PAEDIATRICS Tutorial 563
Anaesthesia for Paediatric Renal
Transplant
Dr Sophie Bloomfield1†, Dr Hannah Lewis2
1
Anaesthetic Resident, FRCA, Evelina Children’s Hospital
2
Consultant Paediatric Anaesthetist, FRCA, Evelina Children’s Hospital
Edited by: Dr William F. Powell Jr, Instructor in Anaesthesia, Mass Eye and Ear, Harvard
Medical School, Boston, MA, USA; Dr Yuanting Zha, Assistant Professor, Department of
Anaesthesiology, Seattle Children’s Hospital, University of Washington, Seattle, WA, USA
†
Corresponding author email: sophie.bloomfield2@[Link]
Published 13 January 2026 DOI: 10.28923/atotw.563
KEY POINTS
• Renal failure is typically congenital in children under 5 and due to acquired disease in older children.
• Kidney replacement therapy has a negative impact on children’s physical and psychological development.
• Transplantation before dialysis has better outcomes, and pre-emptive transplant rates have increased with earlier
referral and a higher rate of living donor transplantation.
• Transplant recipients require multidisciplinary work-up and close liaison between transplant surgeons, nephrologists,
anaesthetists, and paediatric intensive care unit.
• Optimizing fluid status, haemodynamic monitoring, and avoidance of perioperative hypotension is directly related to
long-term graft survival.
• Paediatric specific considerations include size mismatch between recipient and adult donor and the physiological con-
sequences of this.
INTRODUCTION
Background to Renal Transplant
The UK Renal Registry records data on children with end-stage renal disease (ESRD) requiring kidney replacement therapy
(KRT), a term which extends to patients either receiving dialysis therapy or renal transplant. The most common causes of
ESRD are shown in Table 1; these vary based on age with tubulointerstitial disease (i.e., renal dysplasia and obstructive urop-
athy), more prevalent in children under 5 years, and acquired glomerular diseases more common in older children.1
Renal function is monitored via serum creatinine levels, and an estimated glomerular filtration rate (eGFR) is produced using
the Modification of Diet in Renal Disease formula that considers age, gender, ethnicity, and urea or albumin levels indexed to
body surface area.2 Transplant is usually considered in patients over 6 months of age, weighing more than 10 kg, and when
the eGFR is below 15 mL/min/1.73 m2 to prevent further end organ damage, enhance physical growth, and improve quality of
life. Ideally, transplant is performed prior to commencing peritoneal dialysis or haemodialysis. Cases are either planned via
direct living or paired or altruistic donor or unscheduled from a deceased donor, with the most common graft being a single
adult kidney. From paediatric donors weighing less than 20 kg, both kidneys and a portion of the aorta and vena cava can be
transplanted en bloc. Paradoxically, older children benefit from en bloc donor organs, whereas small paediatric patients less
than 20 kg benefit from receiving single adult kidneys because this approach is less prone to vascular and other complications.
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ATOTW 563 — Anaesthesia for Paediatric Renal Transplant (13 January 2026) Page 1 of 6
% Children of Kidney Male : Female
Renal Disease Replacement Therapy Ratio
Tubulointerstitial disease—98% congenital anomalies of the kidney 49.3% 3
and urinary tract, i.e., renal dysplasia and reflux, obstructive uropathy
Glomerular disease 16.7% 0.9
Familial or hereditary nephropathies, i.e., polycystic kidney disease 15.3% 0.9
or Alport syndrome
Systemic diseases affecting the kidneys, e.g., lupus nephritis 5.0% 1.2
Miscellaneous disorders 13.8% 0.9
Table 1. Causes of ESRD in UK Paediatric Population From the UK Renal Registry 26th Annual Report
Absolute contraindications to transplant include incompatible cross-match (although blood group incompatible transplants are
a current area of development), recent or active malignancy, and ongoing sepsis. Relative contraindications include active blood-borne
viral infection (hepatitis B, hepatitis C, or human immunodeficiency virus) and inability to adhere to postoperative immunosuppression,
which can lead to poor outcomes. Due to development of multidisciplinary services, an increase in living donor numbers, and improved
immunosuppressive regimens, graft survival rates are excellent with 99.5% functioning at 1 year and 94.9% at 5 years.3
Preoperative Assessment and Preparation
Chronic kidney disease (CKD) can occur in isolation or as part of a syndrome with other systemic involvement, some of which
are referenced in Table 2.
