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16. Renal Transplant (484) > 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)

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41
Q

how to treat antibody mediated acute rejection

A

second line therapies (OKT3, plasmapheresis, IVIG)

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42
Q

gross findings in chronic rejection

A

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

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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)
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44
Q

intimal arteritis of chronic allograft nephropathy histo findings

A

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

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45
Q

2 types of chronic allograft nephropathy

A

antigen dependent and independent

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46
Q

what is antigen dependent CAN - 3

A

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

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47
Q

antigen independent CAN - 5

A

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

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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

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49
Q

common maintenance cocktail

A

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

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50
Q

cyclosporine and tacrolimus - what class r they

A

calcineurin inhibitors

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51
Q

most common side effect of calceneurin inhib - 2

A

nephrotoxic and bone marrow toxic

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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

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53
Q

calcineurin inhib MOA

A

blocks IL2 gene transcription, preventing T cell activaiton early on

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54
Q

calcineurin inhib side effects - 5

A

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

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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

99
Q

What is the criteria for initiating renal replacement therapy (RRT)?

A

GFR < 10mL/min + symptomatic

100
Q

At what level of renal function should a patient meet with the transplantation team

A

GFR < 20ml/min

101
Q

What are absolute contraindications to renal transplantation?

A
  1. Unable to adhere to medication regimen
  2. Active infection
  3. Active malignancy
  4. Mentally challenged
  5. Reversible cause of renal failure
  6. High probability of peri-operative mortality
  7. Anatomic issues (significant vascular disease)
102
Q

What renal diseases have a high risk of recurring in the transplanted kidney?

A
  1. FSGS
  2. Hemolytic uremic syndrome
  3. Membranoproliferative glomerulonephritis
  4. Primary Oxalosis
103
Q

What renal diseases have an intermediate risk of recurring in the transplanted kidney?

A
  1. Sickle cell
  2. Amyloidosis
  3. Fabry disease
  4. IGA nephropathy
  5. HTN nephropathy
  6. Diabetic Nephropathy
104
Q

What renal diseases do NOT recur in a transplanted kidney?

A
  1. ADPCKD
  2. Cystinosis
  3. Renal dysplasia
  4. Alport syndrome (without anti-GBM antibodies)
105
Q

How do you manage malignancy in transplant candidates?

A

Need to ensure disease cure, with disease free period dependent on type of CA. Oncology consults should be obtained to determine risk of recurrence, surveillance and long term prognosis. Patients should be screened for malignancy appropriate to age and gender

Melanoma - 5 years
Any metastatic malignancy - 5 years
High grade, invasive urothelial CA - 5 years
Any localized malignancy - 2 years

106
Q

When is cholecystectomy advised prior to receiving a transplant?

A
  1. Gallbladder polyps greater than 1cm

2. Patients with diabetes and gallstones (increased morbidity in acute cholecystitis after transplantation)

107
Q

What should a patient be assessed for prior to transplantation?

A
  1. Peripheral vascular system (claudication, past vascular procedures, femoral pulses) - if concerns doppler U/S or CT to assess
  2. Abdominal exam for surgical scars and information about past surgical history
108
Q

What are the indications for a pre-transplant nephrectomy?

A
  1. Symptomatic renal stones not cleared by minimally invasive techniques or lithotripsy
  2. Polycystic kidneys that are symptomatic, extend below the iliac crest, have been infected or have solid tumors.
  3. Persistent anti-GBM antibody levels
  4. Significant proteinuria not controlled with medical nephrectomy or angioablation
  5. Recurrent pyelonephritis, or chronically infected kidney
  6. Grade 4 or 5 VUR with urinary tract infections
109
Q

How should bladder outlet obstruction be managed in the transplant patient?

A

First line: medical management - alpha blockers and 5-alpha reductase inhibitors

Second line: TURP = should NOT be performed in anuric/oliguric patients as high risk contracture and strictures

Third line: CIC or indwelling catheterization

110
Q

What are the guidelines for determination of neurologic death? (DND kidney)

A
  1. Complete cessation of all brain stem function (must be irreversible)
    Determined by coma + absence of brainstem reflexes
  2. Apnea challenge
    Determined by no respiratory effort at PaCo2 60 or greater
  3. Negative confirmatory tests if doubt exists.
111
Q

What are the criteria for donation after circulatory death (DCD)?

A
  1. Donor does not meet neurologic death criteria, despite being comatose
  2. Decision made by family to withdraw cardio-pulmonary support.
  3. Death declared by absence of spontaneous respiration and sustained systole for 5 minutes.
112
Q

What are the steps in the harvest of organs from a deceased donor?

A
  1. Median sternotomy and midline incision
  2. Organ inspection for signs of disease
  3. Vascular control - above and below organs for donation
  4. Cannulas inserted for the administration of preservation solution inserted into aorta, clamps are applied, venous effluent is vented and organs are flushed.
  5. Organs are extirpated.
  6. Immediately are cooled with slush once removed.
  7. Spleen and lymph node sections removed for histocompatibility.
113
Q

How are kidneys preserved once extirpated?

A
  1. Hypothermia (4C) reduces energy expenditure
  2. Pulsatile preservation pumps may reduce vascular spasm
  3. Preservation solution (wisconsin solution) designed to maintain intracellular electrolyte composition
114
Q

What are the contents of Wisconsin solution?

A

K lactobionate, KH2PO4, MgSO4, Raffinose, Adenosine, Insulin, glutathione, dexamethasone, allopurinol, penicillin, potassium, sodium

115
Q

What are the four categories of kidney donors?

A
  1. Standard criteria donor younger than 35
  2. Standard criteria donor older than 35
  3. Expanded criteria donor
  4. Donation after circulatory death
116
Q

What are the criteria of an expanded criteria donor?

