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RENAL TRANSPLANT
Dr. Sandeep B. More
Essential functions of kidney :
1) regulate ionic composition of plasma
2) maintain fluid volume
3) elimination of nitrogenous wastes and drugs
4) Erythropoetin production
5) maintenance of pH
 First kidney transplant in 1950
Indications of renal transplant:
 Patients with Chronic kidney disease or End Stage
Renal Disease (ESRD) caused by 1) DM 31% 2) CGN 28%
3)polycystic kidney 12% 4)hypertension 9% 5) SLE 3%
6)interstitial nephritis 7) smoking 8) tuberculosis 9)
HIV, HEP B & C 10) lead, cadmium, mercury
 Renal graft failure is a new indication for renal
transplant .
 What is ESRD: it is final progression of chronic kidney
disease when renal function is irreversibly impaired
and can be fatal without RRT(GFR < 25%)
Uremic syndrome : Extreme form of CRF with GFR <
10% regulation of ECF volume & composition and
excretion of waste products hampered  that cause
1) Water homeostasis alterations causing : ECF
expansion
2) Electrolyte & acid base disturbances cause :
Hyponatremia, hyperkalemia, hyper/hypo calcemia,
hyperphosphatemia, hypermagnesemia, metabolic
acidosis
3) Endocrine changes cause : renal osteodystrophy,
decreased glucose intolerance, hypertriglyceridemia,
atherosclerosis
ESRD Pathophysiology:
Indications for Dialysis
1) GFR <10 without DM
2) GFR<15 with DM,
3) Uremic syndrome (nausea, vomiting, wt loss,
pericarditis, pleuritis),
4) Potassium >6 mEq/L with ECG changes
5) CCF
6) metabolic acidosis
ESRD and CVS:
 Cardiovascular disease is the most common cause of
morbidity and mortality in patients with ESRD
 35-40% of deaths in pts on HD
 Even after renal transplant cardio vascular disease remains
the most common cause of death in the form of:
1) MI 2) CCF 3) atrial fibrillation
 ESRD causes  increased atherosclerosis leading to
ischemic vascular disease coronary, cerebral or
peripheral vascular diseases
 And the incidence is more in pts with DM and HTN
 HTN causes ESRD in 30% pts
 ESRD leads to hyper-reninemia, hypervolemia, renal
vascular changes finally leading to HTN
 2DECHO: concentric LVH and diastolic dysfunction(early and
common changes)
 Heart failure due to dilated cardiomyopathy is also common
 Cardio-renal syndromes 5 types: renal and cardiac
interconnection
 Correction of renal function by transplant  improves
systolic function and reverse LV dilatation and hypertrophy
 Arrhythmias: because of cardiac disease, MI, electrolyte
imbalance
 Atrial fibrillation most common (13 to 27%)  stroke risk
 Normochromic, normocytic anemia due to 1) EPO deficiency,2)
nutritional (iron & folate), 3)chronic inflammatory state, 4)bone
marrow fibrosis
 Hb can be as low as 5-7mg/dl with Hct 15-25%
 Compensation by increased cardiac output & RBC 2,3 DPG  shift
of O2 dissociation curve to right
 Hb target should be 10 mg/dl with drugs
 Avoid blood transfusion as far as possible to prevent
sensitization
 Platelet dysfunction (abnormal adhesion, aggregation),
decreased vWF & factor 8 coagulation disorders
 Increased coagulation & endothelial activation 
hypercoagulable state
 HEMATOLOGIC CHANGES OF HYPERCOAGULABILITY
ARE RESOLVED AFTER SUCCESSFUL KIDNEY
TRANSPLANT
Hematological
 Gastrointestinal: nausea, vomiting, abdominal pain,
decreased gastric motility(gastroparesis)
 Delayed gastric emptying because of ESRD or presence of
diabetes and obesity
These patients are considered always full stomach because
of theses factors with increased risk of aspiration so they are
the candidates for Rapid sequence induction for GA
 CNS: due to accumulation of nitrogenous products
 Memory loss, attention deficit, irritability
 Asterixis, seizures
 Uremia disrupts BBB
Muscle weakness, uremic osteodystrophy (osteomalacia,
osteosclerosis, osteitis fibrosa cystica)
Hypertriglyceridemia, carbohydrate intolerance, secondary
hyperPTH, vit D deficiency
stage Kidney damage GFR (ml/min/1.73m2 BSA)
1 -- Normal or increased (>90)
2 mild 60-89
3 Moderate 30-59
4 severe 15-30
5 ESRD <15
KDQI staging for CRF:
 It is an intermediate risk procedure in the AHA guidelines.
