1. Kidney Transplant
Dr. Basu

2. Type of Grafts 1
Allograft: An organ or tissue transplanted from one individual to another of the same species, i.e. human to human.
Auto graft: Tissue that is taken from one site and grafted to another site on the same person; "skin from his thigh replaced the burned skin on his arms“

3. Type of Grafts 2
Xenograft: A xenograft is a transplantation of tissue from a donor of one species to a recipient of another species
Fetal tissue grafts: Less chance of reaction.

4. Mechanism of graft rejection
T cell mediated reaction
Involve Cytotoxic T cell ( CD8+)
Type IV hypersensitivity reaction
Antibody mediated reaction
(mainly by ADCC)= a variant of Type II.

5. When you give a graft The organ contains Tissues of the organ
Some lymphocytes of the donor
Some macrophage (APC) of the donor that contain MHC I and MHC II receptor.

6. Rejection
Direct pathway
Indirect pathway

7. In the direct pathway Donor’s
MHC I receptor on APC activate CD 8+ cytotoxic cells of host → → kill graft cells directly.
MHC II receptor on APC activate CD4+ helper T cells of host → cytokines→ tissue damage.

8. In the indirect pathway
The host develop antibody against graft antigen
Later that produce Ab-Ag complex.
This complex produce vasculitis ( Fibrinoid necrosis) →tissue damage.

9. Types of rejection reaction
Hyper acute rejection
Acute rejection:
Chronic rejection
Hyper acute ↓
Acute rejection
Chronic rejection
Minutes to hours
Within months
Years

10. Hyperacute rejection
Hyperacute rejection occurs when preformed antidonor antibodies are present in the circulation of the recipient.

11. Kidney change
Hyper acute rejection
kidney rapidly becomes cyanotic, mottled, and flaccid and may excrete a mere few drops of bloody urine.
Swollen necrotic epithelial cells with nuclear pyknosis.

12. Transplant reaction Hyper acute rejection Antibody mediated.
Ag-Ab reaction
Fibrinoid necrosis of arterioles, thrombus in vessels, Neutrophils in the area.
Acute rejection
2 types
1. Acute
cellular rejection→
CD4+ and CD8+ cell in tissue.
2. Acute Humoral rejection→
Necrotizing Vasculitis. And Neutrophils in the tissue.

13. Antibody mediated vascular damage
Chronic Rejection
Antibody mediated vascular damage
Vascular intimal proliferation. Perivascular fibrosis.
Mononuclear cells + eosinophils.
Atheroma formation.

14. Management
Drug cyclosporine (block nuclear factor of activated T cells- thus inhibit the gene for IL-2).
Monoclonal anti-T-cell antibodies (e.g., monoclonal anti-CD3 and antibodies against the IL-2 receptor α chain).

15. Thank you