A
  1. Age over 60
  2. Age between 50-59 with 2 or more of (death from stroke, HTN, elevated Cr just before organ recovery (1.5mg/dL)

*ECD has 80% 2 year graft survival versus 88% for SCD)

117
Q

What happens in ABO incompatibility?

A

Acute rejection - antibodies bind to perceived antigen, trigger complement cascade, leading to coagulation, thrombosis and rapid graft loss.

118
Q

What two classes of HLA’s are used in kidney allocation

A

HLA Class I (HLA-A, HLA-B, HLA-C)
- expressed by all nucleated cells through MHC
HLA Class II (HLA-DR, HLA-DQ, HLA-DP)
-Expressed by antigen presenting cells (dendritic cells, monocytes, macrophages, and B-lymphocytes)

119
Q

What increases the risk of antibody and cellular rejection?

A
  1. Pregnancy
  2. Blood transfusion
  3. Prior transplantation
  4. Some infections

These things increase risk of forming HLA antibodies
individuals with antibodies directed at 20% of population are said to be sensitized
highly sensitized if antibodies directed at 80% of the population.

120
Q

What are the three classes of renal rejection?

A
  1. Hyperacute - immediate (ABO incompatibility)
  2. Acute - 5 days after allogenic transplant (cellular +/- Ab bx to determine
  3. Chronic - gradual deterioration (vascular
121
Q

What are contraindications to donation of a kidney?

A
  1. Renal disease (GFR < 80)
  2. Transmissible infection
  3. Active malignancy
  4. Mental disorder (incompetent)
  5. High operative risk
  6. Minor
  7. Anatomic unfeasibility
122
Q

What are the indications for dialysis

A
  1. Acidosis (metabolic)
  2. Electrolytes (hyper-K)
  3. Intoxicants
  4. Volume overload
  5. Uremia (pericarditis, pericardial effusion)
123
Q

What is the differential diagnosis of a fluid collection found post-operatively from a renal transplant

A
  1. Seroma
  2. Lymphocele
  3. Abscess
  4. Hematoma
  5. Urinoma
124
Q

When should you intervene in a post-operative renal transplant fluid collection?

A
  1. Fever
  2. Pain
  3. Obstruction
  4. If may be contributing to decreased renal function
125
Q

List causes of early graft dysfunction?

A
  1. ATN
  2. Calcineurin inhibitor toxicity
  3. Rejection
  4. Infection
  5. Obstruction
  6. Hyperglycemia
126
Q

What is the definition of delayed graft function?

A

Requirement for dialysis during the first week of transplantation.

127
Q

What are the classes of immunosuppressants and how do they work?

A
  1. Antiproliferative agents (azathioprine, and MMF) - Block DNA/RNA prodction
  2. Calcineurin inhibitors (cyclosporin and tacrolimus) - inhibit T-cell activation
  3. Monoclonal antibodies (Anti-CD25, basiliximab, daclizumab) - block IL2 receptor
  4. Rapamycin - mTOR inhibitor
  5. Corticosteroids - inhibit gene transcription and IL2 activity
128
Q

What is commonest cause of microscopic haematuria in a man below 40 years?

A. IgA nephropathy
B. IgM nephropathy
C. Alport syndrome
D. Goodpasture syndrome

A

A. IgA nephropathy

129
Q

What electolyte abnormalities occur with the use of stomach for urinary diversion?

A. Hypochloremic metabolic alkalosis
B. Hypochloremic metabolic acidosis
C. Hypochloremic metabolic alkalosis
D. Hypochloremic, hypernatremic metabolic acidosis

A

A. Hypochloremic metabolic alkalosis

130
Q

Which statement is correct concerning the use of ureteric stents in kidney transplantation?

A. They are associated with higher risk of bleeding
B. Stents should stay for at least a month after transplantaion
C. It is not necessary when performing a uretero-ureteral anastomosis
D. There is clear evidence recommending its use in ureteral reimplantation

A

D. There is clear evidence recommending its use in ureteral reimplantation

131
Q

The use of a double-J stent in ureteral reimplantation in transplantation:

A. Is associated with a higher risk of infections
B. Does not change the incidence of haematuria
C. Has no proven benefit
D. Is associated with at higher risk of late stenosis

A

A. Is associated with a higher risk of infections

132
Q

Following renal transplantation, the most important factor which causes renal artery stenosis is:

A. Angulation of hte artery
B. Immunosuppressive treatment
C. Small diameter of the renal artery
D. Arterial anastomosis not perfectly carried out

A

D. Arterial anastomosis not perfectly carried out

133
Q

Which statement about parathyroid hormone is correct?

A. It enhances tubular calcium reabsorption
B. It decreases production of 1.25 dihydroxy-vitamin D
C. It increases tubular reabsorption of inorganic phosphates
D. It enhances hydrogen ion secretion in the proximal tubule

A

A. It enhances tubular calcium reabsorption

134
Q

Which drug may cause acute renal failure?

A. Quinolones
B. Desmopressin
C. Opiate analgesics
D. Non-steroidal anti-inflammatory drugs

A

D. Non-steroidal anti-inflammatory drugs

135
Q

Which hormone is most important in urine production at night?

A. Aldosterone
B. Corticosteroids
C. Renin-angiotensin system
D. Vasopressin

A

D. Vasopressin

136
Q

Oliguria is likely to be caused by pre-renal (impaired perfusion) failure rather than by intrarenal (renal parenchymal) failure, if:

A. The urine contains no cells or casts
B. The urinary sodum is less than 10mmol/l
C. The urinary osmolality is less than 350mOsm/l
D. The child has hypertension, raised central pressure and good peripheral perfusion

A

B. The urinary sodum is less than 10mmol/l

16. Renal Transplant (484) (4 decks)

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