Recipient undergoes a multidisciplinary assessment to
determine the candidacy
 Two types:
 Cadaveric : urgent procedure as harvested kidney can tolerate
cold ischemia only for less than 24 hrs
 Living donor transplant: the ischemia time of harvested kidney
can be less than one hour
So thorough preop assessmernt of the recipient and the donor
can be done so as to minimize intraop and postop complications in
both donor and recipient and to decrease incidence of graft
rejection improving postop survival of the recipient
 Nephrology, Medicine, cardiology, psychiatry, dental, gastromed
(and OBGY for females)
Preop work up for renal transplant
 HIV positive not absolute contraindication if stable on
HAART, RNA negative, CD4> 200 cmm however if pt is
diagnosed with AIDS then it is a contraindication for
transplant
Other recommendations for prospective recipient:
 Stop smoking
 Weight reduction
 BP control
 Dental care
 Exercise
Pre-op
 Blood cross matching (recipient blood with donor
blood cells)
 Human leukocyte antigen (HLA) profile of recipient
determined & compared with donor HLA
 Blood Transfusion, prior transplantation and
pregnancy lead to  preformed antibodies 
positive cross matches against living donor tissue
antigens  PREOP PLASMAPHERESIS to remove
these Abs & immunoglobulins  living donor
transplant is conducted when the cross match turns
negative  additional plasmapheresis and
immunoglobulins to be given postop: hence blood
transfusion is avoided as far as possible with anemia
treated with hematinics and erythropoetin
Organ matching and allocation :
 Ideal cadaveric donor : with prior family consent and
registration
1. Age 5 to 49yrs
2. Nonhypertensive
3. Cause of death other than cerebrovascular accident
4. Creat <1.5
Expanded criteria : age 50 to 59 yrs with 2 additional
risk factors i.e. hypertensive, CVA death or creat >1.5 to
increase pool of donors
Donor criteria:
 Living Donor:
 surgeries scheduled simultaneously  advantage is
minimal ischemia time (<1 hour)  immediate graft
function, high UO, creat clearance
 Exchange donor or kidney swap
 Chain of paired kidney donations
 Continue dialysis as per schedule
 Dialysis before surgery : to be done in pts with increased
intravascular volume, hyperkalemia, acidosis
 CBC (platelet)
 LFTs with enzymes
 RFTs with electrolytes
 PT/INR, aPTT
 CXR
 ECG
 2D ECHO
Pre-requisites:
 Pt typically undergoes dialysis within 48 hrs of
surgery
 Intravascular volume maybe assessed using their
current weight and dry weight
 Pt maybe hypovolemic and prone to hypotension if
loss during dialysis is more than 2 kg
 Preloading with non potassium containing saline or
colloid maybe required if hypotension present
 In case pt is hypervolemic then preloading can
precipitate CCF
 Monitors:
 ECG
 pulse oximeter
 NIBP
 IABP
 CVP monitoring with central line
 Urine output
 Temperature monitoring
 (AV fistula to be palpated and protected)
Preoperative:
Goals: adequate depth, hemodynamic stability, appropriate relaxation
Preanesthetic medication:
Diazepam : protein bound  increased duration
Midaz: water soluble  can be used
Antacid (Na citrate 30 ml) and H2 blocker as pre anesthetic medications
Rapid sequence induction with cricoid pressure is recommended i/v/o incresed
risk of aspiration because of associated DM and obesity and delayed gastric
emptying
Induction agent : Symp responses is blunted because of anti HTN t/t and diabetic
autonomic neuropathy causing impaired vasoconstriction resulting in
hypotension. Also because of preop dialysis pt can be hypovolemic and there is
increased CNS sensitivity. All this make pt susceptible for hypotensive effects of
induction agents. So induction agent should be given slowly and in lower dose to
avoid hypotension.
