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Renal I > Renal Immunology > Flashcards

Renal Immunology Flashcards

1
Q

What are the two ‘categories’ of antigen that are responsible for Renal Immune disease ?

A 
Renal
   Self: GBM Collagen IV,
   Foreign: HLA from Transplants 
Non-Renal
   Self: Nucleic acids, Tumor antigen, Cryoglobulin
   Non-Self: Infectious, allergens,Drugs
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2
Q

In order for antigen to create an immune Rxn in the kidney it must either be endogenous in the kidney or be deposited (non-renal). What do most non-renal antigens form in order to be deposited in the Kidney ?

A

Immune complexes (Type III) floating in the blood

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3
Q

Where are the 4 sites that immune complexes will deposit in the kidney ?

A

Glomerular mesangium
Glomerular Basement Membrane (GBM)
Endothelial cells lining the inside of the GBM
Endothelial cells lining the outside of the GBM

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4
Q

In Berger Disease (IgA nephropathy) where will IgA deposit ? Why ?

A

In the mesangium

IgA is a large molecule and will not penetrate to the GBM

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5
Q

Where will bacterial antigens complexed with IgG tend to localize ?

A

WIthing the GBM or on the epithelial side of the GBM.

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6
Q

Is Berger Disease diffuse or focal ?

A

Focal (only occurs in a small portion

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7
Q

Berger disease usually presents with which renal complication ?

A

Hematuria

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8
Q

Berger disease usually follows what occurrence in young males ?

A

Upper respiratory infection

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9
Q

What systemic disease is associated with Berger Disease ?

A

Henoch-Schonlein Purpura

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10
Q

What is unusual about glomerular capillary beds ?

A

It is situated between two arterioles instead of an arteriole and a venule

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11
Q

Normally, Capillary pressure should always be higher than Bowman space thus leading to ….

A

filtration

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12
Q

What type of Ig mediates Type I hypersensitivity ?

A

IgE

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13
Q

What type of Ig mediates type II hypersensitivity ?

A

IgM, IgG (Direct binding)

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14
Q

What type of Ig mediates Type III hypersensitivity ?

A

IgM, IgG ( Immune Complex)

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15
Q

What mediates Type IV hypersensitivity ?

A

T-Cells

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16
Q

Besides the hypersensitivity run’s, Ag-Ab complexes initiate immune inflammatory injury via which two mechanisms ?

A

Direct Compliment activation
Immunodeficiency disorders
AIDS, etc

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17
Q

Anti-GBM disease, Anti-TBM, hyper acute rejection and Wegner Granulomatis are all associated with which kind of hypersensitivity ?

A

Type II (Direct Cytotoxic )

Leads to linear deposition (smooth, not lumpy bumpy)

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18
Q

Anti GBM disease is due to Ab’s directed at which antigen ?

A

GBM (Type II)

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19
Q

Anti-TBM disease is due to Ab’s directed at which antigen ?

A

Tubular membrane antigens (Type II)

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20
Q

Hyper-acute rejection syndrome is due to Ab’s directed at which antigen ?

A

Class I -HLA (Type II)

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21
Q

Wegner Disease is due to Ab’s directed at which antigen ?

A

Cytoplasmic MPO of neutrophils

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22
Q

What is the distinction given to Immune complex associated Glomerulonephritis (GN) on immunofluorescence ?

A

Lumpy-Bumpy deposition ( Type III)

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23
Q

Chronic Renal Allograft rejection is due to cell mediated hypersensitivity (Type IV). What antigen is this immune response directed at ?

A

Class II HLA antigens

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24
Q

What pattern of damage do you see in Cell mediated hypersensitivity in the kidney ?

A

Diffuse, granular

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25
Q

What kind of immune reactions is responsible for Chronic GN ?

A

Type IV (cell mediated) directed at renal antigens

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26
Q

Immmune tubular interstitial disease is mediated by which kind of immune run ?

A

Type I (IgE mediated)

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27
Q

Membranoproliferative GN is due to which kind of immune rxn ?

A

Direct C mediated (Alternative pathway). Immune compled to C3 nephritic factor.

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28
Q

In AIDS you will see focal segmental GN due to which antigen ?

A

HIV !

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29
Q

Lupus- Like Syndrome is due to deficiency in what immune product ?

A

Complement

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30
Q

Hemolytic uremic syndrome is due to deficiency in which factor ?

A

Factor H deficiency.

