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review course > renal transplant > Flashcards

renal transplant Flashcards

1
Q

what is criteria for DCD

A

absence of circulation, not EKG silence

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2
Q

causes of graft failure after first yr - 5

A

chronic allograft nephropathy (scarring) 40%, death 30% (CVD), acute rejection 7%, noncompliance 3%, recurrence 2%

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3
Q

top 3 causes of ESRD leading to txp

A

glomerular disease (30%), DM (20%), HTN (20%)

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4
Q

major factors affecting long term outcome - 5

A

HLA match, rejection (acute/ chronic), prior failed txp, comorbidities, race

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5
Q

relative contraindications to txp - 6

A

active infection, malignancy (document cure), active ongoing renal disease (SLE), hyperoxaluria type 1, severe atherosclerosis with uncorrectable disease, social problems (non compliance, psych, morbid obesity)

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6
Q

problem with FSGS and transplant

A

25% recur leading to upto 65% graft failure

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7
Q

what is extended criteria

A

> 60 yo, OR > 50 yo with 2(cr > 1.5, HTN, CVA death)

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8
Q

where are HLA found

A

surface of NUCLEATED cells

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9
Q

what chromosome is HLA on

A

6

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10
Q

parts to class 1 HLA antigen

A

3 alpha and 1 b2microglobulin with 1 carboxy terminal through cell membrane

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11
Q

parts to class 2 HLA antigen

A

2 alpha, 2 beta, 2 carboxy

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12
Q

how does rejection happen

A

HLA molecules on surface shed into circulation, APC’s (host or donor) in LN’s present molecule to T cells, stimulates cytokine release, which then go to graft to damage

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13
Q

what is signal 1

A

APC’s (host or donor) in LN’s present MHC to T cells - difference in binding cleft between alpha subunits sends signal

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14
Q

what is the result of signal 1

A

STARTS cytokine production

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15
Q

what is signal 2

A

AKA costimulation. sets of receptors on APC bind to t-cell –> stimulation

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16
Q

what is signal 3

A

cytokine IL2 released by CD4 is most potent. Stimulates CD8 t cells to become cytotoxic and attack organ with HLA organ it was sensitized to

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17
Q

CD4 vs CD8 t cells

A

CD4 (helper) activate CD8 (killer) and b-cells, CD8 = cytotoxic via perforins

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18
Q

class 1 vs 2 HLA and CD4 vs 8 T cell

A

class 1 has binding site for CD8, class 2 for CD4

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19
Q

what types of cells mediate acute rejection

A

donor APC’s present MHC to recipient T cells immediately

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20
Q

what types of cells mediate chronic rejection

A

recipient APC re-packages MHC to recipient t-cell

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21
Q

what is costimulation

A

signal 1 and 2

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22
Q

significance of co-stimulation

A

nieve t-cells become anergic/ undergo apoptosis without signal 2

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23
Q

hyperacute timing

A

min - hrs

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24
Q

acute timing

A

d- yrs

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25
Q

chronic timing?

A

mo - yrs

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26
Q

hyperacute mediating factors

A

preformed ab’s (humoral)

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27
Q

acute mediating factors - 2

A

cellular/ humoral (ab’s) responses

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28
Q

chronic mediating factor - 3

A

cellular/humoral response/ viral

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29
Q

hyperacute rejection primary finding

A

intravascular coagulation/ hemorrhagic necrosis

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30
Q

acute rejection primary finding

A

tissue destruction

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31
Q

chronic rejection primary finding

A

obliterative fibrosis

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32
Q

vessel endothelium @ hyperacute rejection

A

ab’s attack walls of endothelium and disrupt vessel

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33
Q

prevention of hyperacute rejection

A

crossmatch to ID if recipient has circulating preformed ab’s to HLA molecules on donor

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34
Q

first step in diagnosing acute rejection

A

biopsy

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35
Q

acute rejection histology - 2

A

infiltrate of mononuclear cells and plasma cells in interstitum

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36
Q

effect of acute rejection on kidney

A

causes tubulitis –> overrides tubules

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37
Q

first line therapy of acute rejection

A

high dose steroids

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38
Q

second line therapy given when? For acute rejection

A

vascular rejection aka Banf grade 2 or 3

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39
Q

how can you identify antibody mediated acute rejection

A

antibodies on artery walls on biopsy.

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40
Q

what are second line therapies for acute rejection - 3

A

anti-t cell ab’s (OKT3), plasmapheresis (remove AB’s), IVIG (block ab’s)

41
Q

how to treat antibody mediated acute rejection

A

second line therapies (OKT3, plasmapheresis, IVIG)

42
Q

gross findings in chronic rejection

A

atrophy/ fibrosis - cortical atrophy, whiteish kidney (fibrosis)

43
Q

histologic findings in chronic rejection - 4

A
  1. interstitial fibrosis / tubular atrophy, 2. vascular intimal hyperplasia, 3. arteriolar hyalinosis, 4. glomerulopathy (double countour GBM)
44
Q

intimal arteritis of chronic allograft nephropathy histo findings

A

lumen occluded - intima inflamed and infiltrated by inflammatory cells - occluding lumen

45
Q

2 types of chronic allograft nephropathy

A

antigen dependent and independent

46
Q

what is antigen dependent CAN - 3

A

after episodes of acute rejection, re-transplantation (preformed ab’s), triggering HLA system

47
Q

antigen independent CAN - 5

A

ischemia/reperfusion at txp, nephrotoxic drugs, viral, hyperlipidemia, HTN

48
Q

how does combination antirejection therapy work

A

use combination drugs that work at different points in cell cycle -synergistic effect and can use lower doses overall to minimize toxicity