Pento : increased Vd & reduced protein binding  reduce dose
Propofol : use in low dose, advantage is reduced ischemia/reperfusion injury
Ketamine : causes hypertension. To be used with caution
Etomidate : well tolerated, stable hemodynamics
Intra op management
Neuromuscular blocker:
1) Scoline can be used safely if potassium less than 5.5
mEq/l (hyperkalemia by 0.5 to 1.0 mEq/L for 10-15 mins)
2) Rocuronium 0.8-1.2 mg/kg IV is the best choice if
sugammadex is available
To counteract DL scopy response :
 Opioids Fentanyl (2-5 mics/kg)
 Esmolol (0.5-1 mg/kg)
 Lignocaine 1-1.5 mg/kg
 Nitroglycerin
 Blood sugar level monitoring perioperatively. And consider
shift from OHA to Insulin if required and follow sliding
scale intraop
Intra-op:
 IV fluid: NS & NS based solutions  to prevent
hyperkalemia due to RL
 NS can cause acidosis
 Intraop targets
1) Systolic BP 130 – 160 mm Hg
2) CVP 12 to 14 mm Hg
3) Pulmponary artery pressure 18-20 mm Hg
 Adequate IV fluid intra-op (30 ml/hr plus previous
hour’s urine output): leads to earliest onset of graft
function, low postop creat, higher postop creat
clearance, improved graft survival
 IV methylprednisolone after induction
Intra-op
 Inhalational: Desflurane and Isoflurane not
associated with nephrotoxicity
 Sevoflurane : potentially nephrotoxic due to
compound A and fluoride but no human data
available
 Analgesia: fentanyl 2-5 mic/kg
 Relaxant : Atracurium 0.5 mg/kg , Cis-atracurium is
best choice if available
 Vec /Roc : prolonged action because hepatic and renal
metabolism
 Pancuronium: avoid because primary renal excretion
 Forced air warmer or fluid warmer : to avoid
hypothermia (temp <35 can l/t delayed recovery)
Maintenance of anesthesia:
 Vertical curvilinear incision from pubic symphysis to
ASIS 20-25 cm
 External iliac vein and artery mobilized  vein
clamped first  artery clamped  anastomosis
performed
 Left kidney preferred as left renal vein is longer
 Renal allograft is placed in Right extrarenal fossa
 Furosemide and Mannitol  before reperfusion
 Mannitol and fluid  avoid ATN
 Adequate fluid  increase blood flow  improve
immediate graft rejection
Surgical Procedure:
 Vascular clamp removal  acute bleeding/ release of
inflammatory products accumulated cytokines,
histamine  vasodilatation  hypotension 
hypotension f/b reperfusion  hypoperfusion of graft
 vascular thrombosis of graft
 T/t hypotension with fluid
 Adrenergic vasopressors can cause renal
vasoconstriction
 Dopa : tachycardia, arrhythmias and MI
 After vascular anastomoses  donor graft ureter
implanted in bladder (bladder filled with NS)
 If recipient’s weight < 20 kg  kidney placed intra-
abdominally posterior to the right colon
 In cadaveric donor transplant : aftere vascular
anastomosis, intra-arterial papaverine/ verapamil is
given to prevent arterial spasm  then release
arterial clamp
 Donors younger than 2 yrs , both kidneys
transplanted en bloc with donor’s aorta, which is then
anastomosed to external iliac artery
 Kidney cocktail : infused during vascular anastomosis
in the recipient for cadaveric kidney: it consists of 600
ml of 0.45% dextrose in 0.45 % NS, 37.5 gm Albumin,
80 mg Frusemide, 37.5 gm Mannitol
 Ischemia time : it starts with clamping of the renal
vessels in the donor and ends with vascular
anastomosis in the recipient
 Shorter ischemia time  better organ preservation
 Warm ischemia time begins with clamping of renal
vessels in the donor, it is interrupted by cold
preservation solution and resumes again when the
kidney is placed in the recipient and ends with the
vascular anastomosis
 Cold ischemia: kidney is preserved by storing at 4
degree celsius for less than 24 hrs