Preoperative history of a child with chronic renal failure presenting for transplant should include:
• Weight of the child; this will have implications for surgical approach and postoperative care with significant alterations above
or below 20 kg (discussed further).
• Whether the transplant is pre-emptive or if the child is already on KRT, this will be either intermittent haemodialysis 3 times
weekly or daily nocturnal peritoneal dialysis. Enquire the time of last dialysis (the timing of surgery aims to be at least 4–
6 hours after haemodialysis to avoid residual blood heparinisation). Peritoneal dialysis patients will need all fluid drained
from the peritoneum prior to coming to theatre.
• Establish patients’ daily fluid targets or restrictions.
• Urine output varies, and children may be polyuric, oliguric, or anuric. Patients on dialysis may have a wet weight predialysis
and a dry weight postdialysis.
• Cause of renal failure and presence of cardiac and respiratory symptoms and other systemic involvement; some syndromes
associated with chronic renal failure are detailed in Table 2.
Syndrome Manifestations
Polycystic kidney disease The most common genetic cause of renal failure; large fluid-filled cysts form in the kidneys which
grow to 3–4 times normal size. The recessive form also causes liver cysts. It can also cause
pulmonary hypoplasia.
Alport syndrome An abnormality of the collagen IV gene which makes up the glomerular basement membrane, 85%
X-linked. Haematuria is often present from birth; hypertension worsens renal failure. Hearing and
sight issues develop in late childhood or early adulthood.
Prune belly syndrome Predominantly impacts males; characterised by a congenital absence of abdominal muscles
giving a wrinkled appearance, undescended testes, and urinary malformation including ureteric
obstruction with or without dilatation. Can cause pulmonary hypoplasia, and 10% have
cardiovascular anomalies.
Denys-Drash syndrome A congenital nephropathy that causes renal failure within first 3 years of life. Individuals often
have recurrent infections and hypertension; 90% have Wilm’s tumour of the kidneys and
abnormalities of genitalia.
Bartter syndrome A salt-wasting tubulopathy. Excessive calcium excretion in the urine and deposition in the kidney
can cause renal stones, hypokalaemia, and hypotension despite raised renin and aldosterone.
Gitelman syndrome Related to Bartter syndrome; can cause low potassium and magnesium and precipitate cardiac
arrhythmias.
Pierson syndrome Characterised by renal and ocular abnormalities.
Table 2. Congenital Paediatric Syndromes Associated With Chronic Renal Failure4
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• Last food and fluids and if symptoms are suggestive of slow gastric emptying or gastroparesis, which can be the result of
electrolyte imbalances and tissue oedema due to CKD. Note: Nil by mouth patients who are anuric need only 50% of the
usual 4-2-1 fluid maintenance regime.
• Full medication history.
Examination:
• General appearance, weight, and nutritional status.
• Presence of existing vascular access devices.
• Observations: heart rate, oxygen saturations, identify blood pressure normal for the patient, temperature.
8 Clinically may have a hyperdynamic circulation, tachycardia, and reduced heart rate variability.
8 Of note, up to 80% of children requiring KRT are hypertensive (systolic blood pressure > 90th decile). The pathogenesis
of this is likely multifactorial; sodium reabsorption in the nephrons is increased, increasing circulating volume, and
decreasing urine output. The decreased glomerular filtration rate (GFR) stimulates the renin-angiotensin axis, resulting in
chronic activation of the sympathetic nervous system. Hypertensive patients may have more pronounced anaesthesia-
induced hypotension due to autonomic dysregulation and impaired baroreceptor reflex sensitivity.5
Preoperative investigations:
• Blood tests: Baseline or postdialysis (if applicable).
