Author: Dilshad Marikar / Editors: Angela Hall, Damian Roland / Reviewer: Jolene Rosario, Raghaventhar manikandan / Code: ACCS LO 2, NepC1, NepC2, NepP2, SLO2, SLO5Published: 22/12/2020 / Reviewed: 07/03/2024


Acute Kidney Injury (AKI) is a sudden decline in kidney function. [1] AKI in children is associated with an increased risk of death and prolonged hospital stay, [2] and increased risk of chronic kidney disease. [3]

Recognition of children at risk in the paediatric emergency department can facilitate the early diagnosis of AKI and help reduce the risk of harm. [1]

This e-learning is based on guidance on AKI from the British Association of Paediatric Nephrology (BAPN) and the National Institute of Clinical Excellence (NICE).



Acute kidney injury (AKI) is defined as a sudden loss of kidney function, leading to a decrease in glomerular filtration rate (GFR). [1]

It is detected through [4]:

  • a decrease in urine output in most cases (< 0.5 ml/kg/hour for 8 hours or more)
  • blood testing – an increased serum creatinine (compared to baseline or reference range)


Despite its wide use, serum creatinine is a poor marker for AKI; it varies with age, weight and sex. It is also a late and insensitive marker for AKI – levels only rise significantly when 25-50% of renal function is lost. [1] There is also a lack of consensus on definition of AKI, with over 30 definitions in the literature. The definition used by the NHS England AKI algorithm described below is based on the Kidney Disease Improving Global Outcomes (KDIGO) classification. [1]

NHS England AKI Algorithm [5]

Standardisation of AKI definition

NHS England has agreed a national algorithm to standardise the definition of AKI, and has recommended that this algorithm is automatically calculated by hospital laboratory systems:

  • Serum creatinine is used to create an ‘early warning’ AKI score for severity of AKI (table 1). This score is calculated by comparing the measured creatinine to previous results if available or to a reference upper limit for the child’s age (table 2).

An AKI score should be automatically calculated, and available alongside the creatinine result (table 1)

Stage 1 AKI is often unrecognised and may be the first sign of dehydration or intrinsic renal disease – early detection can reduce progression and harm.

Table 1: Acute Kidney Injury (AKI) Warning Score, based on the NHS England AKI algorithm

AKI Stage Measurement
Stage 1 Measured creatinine is more than 1.5 to 2 times either previous baseline creatinine result or upper reference creatinine limit for age.
Stage 2 Measured creatinine is more than 2 to 3 times either previous baseline creatinine result or upper reference creatinine limit for age.
Stage 3 Measured creatinine is more than 3 times either previous baseline creatinine result or upper reference creatinine limit for age.

Table 2: Paediatric reference ranges for creatinine (Source: UK Paediatric Laboratory Medicine Network)

Age Group Male (Creatinine mol/l) Female (Creatinine mol/l)
Lower Limit Upper Limit Lower Limit Upper Limit
0 – <14days 27 81 27 81
14d – <1yr 14 34 14 34
1 – <3yr 15 31 15 31
3 – <5yr 23 37 23 37
5 – <7yr 25 42 25 42
7 – <9yr 30 48 30 48
9 – <11yr 28 57 28 57
11yr 36 64 36 64
12yr 36 67 36 67
13yr 38 76 38 74
14yr 40 83 43 75
15yr 47 98 44 79
16yr 54 99 48 81
>16 yr Adult Range Adult Range
59 104 45 84


A large US epidemiological study of hospitalised children [2] reported:

  • A Paediatric AKI incidence rate of 3.9 cases per 1000 admissions.
  • Children with AKI had a significantly higher absolute mortality rate (15.9%) compared to children without AKI (0.6%).
  • Mortality increased in children with AKI who were under 1 month of age (31.3% v 10.1%), required paediatric intensive care (32.8% v 9.4%), or required dialysis (27.1% v 14.2%).

The same study reported the following factors associated with Paediatric AKI:

  • Shock
  • Sepsis
  • Intubation/Mechanical Ventilation
  • Extracorporeal Support
  • Circulatory Disease
  • Cardiac congenital abnormalities


The aetiology of acute kidney injury in children has been traditionally divided into pre-renal, intrinstic/renal and post renal causes. The majority of these cases of AKI will be pre-renal due to hypovolaemia (e.g. gastroenteritis) that can be corrected with adequate fluid replacement. [6]

A Norwegian study of AKI in children managed at tertiary centres identified the most common aetiologies [7]:

Pre-renal (hypoperfusion)

  • Dehydration/hypovolaemia (e.g. gastroenteritis)
  • Sepsis
  • cardiac disease

Renal causes

  • Nephritic Syndrome
  • Haemolytic Uraemic Syndrome
  • Drugs related

Post renal causes

  • Congenital anomalies of the kidney and urinary tract.

History Taking – Risk Stratification

In assessing children with acute illness or a history of decreased urine output, you must assess whether they are at increased risk of AKI. Guidelines from the British Association of Paediatric Nephrologists (BAPN) identify two groups who are at increased risk of AKI:

  • Children with pre-existing diseases or risk factors – high risk groups (table 1)
  • Children presenting with acute high-risk scenarios (table 2)

Children in high-risk groups OR high-risk scenarios are at risk of AKI and should have a serum creatinine according to BAPN guidelines.