 EXTUBATION:
 Avoid extubation response to avoid coughing on tube
 Extubation only after adequate reversal of
neuromuscular blockade and presence of normal
reflexes as they are prone for aspirations
 Monitor : BP, UO, GCS, reflexes
 Adequate fluid : CVP may decline 1-2 hrs after
revascularization (25-50%) due to redistribution of
fluids, changes of vascular permeability, increased
nitric oxide levels 
 Postop complications : vascular thrombosis(1-2%), wound
hematomas(1-2%), infection
 Cardiac monitoring
 Pain: opioids preferred (avoid NSAIDs as may exacerbate HTN,
precipitate edema, increased CVS complications)
 Epidural : better analgesia but better avoided because of
presence of coagulopathy and increased incidence of
hypotension
 Preop TAP block
 Graft rejection : Interleukin 2 mediated activation of
lymphocytes is a critical factor in the cellular immune response
of rejection
Post op management:
 Post transplant: Pt is considered as stage 2 or 3 CKD
as GFR >30 ml/min (GFR decrease by 1.4 – 2.4
ml/min/year)
 Assess renal function
 Rule out rejection
 Cause of death : CVS
 Survival : IHD, cerebrovascular and peripheral vascular
disease
 Immunosuppression: hyperlipidemia, HTN, diabetes
 Obesity and metabolic syndromes
 Post transplant malignancies, anemia,
osteodystrophy
Post transplant pt for other surgery:
 Infection: CMV (CMV negative blood if BT required)
 Immunosuppressants : prevent acute and chronic T
cell allo immune rejection. They may not present with
typical signs & symptoms of intra abdominal sepsis
such as fever, increased TLC, peritonitis signs
 4 classes:
1. Corticosteroids
2. Calcineurine inhibitors (cyclosporine, tacrolimus)
3. Antimetabolites (mycophenolate mofetil,
mycophenolate sodium, azathioprine)
4. Sirolimus (rapamycin inhibitor)
 started in immediate preop period
Infections and immunosuppression:
Corticosteroids: In the early 1960s, Goodwin and Mims reported
that they had used corticosteroids to reverse acute rejection in a living-
donor kidney transplant recipient. Starzl and Marchioro, in 1963,
confirmed the efficacy with corticosteroids and the “almost miracle”
effect. But over the years with recognition of severe irreversible side
effects of corticosteroids and availability of newer and relatively safer
drugs corticosteroids are not advocated now.
1]Calcineurin inhibitor : main stay
1)Cyclosporine : HTN, hyperlipidemia, hyperkalemia,
hypomagnesemia, gum hypertrophy, nephrotoxicity
with renal fibrosis. Lower seizure threshold (avoid
hyperventilation), hirsutism
Potentiate NMB & post op respiratory failure
2)Tacrolimus : inhibits the formation of cytotoxic
lymphocytes which are regarded as being primarily
responsible for graft rejection.
Adv : less HTN & hyperlipidemia. Nephrotoxic but
improves long term post-transplant renal function
S/E : DM, tremors, diarrhoea, neurotoxic
Both can cause chronic allograft nephropathy. In case
of Acute rejection on cyclosporine switch over to
tacrolimus can be considered
2] Antimetabolites :
Mycophenolate mofetil : inhibits de novo purine synthesis in
lymphocytes. No nephrotoxicity. Oral bioavailability 94%
Side effects : diarrhoea,constipation, nausea, indigestion, fluid
retention
Azathioprine : Used in combination with cyclosporin or tacrolimus
or sirolimus
Side effects; skin rash , myalgias, fever, headache, vomiting
bone marrow suppression & pancytopenia
3) Sirolimus: inhibits T cell activation induced by most stimuli by
blocking calcium dependent and calcium independent intracellular
signal transduction. its effects are mediated by a mechanism that
is different from that of cyclosporin, tacrolimus and other
immunosuppressive agents.
