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Why the need ?
 Only treatment of choice for end-stage organ failure
What is Major Histocompatibility
Complex?
 Cell surface antigens
 Synonymous to HLA (Human leukocyte antigen)
 Multiple genes involved and regulate the antigenic
expression
Human Leukocyte Antigen
3 class
 Class I - determine histocompatibility and the
acceptance or rejection of allografts
 Comprises A, B, C loci
 Class II – regulate immune response
 DR, DQ & DP
 Class III – components of the complement system
 C2 and C4 of the classical pathway
Types of Grafts
 Recongnition of Graft Alloantigens
 Direct
 Indirect
 T-cell mediated Rejection
 Acute cellular rejection
 Chronic rejection
 Antibody mediated rejection
 Hyperacute
 Acute
 Chronic
T cell mediated
 In acute cellular rejection, direct killing of graft cells
by CD8+ CTLs
 Cytokines secreted by activated CD4+ T cells
 Increased vascular permeability and local
accumulation of mononuclear cells
 Activated lymphocytes damage graft cells
In chronic rejection, lymphocytes
reacting against alloantigens in the
vessel wall secrete cytokines that
induce local inflammamtion and
stimulate the proliferation of vascular
endothelial and smooth muscle cells.
Antibody-mediated Rejection
 Affects recipients sensitised with pre-transplant
donor-specific antibodies to HLA or post-transplant
de novo HLA or non-HLA antibodies.
 Coexists with Acute cellular rejection
Pathogenesis of AMR
 Hyperacute
 Preformed antibodies present in the circulation of the
recipient
 Acute
 Produced after transplant, complement activation,
inflammation, antibody dependent cell mediated
cytotoxicity
 Chronic
 Insidious in onset, affects vascular components
Risk Factors
 Younger age
 Female gender
 Prior sensitization to
OKT3
 Cytomegalovirus
seropositivity
 Pregnancy
 Previous transfusion
 Surgery
 Transplantation
 Cardiac support
 hemodialysis
Limited treatment options
 Plasmapheresis
 Immunoadsorption
 Intravenous immunoglobulin
 Intensive immunosuppression
 Monoclonal antibodies
Organs we’ll be dealing
with
 Kidney
 Heart
 Liver
 Lung
Kidney
 Sample to be collected in
 10% buffered formalin for histopathological
examination
 Glutaraldehyde for electron microscopy
 Michel’s medium for immunoflouresence
Adequacy criteria of a core
Number of glomeruli for adequate
diagnosis:
an intact blood vessel along with
For glomerular lesions: 5
For tubulointerstitial lesions: 6-10
For transplant kidney: 7
4 routine stains performed
Case 1
76 year old male presented with rapidly rising serum
creatinine levels after renal transplant 12 hours ago.
 Congested capillaries
 accumulation of t lymphocytes
 fibrinoid necrosis
 thrombotic microangiopathy
IgG and IgM linear deposits along with C4d
Hyperacute Rejection
Case 2
72 year old female presented with hematuria after a
week of renal transplantation
 prominent interstitial
 mononuclear cell infiltrate
 Tubulitis is the hallmark of acute interstitial rejection.
 rupture of the tubular basement membrane (which is
periodic acid-Schiff positive), with subsequent
invasion of the tubular epithelium by inflammatory
cells. A mitotic cell is also seen in the middle.
CD 3
Granular patchy c3
Acute Rejection
Case 3
65 year old male presented with increase BUN and
oliguria, 6 months post renal transplantation
 prominent fibrous intimal thickening
 severe narrowing of the arterial lumen
Chronic rejection
Banff Classification
 6 diagnostic categories
 Normal
 Hyperacutre
 Boderline
 Acute rejection
 Chronic rejection
 Other (features not related to rejection)
 The diagnosis of renal AMR is multidisciplinary and
requires DSA positivity, C4d deposition in peritubular
capillaries and histological features of AMR.
Acute Rejection
 Grade I : moderate interstitial infiltrate with tubulitis
but no vascular changes
 Grade II : moderate to severe interstitial infiltrate
with severe tubulitis, possible mild to moderate
intimal arteritis
 Grade III: severe intimal arteritis with fibrinoid
necrosis, infarcts, interstitial hemorrhage, severity of
interstitial infiltrate is irrelevant
Chronic Rejection
 Grade I : Mild interstitial fibrosis with tubular atrophy
 Grade II : Moderate interstitial fibrosis with tubular
atrophy
 Grade III : Severe interstitial fibrosis with tubular
atrophy or loss
Hyperacute rejection
 is an antibody-mediated process characterized
 by necrotizing arteritis
 a polymorphonuclear infiltrate
 ischemic damage to the organ
 is a rare event in the liver
Acute rejection
 characterized by a mixed portal infiltrate predominantly
 composed of lymphocytes with intermixed neutrophils and
eosinophils.