Table 1: High risk groups for Paediatric AKI

High risk groups Examples
Nephro-urological, cardiac or liver disease Henoch-Schnlein Purpura (HSP) with renal involvement, Nephritic Syndrome, Polycystic Kidneys, Heart failure, Kidney/Liver Transplant
Malignancy and/ or a bone marrow transplant Acute Lymphoblastic Leukaemia (ALL)
Dependence on others for access to fluids Neonates, infants, children with severe neurodisability
History of taking medication that may adversely affect renal function ●      ACE Inhibitors/Angiotensin 2 receptor blockers – e.g. enalapril, captopril, losartan

●      NSAIDs – e.g. ibuprofen

●      Aminoglycoside antibiotics – e.g. gentamicin

●      calcineurin inhibitors – e.g. tacrolimus for children post transplantation

Table 2: High risk scenarios for Paediatric AKI

High risk scenarios
History of reduced urine output**(<0.5 ml/kg/hour for 8 hours)
Hypoperfusion or dehydration
History of exposure to drugs or toxin that may adversely affect renal function
Renal disease or urinary tract obstruction
Major surgery

AKI Risk Stratification and clinical judgement

For a child identified as being at increased risk of AKI using the BAPN guidelines, clinical judgement can be used to determine whether serum creatinine testing is needed. In particular:

  • Children in high-risk groups who do not have a history of reduced urine output and are not acutely unwell, e.g. a child with cardiac disease who has a simple fracture do not need creatinine blood testing.
  • In children with suspected gastroenteritis and a history of reduced urine output or mild to moderate dehydration, a trial of oral rehydration can be performed and the child reassessed before considering blood testing. This approach is consistent with NICE guidance on gastroenteritis for children under 5 years of age. [8]


  • NICE guidance on AKI advises that acutely unwell children with severe diarrhoea (children with bloody diarrhoea are at particular risk) should have a serum creatinine measured. [6] This requires clinical judgement, as a definition of severe diarrhoea is not provided.
  • Be aware that NICE guidance on children with gastroenteritis [8] identifies children who have passed more than five diarrhoeal stools in the previous 24 hours as at increased risk of dehydration; these children require careful evaluation.

Children should be assessed using an ABCDE approach, and potentially life-threatening problems such as shock and sepsis addressed before careful assessment to find an underlying cause.

Key examination points

The Clinical assessment of dehydration is difficult and subject to variability between clinicians, even when standardised scoring systems are used. [6]

The “gold standard” of assessing clinical dehydration is to weigh the child and compare this to previous weight (where available) and subsequent weights after rehydration.

1: What is the child’s fluid Status?

  • Is there clinical evidence of dehydration or shock
  • Have your weighed the child?
  • Is there evidence of hypertension?
  • Does the child appear to have a normal hydration status?
  • Or does the child show evidence of fluid overload – eg peripheral oedema?

Learning Bites

  • Children who have passed more than five diarrhoeal stools in the previous 24 hours as at increased risk of dehydration and require careful evaluation. [8]
  • Euvolaemia, hypervolaemia or hypertension may point to intrinsic renal causes, eg nephritic or nephrotic syndrome. Perform urinalysis to look for proteinurea and/or haematuria.

2) Is there evidence of sepsis? Sepsis is a common cause of AKI in paediatrics [7]

3) Is there evidence of urinary tract obstruction? Examine for a palpable bladder or other abdominal masses

Resource for assessment of dehydration and shock [9]

The British Association of Paediatric Nephrologists (BAPN) recommend the following first-line investigations where AKI is suspected:

Investigations Comment
Full blood count, creatinine, electrolytes, bone profile, bicarbonate A raised white cell count and falling platelets may indicate early Haemolytic Uraemic Syndrome (HUS) – also look for falling haemoglobin and fragmented RBCs on blood film
Urinalysis proteinuria/haematuria may indicate intrinsic renal disease
Urine microscopy To look for evidence or urinary tract infection. Red cells casts may indicate glomerulonephritis
Urinary tract ultrasound* May identify a cause for AKI, eg hydronephrosis


As the majority of cases of AKI are due to hypovolemia and will be corrected with adequate fluid replacement, unless there is suspicion of urinary tract obstruction, performing an urgent urinary tract ultrasound in the paediatric emergency department may not be indicated.

Intrinsic renal disease in may cause AKI in children, and early detection will aid specific management and may help reduce the risk of progression to chronic kidney disease. Look out for

  • Haematuria/proteinuria: May indicate nephritic, nephrotic or haemolytic uraemic syndrome (HUS)
  • Rash: Palpable purpura are present in Henoch Schonlein Purpura (HSP); all children should have a urine dip performed to look for renal involvement
  • Bloody Diarrhoea: May indicate Haemolytic Uraemic Syndrome (HUS)

Haemolytic Uraemic Syndrome (HUS) is a triad of:

  • microangiopathic haemolytic anaemia,
  • thrombocytopaenia
  • acute renal failure

It is a common cause of acute kidney injury in children and is typically infection-induced, most commonly by vero cytotoxin-producing Escherichia coli (VTEC).

