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Renal > Renal Transplantation > Flashcards

Renal Transplantation Flashcards

1
Q

Notes on deceased vs living donor kidney transplants

A

Deceased

  • Higher earliy morality rate, lower mortality risk in long term

Live donor

  • Trump deceased donors for graft survival in long term
    • 5YS graft = 90% in living donor 80% in deceased
    • 5YS patient = 96% living donor, 90% with deceased
  • Allows pre-emptive treatment → graft and patient survival improved in pre-emptive vs non-preemptive treatment
  • 25% Tx Australia are living donor
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2
Q

Notes on HLA incompatibility

A
  • HLA sensitised patients remain difficult to match. HLA sensitisation from:
    • Previous transplants (poorly HLA matched)
    • Pregnancies
    • Blood transfusions → avoid where possible (EPO helps to reduce blood transfusions in CKD and reduce risk of HLA sensitisation)
  • To detect donor specific anti-HLA antibodies against any potential donor:
    • Options are cdc (compleent dependent cytotoxicity crossmatch, flow cross match, virtual crossmatch (single antigen bead).
    • Risk of rejection/graft loss if positive test: CDC > flow > virtual XM
    • If you have a “reasonably weake: donor specific antibody from virtual XM and phycial one if negative outcomes can be ”quite reasonable” compared to Tx without a donor specific antibody in terms of graft survival
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3
Q

Notes on ABO incompatible kidney transplants

A
  • ABO incompatible kidney transplant has been occurring in Japan for several decades (deceased donor option quite limited)
    • In “contemporary era” - graft survival almost equivalent to ABO compatible transplants
  • Australia/NZ
    • First month - increased death censored graft loss and rejection (still very low)
    • In the long-term no difference in the graft or patient survival compared with APO compatible transplant
  • Antibody removal via plasma exchange
  • Try to maintain antibody levels at a low level for 2-4 weeks to allow for process called accommodation
    • Kidney biopsy - antigen-antibody interaction (positive C4D staining) without any evidence of rejection - quite specific for ABO incompatible kidney transplants
    • Not performed for HLA donor specific antibodies
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4
Q

Eligibility criteria for kidney transplant

A
  • ESKD requiring dialysis (in NZ, eGFR < 15, don’t need to be on dialysis)
  • Low perioperative mortality risk
  • Reasonable post transplant patient and graft survival with liklihood of significant benefit from transplant
  • Age not a contraindications
    • Carefully selected > 70 years, limited comorbidities
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5
Q

Risk of ESKD post kidney donation

A

Low absolute but increased risk of ESKD post donation. Lifetime risk <1%

Lifetime risk higher in the younger donor candidates

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6
Q

General standard immunosuppression following renal transplant

A

Basiliximab induction following triple therapy 1. Prednisone 2. Calcineurin inhibitor - tacrolimus (usually ciclosporin in NZ) 3. Anti-metabolite - mycophenolate vs azathioprine

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7
Q

Basiliximab vs ATG in induction therapy for renal transplant

A

Basiliximab: human/mouse chimeric Ab, binds to IL-2 receptor (anti CD25) on activated T cells, reduction in acute rejection vs placebo - benefit less clear in tacrolimus era, minimal side effects (expensive) ATG: rabbit polyclonal Ab, targets T cells, reduction in acute rejection (superior vs Basiliximab in high immunological risk group - less clear in long term graft survival). Increased risks of infections and malignancies. EBV donor positive, recipient negative - post transplant lymphoproliferative disorder Mostly used for treatment of steroid resistant rejection rather than induction therapy

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8
Q

Calcineurin inhibitors in renal transplant

A

Tacrolimus and ciclosporin

  • Both nephrotoxic - acute and chronic -
  • Hypertension, hyperlipideamia
  • TMA - No bone marrow suppression
  • “Safe in pregnancy

Tacrolimus

  • Less acute rejection and early graft loss L
  • ess de novo DSA (A/W chronic rejection and graft loss)
  • More post transplant diabetes
  • Magnesium and phosphate derangements,
  • Tremor
  • More nephrotoxic than ciclosporin M
  • More hair loss compared to ciclosporin

Ciclosporin

  • Gum hypertrophy, hirsutism - more so than Tacrolimus
  • Lowers levels of mycophenolate → one reason for less rejection with tacrolimus
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9
Q