 The major targets of attack are bile duct epithelium and venous
endothelium
 The hepatocytes are not a major target of attack in acute
disease.
 Other features seen in rejection
 loss of bile ducts, arteritis, and/or central ischemic damage in
the form of hepatocellular ballooning and dropout of clusters
of hepatocytes
Chronic Rejection
 Two forms have been recognized:
 chronic vascular rejection with ischemic damage to
hepatocellular parenchyma
 and chronic biliary rejection with total loss of bile
ducts
 The hallmark of chronic vascular rejection is
 obliterative endarteritis
 the obstruction of arteries by subintimal fibrosis
 or the accumulation of foamy histiocytes
Grading
 pAMR 1 – either pAMR1(h+) or pAMR1(i+)
 pAMR 2 – both histopathological changes and
immunopathological findings
 pAMR 3 – histo and immuno findings of extensive
myocardial damage and disruption of
microcirculation
Concomitant ACR is frequently found and should be
graded separately.
 True incidence unknown as definitions and
diagnostic criteria are currently lacking
 Known patterns of immunologic injury include
 Lymphocytic bronchiolitis
 Bronchiolitis obliterans syndrome
 Capillary C4d deposition
 Diffuse alveolar damage
Conclusion
 Microscopic features coomon to all are
 Capillary endothelial activation
 Microvascular inflammation
 IV inflammatory cells - macrophages
 Capillary deposition of C4d

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Antibody mediated rejection pathology histopathology

  • 1.
  • 2. Why the need ?  Only treatment of choice for end-stage organ failure
  • 3. What is Major Histocompatibility Complex?  Cell surface antigens  Synonymous to HLA (Human leukocyte antigen)  Multiple genes involved and regulate the antigenic expression
  • 5. 3 class  Class I - determine histocompatibility and the acceptance or rejection of allografts  Comprises A, B, C loci  Class II – regulate immune response  DR, DQ & DP  Class III – components of the complement system  C2 and C4 of the classical pathway
  • 6.
  • 8.  Recongnition of Graft Alloantigens  Direct  Indirect
  • 9.
  • 10.
  • 11.  T-cell mediated Rejection  Acute cellular rejection  Chronic rejection  Antibody mediated rejection  Hyperacute  Acute  Chronic
  • 12. T cell mediated  In acute cellular rejection, direct killing of graft cells by CD8+ CTLs  Cytokines secreted by activated CD4+ T cells  Increased vascular permeability and local accumulation of mononuclear cells  Activated lymphocytes damage graft cells
  • 13. In chronic rejection, lymphocytes reacting against alloantigens in the vessel wall secrete cytokines that induce local inflammamtion and stimulate the proliferation of vascular endothelial and smooth muscle cells.
  • 14. Antibody-mediated Rejection  Affects recipients sensitised with pre-transplant donor-specific antibodies to HLA or post-transplant de novo HLA or non-HLA antibodies.  Coexists with Acute cellular rejection
  • 15. Pathogenesis of AMR  Hyperacute  Preformed antibodies present in the circulation of the recipient  Acute  Produced after transplant, complement activation, inflammation, antibody dependent cell mediated cytotoxicity  Chronic  Insidious in onset, affects vascular components
  • 16. Risk Factors  Younger age  Female gender  Prior sensitization to OKT3  Cytomegalovirus seropositivity  Pregnancy  Previous transfusion  Surgery  Transplantation  Cardiac support  hemodialysis
  • 17. Limited treatment options  Plasmapheresis  Immunoadsorption  Intravenous immunoglobulin  Intensive immunosuppression  Monoclonal antibodies
  • 18.
  • 19. Organs we’ll be dealing with  Kidney  Heart  Liver  Lung
  • 20.
  • 21.
  • 22. Kidney  Sample to be collected in  10% buffered formalin for histopathological examination  Glutaraldehyde for electron microscopy  Michel’s medium for immunoflouresence
  • 23. Adequacy criteria of a core Number of glomeruli for adequate diagnosis: an intact blood vessel along with For glomerular lesions: 5 For tubulointerstitial lesions: 6-10 For transplant kidney: 7
  • 24.
  • 25. 4 routine stains performed
  • 26.
  • 27.
  • 28.
  • 29. Case 1 76 year old male presented with rapidly rising serum creatinine levels after renal transplant 12 hours ago.
  • 30.
  • 31.  Congested capillaries  accumulation of t lymphocytes  fibrinoid necrosis  thrombotic microangiopathy
  • 32. IgG and IgM linear deposits along with C4d
  • 34. Case 2 72 year old female presented with hematuria after a week of renal transplantation
  • 35.
  • 36.
  • 37.  prominent interstitial  mononuclear cell infiltrate  Tubulitis is the hallmark of acute interstitial rejection.  rupture of the tubular basement membrane (which is periodic acid-Schiff positive), with subsequent invasion of the tubular epithelium by inflammatory cells. A mitotic cell is also seen in the middle.