49
Q

common maintenance cocktail

A

calceneurin inhibitor, antiproliferative agent, steroid –> tacrolimus, mycophenolic acid, prednisone

50
Q

cyclosporine and tacrolimus - what class r they

A

calcineurin inhibitors

51
Q

most common side effect of calceneurin inhib - 2

A

nephrotoxic and bone marrow toxic

52
Q

role of calineurin in CD4 T cell activation

A

CD4 - MHC engagement + 2nd signal + CD3 = increased intracellular calcium –> calcineurin activation –> dephosphorylation of NFAT and transfer to nucleus –> t cell activation and IL2 production

53
Q

calcineurin inhib MOA

A

blocks IL2 gene transcription, preventing T cell activaiton early on

54
Q

calcineurin inhib side effects - 5

A

nephrotoxic, HTN, DM, cosmetic changes (hersutism, gingival hyperplasia), neurotoxic

55
Q

what is C2 level

A

cyclosporin Area under the curve level 2 hrs after po dose

56
Q

how to monitor tacrolimus level

A

trough

57
Q

sirolimus class

A

mtor inhibitor

58
Q

mtor side effects - 3

A

marrow toxic, hyperlipidemia, slow wound healing

59
Q

OKT3 MOA

A

monoclonal ab blocking CD3 and t cell activation

60
Q

thymoglobulin MOA

A

AB’s against multiple cell surface antigens = profound T cell activation for weeks

61
Q

mycophenolate mofetil, azathioprine - what class?

A

antiproliferative or antimetabolites agents

62
Q

antiproliferative agent common side effect

A

bone marrow supression

63
Q

mycofenolate side effect - 1

A

GI toxicity, diarrhea

64
Q

azathioprine side effect - 1

A

liver toxicity

65
Q

what is carrel patch

A

take a piece of aorta and place onto iliac when multiple vessels

66
Q

pediatric pt receiving adult kidney - where?

A

anastamosed to aorta/ivc

67
Q

pediatric en bloc to adult - vascular anastamosis

A

pediatric aorta and ivc attached to iliac

68
Q

initial workup of txp dysfunction (non-immune causes) - 4

A

eval volume status, r/o bladder ourlet obstruction, screen for infection (blood/urine), check calcineurin levels

69
Q

def of transplant dysfxn

A

cr > 20% baseline

70
Q

effect of large pelvic lymphocele

A

can compress illiacs –> leg edema, decreased flow to kidney, DVT

71
Q

most common viral post txp infection

A

CMV in 10-20%

72
Q

cmv prophylaxis

A

gancyclovir

73
Q

CMV features- 5

A

happens at 42 days postop, affected organs: GIT, liver, glomerulopathy, retinitis

74
Q

BK virus sx - 5

A

rising cr (BK nephropathy), hemorrhagic cystitis, ureteral stenosis, sterile pyuria (viuria)

75
Q

BK virus mgmt

A

reduce immunosupression, stop mycophenolate, start lefunomide (pyrimidine synthesis inhibitor) and cidofovir

76
Q

most common fungal infections - 2

A

candida and torulopsis

77
Q

fungal prophylaxis

A

fluconazole

78
Q

opportunistic infection and prophylaxis

A

pcp & bactrim

79
Q

live donor exclusion - age - 2

A

< 18 (consent) or > 70 - anesthetic risk and poor kidney

80
Q

live donor exclusion - BP

A

> 140/90 in blacks, 1 drug HTN in whites w/ no LVH in whites considered

81
Q

live donor exclusion - kidney - 4

A

proteinuria > 200 F 250 M, GFR< 80, ADPKD, kidney stones (multiple or clinically active)

82
Q

live donor exclusion - others - 5

A

DM, prior cancer, hypercoagulable, psychosocial stressor, very abnormal CT

83
Q

which kidney to remove in donor -4

A

single renal artery, left kidney (longer vein), smaller kidney, the one with abnormalities

84
Q

general principal of donor nx

A

leave donor with better kidney

85
Q

renal recovery in donor

A

under 50 yo have hypertrophy to final 65-75% total renal function

86
Q

what is a pretransplant gu eval for recipient? - 4

A

sterile urine, VCUG if suspected abnormality, BPH - resect if not anuric

87
Q

living vs cadaveric donor and success

A

poorly matched living is better than matched cadaveric

88
Q

crossmatch: positive T cell/ class 1

A

no txp

89
Q

who gets first transplant only - 3

A

pos T cell flow crossmatch only, negative T cell positive B cell, positive B cell flow

90
Q

perioperative maneuvers that reduce impact of ischemia reperfusion - 5

A

hydration, mannitol, lasix, intra-arterial verapamil, low dose dopamine

91
Q

which branching vessels can be tied off

A

small upper pole, not lower pole as may supply ureter

92
Q

vascular thrombosis/leak mgmt

A

reoperate

93
Q

urine leak/ureteral obstruction mgmt

A

endoscopic mgmt, or reoperation if endoscopy fails or necrosis

94
Q

lymphocele presentation - 2

A

ureteral obstruction (rising cr), or iliac vein compression (leg edema/DVT)

95
Q

lymphocele mgmt - 3

A

large and symptomatic require tx: percutaneous drainage, sclerosis, peritoneal window

96
Q

ipp post TXP

A

considered safe

97
Q

ureteral stents and transplant

A

higher risk of infection unless abx added

98
Q

drug used to prevent and treat acute rejection

A

thymoglobulin

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