Mechanism of action of myocphenolate

A

Inhibits IMPDH (inosine-5 monophosphate dehydrogenase) involved in purine synthesis

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10
Q

Adverse effects of mycophenolate

A

GI upset - dose dependent response
Myelosupression - 2-6 months after initiation
Infection
Malignancy
Teratogenic
Levels lowered by cyclosporin but not tacrolimus

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11
Q

Anti-metabolites in renal transplant - mycophenolate vs azathioprine

A

Mycophenolate

  • Less acute rejection and ?graft loss compared to azathioprine
  • More diarrhoea
  • Teratogenic - contraindicated in pregnancy - need to switch to azathioprine in pregnancy (usual regimen CNI + AZA + pred)
  • No drug interactions with allopurinol/febuxostat (role of xanthine oxidase in purine metabolism)
  • No issue with TMPT deficiency
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12
Q

Sirolimus - mechanism of action and side effects

A

Mammalian target of rapomycin (mTOR) inhibitor. Binds to FK binding protein and inhibits mTOR -> inhibits IL2 signalling
Side effects - wound compliations/fluid collection, proteinuria, haematological - cytopaenia with antimetabolite, TMA (W/ CNI - esp sirolimus compared to everolimus), hyperlipidaemia, mouth ulcers, oedema, interstitial pneumonitis, contraindicated in pregnancy

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13
Q

Use of mTORi (sirolimus and everolimus) in renal transplantation

A
  • Previously as CNI sparing with mycophenolate (avoid tac/cyclo) - to avoid CNI nephrotoxicity and hopefully late graft loss
    • However more rejection and graft loss, high discontinuation rate
  • More recently - used with reduced dose CNI and prednisolone (to replace mycophenolate)
    • Similar rejection rate and GFR
    • Less viral infection (especially CMV)
    • Less skin malignancy
    • Less neutropenia and diarrhoea
    • Still quite high discontinuation rate, long term follow up lacking for everolimus with tacrolimus
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14
Q

Cells involved in acute cellular rejection in renal transplantation

A

T lymphocytes

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15
Q

Opportunistic infection 6 months post renal transplant:

A

Aspergillus
Nocardia
BK virus - should be associated with decline in renal function
Herpes Zoster
Hepatitis B
Hepatitis C

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16
Q

Principles of treatment for rapidly progressive glomerulonephritis

A

Induction:

Cyclophosphamide and IV methyprednisolone

Maintainence

Azathioprine

17
Q

Early infections (1-6 months) post renal transplantation

A

PCP

CMV

Hepatitis B& C

Legionella

Listeria

18
Q

Notes on chronic allograft nephropathy

A
  • Poor term
  • Immunological vs non-immunological
  • Historically thought to be due to CNI toxicity
    • Still a factor → ESKD in non-renal solid organ transplant recipients
  • Chronic antibody mediated rejection probably most significant contributor
    • Early rejection not resolved
    • Non-adherence, under immnuosuppression (low Tac levels) + poor HLA matching synergistic
    • Associated with de novo donor specific antibodies - especially class 2, DQ
    • Eventually → graft loss (may take months to years after diagnosis)
    • No proven effective treatment
19
Q

Notes on delayed graft function

A

See slide

20
Q

Differentials for worsening graft function < 12 months post- transplant

A
  • Acute rejection
    • To be excluded with biopsy
  • CNI toxicity
  • Renal artery stenosis
  • Obstruction +/- leak +/- collection
    • After ureteric stent removal
  • BK nephropathy
  • Recurrent disease
    • Early: Primary FSGS, aHUS, MPGN, ANCA
    • Late: IgAN, membranous, MPGN
21
Q

Notes on acute rejection in renal transplants

A

See slides

22
Q

Notes on BK virus

A
23
Q

Notes on CMV in renal transplants

A
24
Q

Notes on cancers post renal transplant

A
  • Higher rates on NHL, kidney (also higher in dialysis patients), melanoma
  • No difference in breast and prostate

Skin cancers

  • Very common
  • Metastatic SCC → common cause of cancer related death post transplant (especially head and neck)
  • Late switch to mTORi → may reduce skin cancer incidence for those with previous skin cancer

Renal (7 decks)

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