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31
Q

When allergen sensitive T-Cells encounter specific antigen, they release which two interleukens that lead to increased IgE production ?

A

IL-4 and 5

32
Q

IgE that is created during a Type I hypersensitivity will attach to Mast and Basophils, activating them. When these Mast Cell/IgE complex come into contact with antigen which vasoactive amine(s) are released ?

A

Histamine…..

Chemokines are also released: MCP-1, RANTES, IP-10

Prostaglandins are produced

33
Q

Allergic Tuberointerstitial disease is often caused by sensitivity to which anti-biotic ? What kind of hypersensitivity is this ?

A

Penicillin

Type I

34
Q

What factor is released during Allergic Tuberointerstial disease that leads to eosinophilia ?

A

ECF (Eosinophil chemotactic pattern)

35
Q

What class of drugs has a good response when used to treat Allergic Tuberointerstitial disease ?

A

Corticosteroids

36
Q

Goodpastures disease is a Type II disease which shows linear deposition of which antibody on which self antigen ?

A

Collagen IV (Anti-Collagen IV anti-body)

37
Q

What is the cause of cell damage in Goodpasture Disease ?

A

Antigen-Anti-body complex activating complement leading to the formation of MAC.

MAC directly damages cells
Complement particles are chemotactic for other inflammatory cells (C5a –> Neutrophils)
Neutrophils lead to the release of lysozyme causing major oxidative damage.

38
Q

Anti-Nuclear Cytoplasic Anti-bodies are specific for cytoplasmic constituents in which cells ?

A

Neutrophils

39
Q

What do ANCA’s target ?

A 
MYELOPEROXIDASE 
lysozyme 
elastase
proteinase 3 (c-ANCA antigen.)
lactoferrin
cathepsins B, D, and G
40
Q

What does it means to be “Pauci-immune” ?

A

No demonstration of immune components on immunofluorescence, however ANCA still plays a role

You will not see IgG or C3 in the basement membrane of the glomerulus

41
Q

What are the three diseases that must be differentiated why referring to Pauci-Immune Rapidly progressing glomerulonephritides ?

A

Type III Idiopathic Crescentic glomerulonephritis
Wegner Granulomatosis
Microscopic Polyangiitis

42
Q

Which of the Pauci Immune diseases is most common of the Rapidly Progressing glomerulonephritides ?

A

Type III Idiopathic Crescentic Glomerulo Nephritis

43
Q

Wegners Granulomatosis is the prototype ANCA related renal disease. What is the most predominant form of ANCA in this disease ?

A

cANCA (90%)

44
Q

The binding of ANCA to cytoplasmic targets in neutrophils leads to the up-regulation of which molecules on neutrophils ?

A

Beta 2 integrin : rolling adhesion
ICAM-1 : Tight Binding
ELAM 1 : Adhesion

Overall this activation leads to increased extraversion into areas of the body, in this case the glomeruli

45
Q

Describe the Histopathology of Wegners ?

A

Rapidly progressing crescentic GN

T-CEll Mediated Granulomas in the Kidney and Respirtory tract

46
Q

how can you tell the difference between WG and Microscopic polyangiitis ?

A

There will be vasculitis without the formation of granulomas or deposition of Ig i

47
Q

What is the difference between WG and Idiopathic Crescentic GN ?

A

Idiopathic Crescentic GN does not include the Lungs whereas WG will include lung lesions

48
Q

Where will immune complexes (Type III) typically aggregate ?

A

Mesangium
Glomerular Capillary Wall
Renal interstitium.

49
Q

In Type III hypersensitivity, what pattern will be shown in immunofluroscopy of Ab-Complement ?

A

“Lumpy Bumpy” not linear deposition seen in Type II.

50
Q

What are the two ways in which immune complex come to be in the kidney ?

A
  1. Antigen is planted in the kidney, circulating Ab binds to it as it passes through
  2. Ag-Ab complex is in the blood flow and settles out –> Deposition in mesangium and glomerular capillary wall
51
Q

What kind Complement pathway is often associated with Type III hypersensitivity ?

A

Classical (needs Ab-Ag complex to be activated)

52
Q

What will the effect of vasoactive substances have on the deposition of immune complexes ?

A

It will allow for increased penetrance of immune complexes since it makes the endothelium more permeable.

53
Q

The CR1 receptor on glomerular epithelial cells is specific for which complement fragment ?

