
Q
  • Role of Th17 Cells in AKI
A
  • Secrete IL-17: Recruits neutrophils
  • Secrete CCL20/MIP-3:
    • ​Recruits monocytes
    • Th1 cells recruited
    • Th17 cells rectuired
    • Other pro-inflammatory leukocyte subsets recruited
      *
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19
Q
  • Antiobdy Mediated Immune Mechanisms in Kidney Injury
A

Type II and Type III hypersensitivity rxns

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20
Q
  • Reactant for Type II hypersensitivity in kidney injury
  • Antigen form
  • MOA
  • Examples
A
  • IgM or IgG
  • Cell-bound antigen
  • IgG or IgM binds cellular Ag, leading to complement activation and cell lysis (IgG can also mediate ADCC w/ cytotoxic T cells, NK cells, Macrophages, and neutrophils)
  • EX: Red blood cell destruction after mismatched blood transfusion, hemolytic disease of the newborn
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21
Q
  • Reactant for Type III hypersensitivity reactions
  • Antigen form
  • MOA
  • EXs
A
  • IgM or IgG
  • Soluble Ag
  • Ag-Ab complexes are deposited in tissues, complement activation induces inflammation and recruits neutrophils (released enzymes damage tissue)
  • EX: Post-streptococcal glomerulonephritis, R.A, Systemic Lupus Erythematous
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22
Q

Barrier to transplantation is _ of donor and recipient

A

Genetic incompatability

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23
Q

_ Ags are the targets for rejection

_ rejection is immediate and caused by antibody

_ rejection occurs days/weeks after transplant and is caused by T cells

_ rejection is seen over months/years and is caused by vascular trauma, inflammatory products of T cells, Abs

Successive transplant depends on the use of _ drugs

A
  • Histocompatability
  • Hyperacute
  • Acute
  • Chronic
  • Immunosupressive
24
Q

Autograft

A
  • Grafts exchanged from one part of a person to another part of that same person
25
Q

Isograft

A
  • Grafts exchanged between different individuals of identical genetic constitutions (Identical Twins)
26
Q

Allograft (most common)

A

Grafts exchanged between nonidentical members of the same species

27
Q

Xenografts

A
  • Grafts exchanged between members of different species
  • Are susceptible to rapid attack by naturally occurring Abs and complement
  • Insertion of human genes into the genomes of donor animal increases chance of successful transplant
28
Q
  • Variables determining transplant outcome
A
  1. Condition of the allograft
  2. Donor-Host Antigenic Disparity
  3. Strength of Host Anti-Donor Response
  4. Immunosuppressive Regimen
29
Q
  • Overview of immune events that take place following transplantation
A
  • APCs trigger CD4 and CD8 T Cells
  • Both local and systemic immune response develop
  • Cytokines recruit and activate immune cells
  • Development of specific T cells, NK Cells or Macrophages play a role in mediated cytotoxicity
  • Allograft rejection
30
Q
  • Non-immunological factors that affect the transplantation process
A
  • Mechanical trauma and ischemia-reperfusion injury
  • When transplanted, graft tissues release mediators that trigger cascades leading to immediate tissue damage
    • ​Clotting cascade (fibrinopeptides)
    • Fibrinopeptides increase vascular permeability and attract neutrophils and macrophages
    • Kinin cascade produces bradykinin (vasodilation-smooth muscle contraction and increased vascular permeability)
  • If these factors are not immediately controlled, can lead to allograft rejection
31
Q

Blood Group Antigens (ABO)

  • Important in transplanting _
  • Not important in transplanting _
  • Incompatibility is not a contraindication to _ cell transplantation
A
  • Important in transplantation of solid organs
  • Less important in transplanting non-vascularized tissue (cornea, heart valve, bone and tendon)
  • Stem Cell
32
Q
  • Matching Blood Group Antigens (ABO)
A
33
Q
  • In a child who needs a kidney transplant, who is the more suitable parent to serve as donor? Why?
A
  • Father
  • During pregnacy, the mother is exposed to Ags of Child and it is likely that she has produced class I and II antibodies against child Ags (occurs in approximately 50% of pregnancies, with 53% producing Class I Abs and 62% producing Class II)
34
Q
  • How do you perform the microcytotoxicity test for preformed Abs?
A
  1. Recipient serum is added to donor cells (Abs should be present in receipient serum)
  2. Recipient serum Abs bind to donor cell
  3. Complement added
  4. Complement forms MACs/pores in cell
  5. Dye is added and accumulated in cells that have MACS

Basically, the results show if dye has accumulated into the cells, that the recipient has made preformed Abs against the Ags present on the donor cells

35
Q
  • The success of transplantation is dependent on matching of _ Ags
  • Encoded by MHC Class I and II
  • HLA is extremely _
  • HLA complex is found on chromosome _
  • There are how many HLA alleles inherited/person?
  • HLA Ags are _ expressed
    *
A
  • HLA
  • HLA Ags
  • Polymorphic
  • 6
  • 10-12
  • Codominantly
36
Q
  • Which HLA class is a strong barrier to transplantation?
  • Why?
A
  • HLA Class 1 (esp HLA-A and HLA-B)
  • HLA Class I is expressed on ALL CELLS
37
Q
  • Three most important HLA Class II Ags for transplantation pairing?
A
  • HLA-DR
  • HLA-DP
  • HLA-DQ

(Doctor DP went to Dairy Queen)