THANK YOU

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Renal transplant: anaesthetic implications & considerations

  • 2. Essential functions of kidney : 1) regulate ionic composition of plasma 2) maintain fluid volume 3) elimination of nitrogenous wastes and drugs 4) Erythropoetin production 5) maintenance of pH
  • 3.  First kidney transplant in 1950 Indications of renal transplant:  Patients with Chronic kidney disease or End Stage Renal Disease (ESRD) caused by 1) DM 31% 2) CGN 28% 3)polycystic kidney 12% 4)hypertension 9% 5) SLE 3% 6)interstitial nephritis 7) smoking 8) tuberculosis 9) HIV, HEP B & C 10) lead, cadmium, mercury  Renal graft failure is a new indication for renal transplant .
  • 4.  What is ESRD: it is final progression of chronic kidney disease when renal function is irreversibly impaired and can be fatal without RRT(GFR < 25%) Uremic syndrome : Extreme form of CRF with GFR < 10% regulation of ECF volume & composition and excretion of waste products hampered  that cause 1) Water homeostasis alterations causing : ECF expansion 2) Electrolyte & acid base disturbances cause : Hyponatremia, hyperkalemia, hyper/hypo calcemia, hyperphosphatemia, hypermagnesemia, metabolic acidosis 3) Endocrine changes cause : renal osteodystrophy, decreased glucose intolerance, hypertriglyceridemia, atherosclerosis ESRD Pathophysiology:
  • 5. Indications for Dialysis 1) GFR <10 without DM 2) GFR<15 with DM, 3) Uremic syndrome (nausea, vomiting, wt loss, pericarditis, pleuritis), 4) Potassium >6 mEq/L with ECG changes 5) CCF 6) metabolic acidosis
  • 6. ESRD and CVS:  Cardiovascular disease is the most common cause of morbidity and mortality in patients with ESRD  35-40% of deaths in pts on HD  Even after renal transplant cardio vascular disease remains the most common cause of death in the form of: 1) MI 2) CCF 3) atrial fibrillation  ESRD causes  increased atherosclerosis leading to ischemic vascular disease coronary, cerebral or peripheral vascular diseases  And the incidence is more in pts with DM and HTN  HTN causes ESRD in 30% pts  ESRD leads to hyper-reninemia, hypervolemia, renal vascular changes finally leading to HTN
  • 7.  2DECHO: concentric LVH and diastolic dysfunction(early and common changes)  Heart failure due to dilated cardiomyopathy is also common  Cardio-renal syndromes 5 types: renal and cardiac interconnection  Correction of renal function by transplant  improves systolic function and reverse LV dilatation and hypertrophy  Arrhythmias: because of cardiac disease, MI, electrolyte imbalance  Atrial fibrillation most common (13 to 27%)  stroke risk
  • 8.  Normochromic, normocytic anemia due to 1) EPO deficiency,2) nutritional (iron & folate), 3)chronic inflammatory state, 4)bone marrow fibrosis  Hb can be as low as 5-7mg/dl with Hct 15-25%  Compensation by increased cardiac output & RBC 2,3 DPG  shift of O2 dissociation curve to right  Hb target should be 10 mg/dl with drugs  Avoid blood transfusion as far as possible to prevent sensitization  Platelet dysfunction (abnormal adhesion, aggregation), decreased vWF & factor 8 coagulation disorders  Increased coagulation & endothelial activation  hypercoagulable state  HEMATOLOGIC CHANGES OF HYPERCOAGULABILITY ARE RESOLVED AFTER SUCCESSFUL KIDNEY TRANSPLANT Hematological
  • 9.  Gastrointestinal: nausea, vomiting, abdominal pain, decreased gastric motility(gastroparesis)  Delayed gastric emptying because of ESRD or presence of diabetes and obesity These patients are considered always full stomach because of theses factors with increased risk of aspiration so they are the candidates for Rapid sequence induction for GA  CNS: due to accumulation of nitrogenous products  Memory loss, attention deficit, irritability  Asterixis, seizures  Uremia disrupts BBB Muscle weakness, uremic osteodystrophy (osteomalacia, osteosclerosis, osteitis fibrosa cystica) Hypertriglyceridemia, carbohydrate intolerance, secondary hyperPTH, vit D deficiency