8 Full blood count can show a normocytic normochromic anaemia due to reduced erythropoietin production.
8 Sodium, potassium, magnesium, calcium, and phosphate levels. The expected levels will vary based whether patients
have already initiated dialysis and on current medication regimes.
n Sodium is often low secondary to hypervolaemia.
n Potassium will be normal or borderline high due to impaired excretion; hyperkalaemia is a medical emergency which
must be managed prior to coming to theatre.
n Magnesium can be high or low.
n Calcium levels can be high if supplementation is excessive or low if gut absorption is impaired due to vitamin D deficiency.
n High phosphate levels are universal in ESRD due to impaired excretion.
8 Blood gases can be performed alongside routine bloods to show acid-base trends.
8 A coagulation screen may identify uraemia induced coagulopathy.
n Platelet function can be abnormal in the context of a normal platelet count.
8 Blood group and crossmatch 2 adult units.
• Electrocardiography to look for evidence of left ventricular hypertrophy secondary to hypertension or any electrolyte related changes.
• Transthoracic echocardiogram (TTE) requirements vary by centre. A TTE is required if any cardiac concerns exist, for exam-
ple, to screen for left ventricular hypertrophy in the context of hypertension or if concerns of fluid overload and potential peri-
cardial effusion exist. Some UK centres mandate a screening TTE prior to being listed for renal transplant.
• Chest x-ray and lung function tests if appropriate for the individual; some patients with chronic fluid overload and capillary leak
can have pulmonary oedema and display obstructive lung defects. Position of a central vascular access device many be noted.
• Ultrasound: Assess vessels if previous central vascular access devices and proposed renal graft site.
Home medications:
Children with hypertension are commonly on antihypertensives such as angiotensin-converting-enzyme inhibitors, calcium channel
blockers, or both. It is usual practice to withhold the dose 24 hours before elective surgery, but this should be clarified with the
nephrology team. For nonelective deceased donor transplants, this is not always possible, and doses given more recently can
cause hypotension under anaesthesia. Beta blocker class medications are usually continued perioperatively. Some patients may
be on anticoagulation or antiplatelet drugs; decisions on timing and withholding these should be made as a multidisciplinary team.
Perioperative immunosuppression drug protocols vary depending on the case and centre. A common regimen is intravenous
(IV) methylprednisolone (600 mg/m2 body surface area, maximum 500 mg) and a dose of IV basiliximab and IV antibiotics
(agent chosen on patient and donor specific characteristics).
Induction of Anaesthesia
See Table 3 for the commonly used anaesthetic drugs and considerations.6 IV or inhalational induction are both appropriate
for patients with renal dysfunction. The sevoflurane metabolite compound A causing nephrotoxicity is a theoretical risk, but this
has not translated into clinically significant renal impairment.7,8 Pre-existing vascular access devices for haemodialysis can be
used for IV induction, provided they are aspirated using an aseptic nontouch technique prior to use to prevent a bolus of hepa-
rinised saline from the line. Once no longer required, they should be flushed with 20 mL of 0.9% saline to ensure all anaesthetic
drugs are removed from the line and locked according to local policy.
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Commonly
Used Drugs in Suggested Modification in Patients
Anaesthesia Renal Handling With Renal Failure Undergoing Transplant
Alfentanil No altered half-life, 92% PPB Dose as in normal renal function
Fentanyl Possibly increased half-life 50% of normal dose in ESRD, still titrated to response
Remifentanil Spontaneous degradation by plasma esterases, May be beneficial to blood pressure lability at the time
no accumulation of graft reperfusion, associated bradycardia, may be
poorly tolerated by patients used to hyperdynamic
cardiac output
Morphine 10% excreted unchanged, normal half-life Reduced doses, extended dosing intervals
Propofol 98% PPB, conjugated by liver Dose as in normal renal function
Ketamine 20%–50% PPB Dose as in normal renal function. Sympathomimetic
effect may exacerbate tachycardia or hypertension.