38
Q
  • What is a method commonly used to type Class I HLA Ags?
  • What sources are used for lymphocytes?
  • Where is the antisera obtained from?
A
  • Complement dependent serology
  • Can use spleen or lymph nodes from cadaver donor or can use peripheral blood (w/ RBC and platelets removed) from living donor
  • HLA antisera comes from volunteers or multiparous women (women who have had more than one child)
39
Q
  • MOA of microcytotoxicity testing for Class I MHC
A
  • Done separately on both donor and recipient cell-results are compared to see if they match or not
  1. HLA-A3 Abs are added to serum samples of both donor and recipient cells
  2. If Ag for this Ab is present on the donor or recipient cells, complement is activated
  3. Compliment forms MAC complexes on cell surface and induces holes
  4. Dye is added
  5. Dye accumulates in cells that have Ag/Ab complex formed
40
Q
  • Microcytotoxicity Test (Class I MHC): HLA Ag are identical
A
41
Q
  • Microcytotoxicity Test (Class I MHC): HLA Ags not identical
A
42
Q
  • Mixed Lymphocyte Response (MLR) (Class II HLA Typing)-Donor and Recipient do not share HLA II
  • MOA
  • Is this good for transplantation?
A
  1. Donor cells are exposed to radiation (thus unable to proliferate but can serve as APCs)
  2. Mix donor and recipient cells
  3. Add H-Thymidine
  4. When Donor and Recipient do not share HLA Class II, proliferation of recipient cells occurs
  5. NOT Good for transplantation (you want the cells to share same HLA Class II)
43
Q
  • Mixed Lymphocyte Response (Class II HLA Typing): MOA when recipient cells share Class II of MHC
  • Is this good for transplantation?
A
  1. Donor cells are exposed to radiation (so they cannot proliferate, but can still act as APCs to recipient cells)
  2. Donor cells exposed to recipient cells
  3. H-3 Thymidine is NOT incorporated into DNA
  4. No Cell proliferation
  5. GOOD FOR TRANSPLANTATION
44
Q
  • Two types of immune responses in transplantation
A

Host versus graft disesae

Graft versus host disease

45
Q
  • Host v. Graft Immune Responses
A
  • Host immune system attacks donor tissue
  • Adaptive response
  • Response is more vigorous and strong than a response against a pathogen
    • ​D/T higher frequency of T cells that recognize the graft as foreign
  • Immune memory of previous encounter with donor Ags is important
    • ​EX; Animal experiments: Second graft performed from the same donor, rejected more rapidly
46
Q
  • Direct v Indirect Allorecognition
A
  • Direct:
    • T Cell recognizes unprocessed MHC molecules on donor APC
  • Indirect:
    • T Cell recognizes processed MHCs bound to Self MHC molecule on host APC
47
Q
  • Host versus Graft Immune Response **
A
48
Q
  • Types of Graft Rejection
A
  1. Hyperacute
  2. Acute
  3. Chronic
  4. Graft v. Host
49
Q
  • Hyperacute graft rejection
A
  • Within minutes of connecting circulation into transplanted organ
  • Caused by pre-existing Abs binding to endothelial cells in blood
    • How does the recipient have pre-existing Abs that are reactive to the donor tissue?
      • ABO incompatability
      • Recipient has been sensitized to donor MHC by previous transplants, blood transfusions, or pregnancy
  • Abs bind to endothelial cells and activate Classical complement pathway
  • Can lead to death of the endothelium
50
Q
  • Acute graft rejection
A
  • Days to week
  • Donor DCs migrate to lymph mnodes and stimulate a primary recipient response
  • T cells migrate to organ and lead to tissue damage by:
    • ​Generating Cytotoxic T cells
    • Induction of delayed type hypersensitivity reactions
  • Both CD4+ and CD8+ cells can cause graft rejection
  • Indirect response can also lead to acute rejection
51
Q
  • Chronic Graft Rejection
A
  • Months-years after transplantation
  • Occurs d/t occlusion of blood vessels and subsequent ischemia of the organ
  • Often accompanied w/ smooth muscle cell proliferation and macrophage infiltration
  • Main pathogenic mechanism is INDIRECT PATHWAY
  • Abs can also be involved
  • DOES NOT RESPOND TO IMMUNOSUPRESSIVE THERAPY
52
Q
  • Non-immunological factors in chronic rejection
A
  • Ischemia-reperfusion damage
  • Recurrence of disease
  • Effects of nephrotoxic drugs
53
Q
  • GVHD:
    • What causes it?
    • What is the reaction directed against?
    • What individuals is it commonly seen in?
    • Often occurs in which type of transplants?
    • How is it classified?
A

Graft Versus Host Disease

  • Caused bt reaction of grafted matrure T cells in marrow of donor cells with the Allo Ags of host
  • Directed agsint minor H Ags od recipient (cuz HLA-A is usually matched for)
  • Immunocompromised recipients (can’t reject allogenic cells in graft)
  • Small bowel, lung, liver
  • Classified as Acute or Chronic
54
Q
  • Acute GVHD
    • What occurs?
    • What are the clinical sx?
A
  • Epithelial cell death in skin, liver, GI tissues
  • Sx:
    • Rash
    • Diarrhea
    • Jaundice
    • GI Hemorrhage
55
Q
  • Chronic GVHD:
    • What occurs?
    • What is the clinical presentation?
A
  • Fibrosis and atrophy of affected organ
  • Dysfunction of affected organ, obliteration of small airways
56
Q
  • What are the two effector mechanisms of GVHD?
A
  • Fas-FasL
  • Perforin/Granzyme

Renal Exam 2 (8 decks)

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