  • 10. stage Kidney damage GFR (ml/min/1.73m2 BSA) 1 -- Normal or increased (>90) 2 mild 60-89 3 Moderate 30-59 4 severe 15-30 5 ESRD <15 KDQI staging for CRF:
  • 11.  It is an intermediate risk procedure in the AHA guidelines. Recipient undergoes a multidisciplinary assessment to determine the candidacy  Two types:  Cadaveric : urgent procedure as harvested kidney can tolerate cold ischemia only for less than 24 hrs  Living donor transplant: the ischemia time of harvested kidney can be less than one hour So thorough preop assessmernt of the recipient and the donor can be done so as to minimize intraop and postop complications in both donor and recipient and to decrease incidence of graft rejection improving postop survival of the recipient  Nephrology, Medicine, cardiology, psychiatry, dental, gastromed (and OBGY for females) Preop work up for renal transplant
  • 12.  HIV positive not absolute contraindication if stable on HAART, RNA negative, CD4> 200 cmm however if pt is diagnosed with AIDS then it is a contraindication for transplant Other recommendations for prospective recipient:  Stop smoking  Weight reduction  BP control  Dental care  Exercise Pre-op
  • 13.  Blood cross matching (recipient blood with donor blood cells)  Human leukocyte antigen (HLA) profile of recipient determined & compared with donor HLA  Blood Transfusion, prior transplantation and pregnancy lead to  preformed antibodies  positive cross matches against living donor tissue antigens  PREOP PLASMAPHERESIS to remove these Abs & immunoglobulins  living donor transplant is conducted when the cross match turns negative  additional plasmapheresis and immunoglobulins to be given postop: hence blood transfusion is avoided as far as possible with anemia treated with hematinics and erythropoetin Organ matching and allocation :
  • 14.  Ideal cadaveric donor : with prior family consent and registration 1. Age 5 to 49yrs 2. Nonhypertensive 3. Cause of death other than cerebrovascular accident 4. Creat <1.5 Expanded criteria : age 50 to 59 yrs with 2 additional risk factors i.e. hypertensive, CVA death or creat >1.5 to increase pool of donors Donor criteria:
  • 15.  Living Donor:  surgeries scheduled simultaneously  advantage is minimal ischemia time (<1 hour)  immediate graft function, high UO, creat clearance  Exchange donor or kidney swap  Chain of paired kidney donations
  • 16.  Continue dialysis as per schedule  Dialysis before surgery : to be done in pts with increased intravascular volume, hyperkalemia, acidosis  CBC (platelet)  LFTs with enzymes  RFTs with electrolytes  PT/INR, aPTT  CXR  ECG  2D ECHO Pre-requisites:
  • 17.  Pt typically undergoes dialysis within 48 hrs of surgery  Intravascular volume maybe assessed using their current weight and dry weight  Pt maybe hypovolemic and prone to hypotension if loss during dialysis is more than 2 kg  Preloading with non potassium containing saline or colloid maybe required if hypotension present  In case pt is hypervolemic then preloading can precipitate CCF
  • 18.  Monitors:  ECG  pulse oximeter  NIBP  IABP  CVP monitoring with central line  Urine output  Temperature monitoring  (AV fistula to be palpated and protected) Preoperative:
  • 19. Goals: adequate depth, hemodynamic stability, appropriate relaxation Preanesthetic medication: Diazepam : protein bound  increased duration Midaz: water soluble  can be used Antacid (Na citrate 30 ml) and H2 blocker as pre anesthetic medications Rapid sequence induction with cricoid pressure is recommended i/v/o incresed risk of aspiration because of associated DM and obesity and delayed gastric emptying Induction agent : Symp responses is blunted because of anti HTN t/t and diabetic autonomic neuropathy causing impaired vasoconstriction resulting in hypotension. Also because of preop dialysis pt can be hypovolemic and there is increased CNS sensitivity. All this make pt susceptible for hypotensive effects of induction agents. So induction agent should be given slowly and in lower dose to avoid hypotension. Pento : increased Vd & reduced protein binding  reduce dose Propofol : use in low dose, advantage is reduced ischemia/reperfusion injury Ketamine : causes hypertension. To be used with caution Etomidate : well tolerated, stable hemodynamics Intra op management
  • 20. Neuromuscular blocker: 1) Scoline can be used safely if potassium less than 5.5 mEq/l (hyperkalemia by 0.5 to 1.0 mEq/L for 10-15 mins) 2) Rocuronium 0.8-1.2 mg/kg IV is the best choice if sugammadex is available To counteract DL scopy response :  Opioids Fentanyl (2-5 mics/kg)  Esmolol (0.5-1 mg/kg)  Lignocaine 1-1.5 mg/kg  Nitroglycerin  Blood sugar level monitoring perioperatively. And consider shift from OHA to Insulin if required and follow sliding scale intraop Intra-op:
  • 21.  IV fluid: NS & NS based solutions  to prevent hyperkalemia due to RL  NS can cause acidosis  Intraop targets 1) Systolic BP 130 – 160 mm Hg 2) CVP 12 to 14 mm Hg 3) Pulmponary artery pressure 18-20 mm Hg  Adequate IV fluid intra-op (30 ml/hr plus previous hour’s urine output): leads to earliest onset of graft function, low postop creat, higher postop creat clearance, improved graft survival  IV methylprednisolone after induction Intra-op
  • 22.  Inhalational: Desflurane and Isoflurane not associated with nephrotoxicity  Sevoflurane : potentially nephrotoxic due to compound A and fluoride but no human data available  Analgesia: fentanyl 2-5 mic/kg  Relaxant : Atracurium 0.5 mg/kg , Cis-atracurium is best choice if available  Vec /Roc : prolonged action because hepatic and renal metabolism  Pancuronium: avoid because primary renal excretion  Forced air warmer or fluid warmer : to avoid hypothermia (temp <35 can l/t delayed recovery) Maintenance of anesthesia:
  • 23.  Vertical curvilinear incision from pubic symphysis to ASIS 20-25 cm  External iliac vein and artery mobilized  vein clamped first  artery clamped  anastomosis performed  Left kidney preferred as left renal vein is longer  Renal allograft is placed in Right extrarenal fossa  Furosemide and Mannitol  before reperfusion  Mannitol and fluid  avoid ATN  Adequate fluid  increase blood flow  improve immediate graft rejection Surgical Procedure:
  • 24.  Vascular clamp removal  acute bleeding/ release of inflammatory products accumulated cytokines, histamine  vasodilatation  hypotension  hypotension f/b reperfusion  hypoperfusion of graft  vascular thrombosis of graft  T/t hypotension with fluid  Adrenergic vasopressors can cause renal vasoconstriction  Dopa : tachycardia, arrhythmias and MI  After vascular anastomoses  donor graft ureter implanted in bladder (bladder filled with NS)  If recipient’s weight < 20 kg  kidney placed intra- abdominally posterior to the right colon
  • 25.  In cadaveric donor transplant : aftere vascular anastomosis, intra-arterial papaverine/ verapamil is given to prevent arterial spasm  then release arterial clamp  Donors younger than 2 yrs , both kidneys transplanted en bloc with donor’s aorta, which is then anastomosed to external iliac artery  Kidney cocktail : infused during vascular anastomosis in the recipient for cadaveric kidney: it consists of 600 ml of 0.45% dextrose in 0.45 % NS, 37.5 gm Albumin, 80 mg Frusemide, 37.5 gm Mannitol
  • 26.  Ischemia time : it starts with clamping of the renal vessels in the donor and ends with vascular anastomosis in the recipient  Shorter ischemia time  better organ preservation  Warm ischemia time begins with clamping of renal vessels in the donor, it is interrupted by cold preservation solution and resumes again when the kidney is placed in the recipient and ends with the vascular anastomosis  Cold ischemia: kidney is preserved by storing at 4 degree celsius for less than 24 hrs
