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Nephrology > Renal Transplant > Flashcards

Renal Transplant Flashcards

1
Q
A
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2
Q

What are the three options for end stage renal failure? Which is best?

A

Transplant
Dialysis
Supportive care

Transplant is best mortality and morbidity

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3
Q

Most kidneys come from living or deceased doners?

A

Deceased

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4
Q

What are the 2 main types of deceased donars? Which ones is best?

A

Brain dead donar (BDD)
- This is the best one because minimal interruption to blood supply to kidney

Donation after circulatory death (DCD)

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5
Q

Does live donation of a kidney increase risk of CKD for the doner?

A

Yes, doners are at increased risk of kidney disease in the future compared to hjealthy non doners

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6
Q

Absolute contraindications for renal transplantation?

A
  • Malignancy (advanced melanoma, thyroid cancer particularly)
  • Uncontrolled or untreated infection
  • Chronic infection
  • Unacceptable anesthetic risk
  • Smoking, eoth , pscyhological
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7
Q

What are the two types of allocation system used for DD kidney allocation in AUs?

A

National allocation
- Used for highly sensitised pts (ie have more kidneys to chose from)
- Used for younger pts generally (ie paeds)

State allocation (80% of all kidneys stay in state of donation)

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8
Q

What are two main factors that dsetermine who get allocated a kidney?

A

Length of time on the waiting list

The degree of matching (ie if find very matched kidney then will get allocated to you)

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9
Q

What are the main ways in which kidneys are matched?

A

ABO compatibility:
- Similar principles to blood transfusions - O can be given to all, AB can receive from all. Others must be matched

Tissue Typing - HLA matching:
- Multiple regions that comprise HLA but the main ones are A, B, DR
- Each person has 2 alleles, so has a types of A, B, and DR. Therefore has 6 HLAs to be matched
- HLA matching is often given as x out 6 mismatch, y out of 6 matching

Panel reactive antibody test (PRA):
- Way of looking at how many antibodies the recipient has that may react with the donar
- Higher the PRA percentage, more sensatise the donar is
- ? quantitative test

Cross match (CDC)
- Looking for donor specific antibodies (? differs from PRA because its a qualatative test)

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10
Q

What are some characteristics of DSAs and the implication?

A
  • MFI (mean fluorescent index) - how much of the antibody is present
  • Ig subclass - IgG is worst. Dont worry about IgM
  • Preformed - found before teh transplant occurs
  • Denovo - develop following transplant
  • C1q binding - DO the DSAs bind complement
  • HLA vs non-HLA - classic Non-HLA is AT1receptor antibodies (can use ARB to reduce the risk)

A sensitized pt means they have a lot of DSAa

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11
Q

What can occur if a highley sensitised pt (lots of DSAs) received a kindey?

A

At increased risk of antibody mediated rejection (ie the DSAs kill the kidney)

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12
Q

What are the types of transplant rejection?

A

Hyperacute rejection
Acute T cell mediated
Antibody mediated rejection
Mixed rejection
Chronic immunological injury
Banff score

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13
Q

What is hyperacute rejection?

A

Preformed DSAs cause rejection usually on the table
- Kidney goes black and mottled, anuric
- Untreatable

Rare form of rejection because predictable cytotoxic cross match (CDC)

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14
Q

What forms of acute rejection are there? when does acute rejection occur?

A

T cell mediated (classical)
- T cells are presented with antigen from kidney and then attack kidney
Antibody mediated (DSAs)

Occurs early in the transplantation, within weeks following transplant

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15
Q

How does acute rejection typically present? Dx?

A

Usually asymptomatic
Will see rising Cr several weeks following transplantation without another obvious cause

If it is severe then may be symptomatic weith graft tenderness and swelling, fever

Only way to Dx is by renal Bx
- therefore low threshold for renal Bx if see early Cr rise

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16
Q

What are the main Dx for Acute rejection?

A

Acute tubular necrosis
Drug SE - mainly AKI from CNIs (tacrolimus)

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17
Q

What is acute vascular rejection?

A

This is a form of acute rejection in which the vasculature of teh transplant is mainly effect leading to damage to the kidney (ie not attacking the renal cells themselves, but the vasculature)

It is most often T cell mediated but can also be antibody mediated. Usually a severe form of acute rejection

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18
Q

What are some histo finding in acute cellular rejection?

What are some histo findings in acute antibody mediated rejection?

A

Cellular infiltrate in the renal interstitium with lots of lymphocutes and monocytes
Tubular infiltrates (tubulitis)

Glomerulitis (cells in the gloms)
Peritubular capilaritis
Arteritis

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19
Q

Pt with risign Cr 2 weeks post renal transplant. Has C4d positive renal Bx stain. What Dx?

A

acute antibody mediated rejection

20
Q

What is chronic allograft nephropathy?

A

This is essentially what is seen in most renal transplant over time
- Multiple pathological changes including interstitial fibrosis, tubular atrophy, etc
- Usually due to mediation effecft, chronic antibody mediated rejection

21
Q

What is the BANFF score? What is most severe?