  • 38. CD 3
  • 41. Case 3 65 year old male presented with increase BUN and oliguria, 6 months post renal transplantation
  • 42.
  • 43.
  • 44.  prominent fibrous intimal thickening  severe narrowing of the arterial lumen
  • 46.
  • 47.
  • 48. Banff Classification  6 diagnostic categories  Normal  Hyperacutre  Boderline  Acute rejection  Chronic rejection  Other (features not related to rejection)  The diagnosis of renal AMR is multidisciplinary and requires DSA positivity, C4d deposition in peritubular capillaries and histological features of AMR.
  • 49. Acute Rejection  Grade I : moderate interstitial infiltrate with tubulitis but no vascular changes  Grade II : moderate to severe interstitial infiltrate with severe tubulitis, possible mild to moderate intimal arteritis  Grade III: severe intimal arteritis with fibrinoid necrosis, infarcts, interstitial hemorrhage, severity of interstitial infiltrate is irrelevant
  • 50. Chronic Rejection  Grade I : Mild interstitial fibrosis with tubular atrophy  Grade II : Moderate interstitial fibrosis with tubular atrophy  Grade III : Severe interstitial fibrosis with tubular atrophy or loss
  • 51.
  • 52.
  • 53.
  • 54. Hyperacute rejection  is an antibody-mediated process characterized  by necrotizing arteritis  a polymorphonuclear infiltrate  ischemic damage to the organ  is a rare event in the liver
  • 55.
  • 56.
  • 57. Acute rejection  characterized by a mixed portal infiltrate predominantly  composed of lymphocytes with intermixed neutrophils and eosinophils.  The major targets of attack are bile duct epithelium and venous endothelium  The hepatocytes are not a major target of attack in acute disease.  Other features seen in rejection  loss of bile ducts, arteritis, and/or central ischemic damage in the form of hepatocellular ballooning and dropout of clusters of hepatocytes
  • 58.
  • 59. Chronic Rejection  Two forms have been recognized:  chronic vascular rejection with ischemic damage to hepatocellular parenchyma  and chronic biliary rejection with total loss of bile ducts  The hallmark of chronic vascular rejection is  obliterative endarteritis  the obstruction of arteries by subintimal fibrosis  or the accumulation of foamy histiocytes
  • 60.
  • 61.
  • 62.
  • 63.
  • 64.
  • 65. Grading  pAMR 1 – either pAMR1(h+) or pAMR1(i+)  pAMR 2 – both histopathological changes and immunopathological findings  pAMR 3 – histo and immuno findings of extensive myocardial damage and disruption of microcirculation Concomitant ACR is frequently found and should be graded separately.
  • 66.
  • 67.
  • 68.
  • 69.
  • 70.
  • 71.
  • 72.
  • 73.  True incidence unknown as definitions and diagnostic criteria are currently lacking  Known patterns of immunologic injury include  Lymphocytic bronchiolitis  Bronchiolitis obliterans syndrome  Capillary C4d deposition  Diffuse alveolar damage
  • 74.
  • 75. Conclusion  Microscopic features coomon to all are  Capillary endothelial activation  Microvascular inflammation  IV inflammatory cells - macrophages  Capillary deposition of C4d

Editor's Notes

  1. Donor APC have HLA and costimulatory factors , draining lymph nodes, damage the vasculature
  2. Recipients own apc, similar to physiological presentation of antigen, cd8+ cannot destroy graft cells because not presented by APC directly
  3. Capillary endothelial cells form the boundary between the allograft parenchyma and the recipient’s blood
  4. Okt3 is the first monoclonal antibody used to treat patient. Its an immunosuppresant drug
  5. PAS
  6. MT
  7. Methenamine silver
  8. Congested capillaries, accumulation of t lymphocytes, fibrinoid necrosis and thrombotic microangiopathy
  9. igG and igM linear deposits along with c4d
  10. prominent interstitial mononuclear cell infiltrate
  11. Tubulitis is the hallmark of acute interstitial rejection. Note the rupture of the tubular basement membrane (which is periodic acid-Schiff positive), with subsequent invasion of the tubular epithelium by inflammatory cells. A mitotic cell is also seen in the middle.
  12. Granular patchy c3
  13. prominent fibrous intimal thickening with severe narrowing of the arterial lumen
  14. inflammatory portal infiltrate with bile ductular destruction. The morphologic evidence of bile ductular damage includes a disordered appearance of bile duct epithelial cells, lack of a visible bile duct lumen, and inflammatory cell infiltrates in the bile duct walls.     
  15. P stands for pathologic
  16. Microvascular inflammation with c4d deposition
  17. Cd68 postive macrophages
  18. Edema, vasculitis, hemorrhage, microvascular thrombosis, capillary damage and myocyte necrosis
  19. Neutrophilic septal infiltrates, congestion, hemorrhage, fibrin deposition,