Midazolam 98% PPB Use sparingly as bolus doses rather than infusion,
higher fraction of unbound drug likely to be available
Dexmedetomidine Hepatically metabolised to inactive metabolites, Dose as in normal renal function
renally excreted
Rocuronium Variable or unpredictable duration of action, Dose as in normal renal function, use of reversal with
metabolised by the liver to less active normal dose of Sugammadex
metabolites, very small renal contribution to
metabolism
Suxamethonium Broken down by plasma cholinesterases Avoid use if possible due to hyperkalaemia risk
Table 3. Commonly Used Anaesthetic Drugs, Renal Handling, and Suggested Modification in Patients With Renal Failure.6
ESRD, end-stage renal disease; PPB, plasma protein bound. Colour Key for medication labels compliant with the International
Organization for Standardization: Blue – opioids; Yellow – induction agents; Orange – Benzodiazepines; Purple – sedative/
anxiolytics; Red – muscle relaxants
Endotracheal intubation is required; nasal intubation may be beneficial for patients likely to need postoperative paediatric intensive
care unit (PICU) admission. This decision will need to be weighed with possible platelet dysfunction causing epistaxis, and if bleed-
ing or difficulty on insertion exists, then an oral tube should be used. Increased risk of difficult airway may exist, as renal failure can
cause airway oedema and narrowing due to fluid overload; uraemia and acidosis can cause laryngeal myopathy and neuropathy,
and concurrent syndromes can include craniofacial abnormalities. Fluid boluses and vasopressor boluses or infusions (noradrenaline
or phenylephrine) should also be prepared. If central venous access is required, for example, if vasopressor use deemed likely, then
siting in the left internal jugular vein is ideal to keep the right side free for access if haemodialysis is required. The femoral veins are
generally avoided. IV access should also include good peripheral access, ideally 2 peripheral cannulas (the exact gauge will depend
partly on the age of the child) sited above and contralateral to the arterial clamp (i.e., not in the lower extremities). A noninvasive blood
pressure cuff is ideally placed on the contralateral upper limb to the graft. Insertion of an arterial line is beneficial for haemodynamic
monitoring, especially in children less than 20 kg or with evidence of cardiovascular compromise. A urinary catheter is inserted but
often clamped throughout the case or until reperfusion. Near-infrared spectroscopy can be considered in patients less than 20 kg or if
aortic cross-clamp is utilised. Temperature probes can be inserted in the nasopharynx, the axilla, or the rectum to monitor temperature.
In-line fluid warmers and forced air warmers are used to maintain normothermia.
For patients with renal failure, an ideal anaesthetic drug would be hepatically cleared and have inactive metabolites. Infants
weighing less than 20 kg have smaller reservoirs for fat-soluble drugs and reduced plasma protein binding. Despite increased
quantities of unbound drugs, the plasma concentration may not be altered due to increased extracellular fluid and higher total
body water. Table 3 references some of the commonly used drugs, but variance between centres exists. For example, use of
rocuronium for neuromuscular blockade and reversal with sugammadex is widely used, but authors of some papers have sug-
gested that sugammadex could encapsulate the methylprednisolone and impair its efficacy for immunosuppression.9 Debate
exists on whether rocuronium, atracurium, or cisatracurium is superior for neuromuscular blockade.
Maintenance of Anaesthesia
The size of the patient determines the surgical access technique. For patients less than 20 kg, an intraperitoneal approach via
midline laparotomy is taken, with their grafts anastomosed to the aorta and vena cava. Patients more than 20 kg will have an
extraperitoneal approach with a lower quadrant incision, with grafts attached to the external iliac arteries and veins. Knowledge
of the steps of the surgical procedure listed in the Figure, along with close communication with the surgeons, helps to antici-
pate and manage physiological changes.
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Step 1: Surgical dissection (timing approximately 1 hour)
• Aim for neutral fluid balance with balanced crystalloid, avoiding excessive fluid administration. Central
venous pressure (CVP) monitoring may be useful as part of the clinical status and as a guide for fluid
administration.