A

Score that gives the risk that this clinical presentation represents rejection
- Score from 0-3
- 3 is most severe and has high risk of rejection occurring

22
Q

Treat for acute rejection?

A

Obtain tissue
- diagnosis and severity

IV methylpred
- >90% effective in managing acute rejection. If not effective then continue with further therapies

If cell mediated rejection and severe (ie steroid resistant of vascular rejection):
- Lymphocyte depleting antibodies (thymoglobulin)

If antibody mediated rejection and severe (ie steroid resistant or vascular rejection):
- PLEX, IVIG
- High dose Tacrolimus and mycophenylate

23
Q

Explain how T cell mediated rejection occurs on the cellular level (ie T cell activation etc)?

A

Signal 1 (Antigen presentation):
- Host dendritic cell presents donar antigen to T cell receptor
OR
- Doner dencdritic cell presents doner antigen to T cell receptor

Signal 2 (Co-stimulation AKA survival signal):
- CD80/86 on dendritic cell binds to CD 28 -> promotes T cell survival and activation

Signal 3 (IL-2 stimulation):
- Activated T cell release of cytokines and growth factors that result in the maturation into CD8 T cell etc

24
Q

Does thymoglubulin work? When is it used?

A

Antibodyt to T cell receptors
- results in destruction of T cell (T cell depletion)

Used for severe (steroid resistance or vascular) T cell mediated acute rejection

25
Q

What are some CNI example? how do they work?

A

Calceneurin inhibitor
- Ex: Tacrolimus, cyclosporin

Work on the calcenurin pathways involved in signal 1 of T cell activation

26
Q

What is belatercept? how does it work?

A

This is an immunusupresive agent used in renal transplant
It is a co-stimulator for CTLA4 thereby promoting T cell inactivation

Works on signal 2 in T cell activation

27
Q

What agents are used for induction prior to renal transplantation?

A

Thymoglobulin and Basiliximab
- Thymoglobulin is T cell depleting therapy
- Basiliximab is MAB against IL2 which stops the activation of T cell (works on signal 3)

28
Q

What are sirolimus and everolimus? how do they work?

A

mTOR inhibitor
Used in renal transplantation
Work on signal 3 of T cell activation

29
Q

Whare are some examples of anti-proliferative mediations used in renal transplant immunosupression?

A

Mycophenylate and azathiprine
- cblock purine synthesis and cause T cell cell cycle arrest

30
Q

What is a typical long term immunosupressive regime post transplant?

A

Tacrolimus, mycophenylate, mofetil, prednisolone

31
Q

Main risk with tac?

A

Neurotoxic
nephrotoxic
DIabetes
Skin cancer risk (esp melanoma)
Thyroid cancer risk

32
Q

Pt post transplant develops diabetes. What medication is responsible?

A

Tacrolimus or cyclosporin

33
Q

What is the primary T cell involved in T cell mediated rejection?

A

CD4 T cell
- the signal 1,2,3 mechanism is in relation to CD4 T cells

34
Q

What is the most common cause of death early post renal transplant? What about late post transplant (ie many years down the line)

A

Cardiovascular death and infection

Cancer death

35
Q

Infections in post transplant pts and the associated time course?

A

Early:
- Wound infections
- Pneumonia
- UTI (often associated with ureteric stent in situ post transplant)

Moderate to late:
- CMV (M2-12)
- PJP (M3-12)
- BK (M2-24+)

Anytime:
- HVS
- Varicella
- Fungal infection

Pneumonia and UTI can also occur anytime just like in the general population

36
Q

Pt 12 months post transplant. Has cough, dysponea and febrile. What is cause?

A

PJP pneumonia

37
Q

Pt 12 months popst transplant. Acute severe diarrhea following non specific infectious prodrome. Dx?

A

CMV colitis

38
Q

Pt 12 months popst transplant. new jaundice and transaminitis. Dx?

A

CMV hepatitis

39
Q

What is the prophylaxis for CMV infection post transplant. Duration?

A

Valgancyclovir
usually 6 months but depends on risk of infection (ie CMV negative host with pos doner)

40
Q

What is PJP prophylaxis in post transplant?

A

Bactrim
- other inc Dapsone, atovaquone, pentamidine

41
Q

What is the effect of BK virus reactivation?

A

Causes graft dysfunction due to interstitial nephritis (tubular interstitial cells are targeted)

42
Q

How does BK nephropathy present? how is it treated?

A

Often asymptomatic rising Cr

treatment involves reduced immunopsupression
- Difficulty is that if you reduce immunosupression and this is actually acute rejection then will get much worse

43
Q

Most significant type of cancer post renal transplant?

A

Skin cancer (mostly non melanoma cancers)
Kaposi sarcoma

44
Q

What is NODAT?

A

new onset diabetes after transplant

45
Q

Most likely GNs to recur post transplant? What are predictors of recurrance?

A

FSGS
MPGN
IgA nephropathy

Rapidly progressive course of initial GN
Previous recurrence (ie already lost transplant to FSGS)

Nephrology (3 decks)

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