A

C3b

54
Q

The Fc receptor for the Fc portion of IgG is found on which cells in the glomerulus ?

A

Mesangial

Interstitial Cells

55
Q

In acute organ rejection of the kidney, MHC1 is processed monocytes and macrophages. These cells will then release IL-1 which leads to IL-2 synthesis. What important function does IL-2 have in Acute Organ Rejection ?

A

Activates T-Helper cells which in turn activate T-cytoxic (CD8) cells which attack the foreign organ Acute Rejection sounds like a Type IV (cell mediated) hypersensitivity ?

Wasn’t sure since in the chart is had said MHCI recognition was hyper-acute and thus type II

56
Q

In Chronic Organ rejection, the activated T-cells produce cytokines. How do these cytokines affect organ transplant success ?

A

Cytokines induce the proliferation of endothelial and smooth muscle cells. This leads to occlusion of renal blood vessel –> destruction of organ tissue due to arteriosclerosis

Delayed Type Hypersensitivity to alloantigens in graft vessels.

57
Q

What occurs in Post-Streptococcal Glomerulonephritis that leads to organ damage/failure ?

A

T-Cells stimulated by Streptococcal wall Ag’s may cross react with glomerular Ag’s leading to sclerosis of parenchyma and progressive death

58
Q

In hyperacute rejection, a presensitized host has preformed Ab’s to to allograft endothelium. Activation of what immune component leads to intravascular thrombosis and sclerosis leading to acute ischemia or infarction of the transplant ?

A

Complement system

59
Q

Are Ab’s involved in direct Complement mediated renal disease ?

A

NOPE !

This is done by the alternative pathway involving (C3 and properidin)

60
Q

In the alternative pathway, properidin stabilizes which molecule to allow for activation ?

A

C3bBb (C3 convertase)

61
Q

C3bBbC3b is also known as ?

A

C5 convertase

62
Q

Direct complement activations results in which disease ?

A

Membranoproliferative Glomerulonephritis (MPGN)

63
Q

What is MPGN characterized by ?

A

proliferation of cellular elements within the renal corpuscle and increased capillary wall thickness.

64
Q

Type I MPGN is associated with what deposited in the sub endothelial sites along the capillary wall.

A

C3 (IgM/G)

65
Q

Type II MPGN is associated with

A

Dense intramembranous deposits of C3 Nephrotic Factor

There is a third one which is a mixture of the first to Membrano Proliferaive Glomerulonephritis.

66
Q

What complement pathway does Type I MPGN activate ?

A

Classical (C3 and IgM/G)

67
Q

What Complement pathways does Type II MPGN activate ?

A

ALternative

68
Q

How does the appearance of the basement membrane in Type I/II MPGN differentiated ?

A

Both Cause thickening, however in Type I you will see : Tram Tracking

In Type II: Ribboning (Due to C3 Nephrotic Factor)

69
Q

Whats is C3 Nephrotic Factor ?

A

IgG auto-antibody to the Alternative Pathway C3b Convertase

Causes Stabilization of C3 Covertase
Acts like Properidin
Protects it from degradation by Factor I

70
Q

HIV is associated with Focal Segmental Glomerulosclerosis (FSGS). Which ethnic group is associated with rapidly progressing FSGS

A

African Americans

IV drug users

Often present with PROTEINURIA

(Whites usually have less quickly progressing, also have no proteinuria seen)

71
Q

Early FSGS is characterized by ….

A

Focal deposition of IgM and C3 –> Scarring of the glomeruli
–> Blood filtration and urine production impaired

72
Q

Later Histopathology of FSGS shows which kind of cells on Renal biopsy ?

A

Many CD8 and CD2+ T-Cell infiltrates and more extensive collapse of entire glomeruli.

73
Q

What structures seen in the glomerular endothelial wall suggest a viral role in late stage FSGS ?

A

Tubuloreticular strutures.

74
Q

Immune Complex- like disease in patients with HIV typically arise from

A

circulation of bacterial, viral, or tumor-associated immune complexes to the kidney, triggering an immune complex-mediated renal disease

75
Q

IgA Glomerulonephritis is seen with which Histocompatability complexes ?

A

HLA-B35 (MHC I) and HLA-DR4 (MHC II)

76
Q

Anti-GBM or Goodpasture syndrome are seen with which Histocompatability complex ?

A

HLA-DR2 (MHCII)

Renal I (8 decks)

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