• Consider starting low dose vasopressor if mean arterial pressure (MAP) is low despite normovolaemia.
Noradrenaline has not shown adverse effects on renal microcirculation. Aim for MAP > 60 mmHg or
>75% of induction blood pressure.
• Monitor acid/base and electrolytes via blood gas sampling
Step 2: Venous cross clamp to graft perfusion (approximately 20-25 minutes)
• Record venous clamp on and off times
• Patients routinely require fluid loading with 20-40ml/kg of fluid immediately prior to unclamping and graft
reperfusion
• Second dose of IV methylprednisolone (same dosing as pre-induction) required prior to clamp removal
Step 3: Arterial unclamping and reperfusion
• Aim for MAP > 60mmHg or >75% of induction blood pressure - dramatic drop in systemic vascular
resistance anticipated (the most potential seen in patients <20kg receiving an adult kidney) – vasodilatory
cytokines are released from the kidney due to ischaemic time and oxygen demand / supply mismatch
• Consider calcium gluconate prior to re-perfusion
• This point will require generous fluid administration – patients can receive up to 60-120ml/kg of crystalloid
fluid cumulatively and vasopressor boluses (phenylephrine / uptitrate noradrenaline), 4.5% albumin could
also be considered for bolus administration
• There is inadequate evidence to recommend inotropes such as dopamine be used routinely to augment
cardiac output and improve graft perfusion; however if the patient is fluid responsive, administration of IV
balanced crystalloid is most common. Some surgeons also advocate the administration of mannitol.
Step 4: Reperfusion to closing (approximately 1.5 – 2 hours)
• Target MAP is dependent on patient baseline and visual inspection of the graft to establish MAP at which
renal perfusion is optimal
• The ureteric anastomosis is tested with methylene blue dye to ensure there are not leaks and then the
urinary catheter will be unclamped. Inspect for evidence of urine output and monitor volume
• Blood gas monitoring, as necessary depending on patient factors and previous blood gas trends
• Post-operative ultrasound for patency of the graft anastomosis is performed before leaving theatres
Figure. Outlining the surgical steps involved in renal transplant and suggested management.
Balanced crystalloids like Plasma-Lyte 148 or Hartmann’s (compound sodium lactate or Ringer’s lactate) do not cause an
increase in the extracellular fluid potassium concentration and avoid hyperchloraemic acidosis associated with excessive 0.9%
sodium chloride. If hypocalcaemic or hyperkalaemic, supplementation with calcium gluconate is helpful for cardiac contractility
and will stabilise the myocardium to prevent arrhythmias. Reperfusion injury of the new kidney can cause metabolic acidosis
and hyperkalaemia for which slow IV sodium bicarbonate 8.4% administration may be helpful in patients (especially those that
are on long-term oral sodium bicarbonate supplementation). Glucose levels should be monitored throughout the case, and IV
glucose supplementation may be needed, especially in smaller children or patients that are continuously fed.
Administering blood products in response to significant bleeding or anaemia is essential for delivery of oxygen and tissue perfu-
sion and 2 adult units of cross-matched blood should be available. Individual centres may have an agreed transfusion trigger, for
example, a haemoglobin of 75 g/L or less. However, this is balanced against the risk of formation of antibodies against the donor
blood which can induce antibody mediated graft rejection of the transplanted kidney. The risk of transfusion related immune sen-
sitisation is reduced by use of leucocyte depleted red cells. If a blood transfusion is required, it should be discussed with the surgi-
cal team at the time.
Postoperative Care
Multiple factors exist in deciding the best place for postoperative care. Smaller patients less than 20 kg will normally require a
PICU admission, but larger patients who have low ventilatory requirements and are haemodynamically stable can be extu-
bated at the end of the case and nursed in a high dependency or renal ward environment.