  • 27.  EXTUBATION:  Avoid extubation response to avoid coughing on tube  Extubation only after adequate reversal of neuromuscular blockade and presence of normal reflexes as they are prone for aspirations
  • 28.  Monitor : BP, UO, GCS, reflexes  Adequate fluid : CVP may decline 1-2 hrs after revascularization (25-50%) due to redistribution of fluids, changes of vascular permeability, increased nitric oxide levels   Postop complications : vascular thrombosis(1-2%), wound hematomas(1-2%), infection  Cardiac monitoring  Pain: opioids preferred (avoid NSAIDs as may exacerbate HTN, precipitate edema, increased CVS complications)  Epidural : better analgesia but better avoided because of presence of coagulopathy and increased incidence of hypotension  Preop TAP block  Graft rejection : Interleukin 2 mediated activation of lymphocytes is a critical factor in the cellular immune response of rejection Post op management:
  • 29.  Post transplant: Pt is considered as stage 2 or 3 CKD as GFR >30 ml/min (GFR decrease by 1.4 – 2.4 ml/min/year)  Assess renal function  Rule out rejection  Cause of death : CVS  Survival : IHD, cerebrovascular and peripheral vascular disease  Immunosuppression: hyperlipidemia, HTN, diabetes  Obesity and metabolic syndromes  Post transplant malignancies, anemia, osteodystrophy Post transplant pt for other surgery:
  • 30.  Infection: CMV (CMV negative blood if BT required)  Immunosuppressants : prevent acute and chronic T cell allo immune rejection. They may not present with typical signs & symptoms of intra abdominal sepsis such as fever, increased TLC, peritonitis signs  4 classes: 1. Corticosteroids 2. Calcineurine inhibitors (cyclosporine, tacrolimus) 3. Antimetabolites (mycophenolate mofetil, mycophenolate sodium, azathioprine) 4. Sirolimus (rapamycin inhibitor)  started in immediate preop period Infections and immunosuppression:
  • 31. Corticosteroids: In the early 1960s, Goodwin and Mims reported that they had used corticosteroids to reverse acute rejection in a living- donor kidney transplant recipient. Starzl and Marchioro, in 1963, confirmed the efficacy with corticosteroids and the “almost miracle” effect. But over the years with recognition of severe irreversible side effects of corticosteroids and availability of newer and relatively safer drugs corticosteroids are not advocated now.
  • 32. 1]Calcineurin inhibitor : main stay 1)Cyclosporine : HTN, hyperlipidemia, hyperkalemia, hypomagnesemia, gum hypertrophy, nephrotoxicity with renal fibrosis. Lower seizure threshold (avoid hyperventilation), hirsutism Potentiate NMB & post op respiratory failure 2)Tacrolimus : inhibits the formation of cytotoxic lymphocytes which are regarded as being primarily responsible for graft rejection. Adv : less HTN & hyperlipidemia. Nephrotoxic but improves long term post-transplant renal function S/E : DM, tremors, diarrhoea, neurotoxic Both can cause chronic allograft nephropathy. In case of Acute rejection on cyclosporine switch over to tacrolimus can be considered
  • 33. 2] Antimetabolites : Mycophenolate mofetil : inhibits de novo purine synthesis in lymphocytes. No nephrotoxicity. Oral bioavailability 94% Side effects : diarrhoea,constipation, nausea, indigestion, fluid retention Azathioprine : Used in combination with cyclosporin or tacrolimus or sirolimus Side effects; skin rash , myalgias, fever, headache, vomiting bone marrow suppression & pancytopenia 3) Sirolimus: inhibits T cell activation induced by most stimuli by blocking calcium dependent and calcium independent intracellular signal transduction. its effects are mediated by a mechanism that is different from that of cyclosporin, tacrolimus and other immunosuppressive agents.