Analgesia requires a multimodal approach. At the end of the case, a transversus abdominis plane block with bupivacaine up to
2 mg/kg maybe beneficial for patients with a laparotomy wound. A continuous incisional infusion of local anaesthetic (CILA)
can be sited by the surgeons for ongoing postoperative analgesia. Remaining local anaesthetic can be infiltrated to any areas
not covered by the CILA, e.g., a drain site. Nonsteroidal anti-inflammatory drugs are contraindicated due to reduction in renal
blood flow, and the mainstay of analgesia is paracetamol and opioid analgesia, usually a fentanyl patient- or nurse-controlled
analgesia for the first 24 hours with ongoing pain team review to decide when to step it down.
One should be aware of both early and late complications. Low or no urine output postop may be evidence of hypovolaemia,
delayed graft function, or vascular complications. Due to immunosuppressive regimes, acute graft rejection is uncommon, par-
ticularly in those less than 5 years who are immunologically naı̈ve. Ultrasound immediately postoperatively assesses adequacy
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of blood flow and excludes vascular thrombosis early, which would indicate return to theatre. To prevent thrombotic complica-
tions, low-dose aspirin is given postoperatively for 1 month. Other complications can include bleeding, ureteric leaks, and
infection. New hypotension, reduced urine output, significant drain losses, or a drop in haemoglobin of more than 20 g/L should
prompt an urgent surgical review. Electrolytes and urine output along with other fluid losses should be monitored hourly and
replaced; improvement in GFR can cause development of polyuria with high urinary sodium, potassium, phosphate, and mag-
nesium losses. Rapid shifts in serum osmolality can risk cerebral oedema.
Anaesthetising patients who are postrenal transplant for other procedures requires discussion with paediatric nephrology for
timing of immunosuppressive medications. Generally, these are critical medications which should not be omitted without dis-
cussion. Despite having a well-functioning graft, patients may still have residual consequences of renal failure like restrictive
lung defects or cardiovascular changes that can persist lifelong. Chronic graft failure is multifactorial and linked to donor age
and ischaemic times, nephrotoxicity of calcineurin inhibitors, and compliance with immunosuppression regime.
SUMMARY
Paediatric transplant recipients require a multidisciplinary team approach of which anaesthetists are a key participant in the
perioperative period. They can present challenges with associated comorbidities, difficult vascular access, and cautious
consideration of drugs administered and blood transfusion. Surgical approach will vary based on patient size and weight
and size of donor organ. Intraoperative management is directly related to long-term graft outcomes, with regards to judicious
fluid administration and maintaining adequate mean arterial pressure at each stage of the procedure.
REFERENCES
1. UK Kidney Association. UK Renal Registry 26th Annual Report. Accessed April 3, 2025. [Link]
research/annual-report/26th-annual-report-data-31122022
2. Den Bakker E, Gemke R, Bökenkamp A. Endogenous markers for kidney function in children: a review. Crit Rev Clin Lab
Sci. 2018;55(3):163-183.
3. British Transplantation Society. Guidelines for Living Donor Kidney Transplantation. 4th ed. March 2018. Accessed April 3,
2025. [Link]
4. National Organization for Rare Disorders (NORD) database. Accessed April 3, 2025. [Link]
5. Guruswamy V, Barbour R. Anaesthesia for children with renal disease. Br J Anaesth. 2015;15(6):294-298.
6. Ashley C, Dunleavy A. The Renal Drug Handbook. 5th ed. Boca Raton, FL: CRC Press; 2018.
7. Park M, Jung K, Cho HS, Min J-J. Renal injury from sevoflurane in noncardiac surgery: a retrospective cohort study. Br J
Anaesth. 2022;129(2):182-190.
8. Hong I, Bigam KD, McConnell BM, Özelsel TJP, Sondekoppam RV. Sevoflurane and its metabolic byproduct compound A
induce nephrotoxicity: a systematic review and meta-analysis of animal studies. Med Gas Res. 2025;15(2):254-265.
9. Voet M, Cornelissen EAM, van der Jagt MFP, Lemson J, Malagon I. Perioperative anesthesia care for the pediatric patient
undergoing kidney transplantation: an educational review. Paediatr Anaesth. 2021;31(11):1150-1160.
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