Clinicians must be alert to bloody diarrhoea which may be present in up to 90% of VTEC cases. Up to 10% of cases of VTEC infection will develop Haemolytic Uraemic Syndrome (HUS)

Clinicians should have a high index of suspicion of VTEC where the patient has been in recent close contact with:

  • ruminant animals (principally cattle, goats, sheep), their faeces, and faecally contaminated environments (such as at open farm visits)
  • contact with another known or suspected case of VTEC
  • where an outbreak of VTEC infection is known, or suspected to be present locally

Public Health England guidance advises all children with bloody diarrhoea should have investigations for HUS including a full blood count and blood film. [10,11]

Henoch Schonlein Purpura (HSP) is a childhood vasculitis which is characterised by palpable purpura in the presence of at least one of the following:

  • Diffuse abdominal pain
  • Acute arthritis or arthralgia
  • Renal involvement (haematuria and/or proteinuria)
  • Biopsy showing predominant IgA deposition

Renal involvement in HSP can come weeks to months after the onset of rash, and may involve haematuria, proteinuria, nephritic or nephrotic syndrome, renal impairment or hypertension.

Children with HSP should have at a blood pressure and urine dip performed, and enquire whether follow up has been arranged.


Management of AKI – the 3Ms – Monitor, Maintain and Minimise

Children at risk of AKI or with confirmed AKI should be managed using the following iterative steps to prevent further harm [12]:

1) MONITOR Children should have urea and electrolytes and creatinine checkedFluid balance Fluid inputs urine output, Weight recorded Urinalysis performed Blood pressure Paediatric Early Warning Score (EWS) Any signs of sepsis should be urgently investigated and treated.
2) MAINTAIN CIRCULATION Urgently address hypoperfusion using with fluid boluses of normal salineGive maintenance fluids and replace ongoing losses (eg diarrhoea)
3) MINIMISE KIDNEY INJURY Reduce further harm by reviewing, adjusting and monitoring medication that may adversely affect renal function (see next section)


Medication in AKI

Children with AKI need a full review of all their medication, which may need to be stopped, avoided or reduced (fig.1). [4]

In the context of the Paediatric emergency department:

  • Non-steroidal anti-inflammatory drugs should not be given.
  • Do not delay administration of antibiotics in suspected sepsis. However, dose reductions may be required once the child’s level of renal function is known.
Fig.1 Summary of drugs to be stopped, avoided, reduced or monitored in AKI [4]
  • Paediatric AKI can be preventable; early detection and appropriate management can reduce harm
  • Risk assessment for Paediatric AKI involves identifying high risk groups and high risk scenarios for AKI and using clinical judgement to determine whether serum creatinine testing is required
  • AKI prevention and management involves careful assessment and monitoring, maintaining circulation and minimising kidney insults (the 3Ms)

Summary flow diagram of British Association of Paediatric Nephrologists(BAPN) AKI guidelines [4]


The following groups of children with AKI are at high risk of requiring renal replacement therapy and require urgent Involvement of the Paediatrics team with nephrology input:

  • Potassium >6.5mmol/l (non-haemolysed sample)
  • Oligoanuria and plasma sodium <125mmol/l
  • Pulmonary oedema or hypertension unresponsive to diuretics
  • Plasma urea >40mmol/l unresponsive to fluid challenge.
  1. McCaffrey J, Dhakal AK, et al. Recent developments in the detection and management of acute kidney injury. Arch Dis Child. 2017 Jan;102(1):91-96.
  2. Sutherland SM, Ji J, Sheikhi FH, et al. AKI in hospitalized children: epidemiology and clinical associations in a national cohort. Clin J Am Soc Nephrol. 2013 Oct;8(10):1661-9.
  3. Mammen C, Al Abbas A, et al. Long-term risk of CKD in children surviving episodes of acute kidney injury in the intensive care unit: a prospective cohort study. Am J Kidney Dis. 2012 Apr;59(4):523-30.
  4. Guidance for clinicians managing children at risk of, or with, acute kidney injury. UK Renal Registry. “Think Kidneys”, 2016. Revised Dec 2019. [Accessed March 2024]
  5. Acute Kidney Injury (AKI) Algorithm. NHS England. [Accessed Dec 2023]
  6. National Institute for Health and Care Excellence (NICE). Acute kidney injury: prevention, detection and management [NG148] 2019. Last updated: 28 September 2023 [Accessed Dec 2023]
  7. Jenssen GR, Hovland E, et al. The incidence and aetiology of acute kidney injury in children in Norway between 1999 and 2008. Acta Paediatr. 2014 Nov;103(11):1192-7.
  8. National Institute for Health and Care Excellence (NICE). Diarrhoea and vomiting caused by gastroenteritis in under 5s: diagnosis and management. [CG84] 2009. [Accessed Dec 2023]
  9. Freeman R. Gastroenteritis in Children under 5 years of age. RCEMLearning, 2021.
  10. Public health operational guidance for Shiga toxin-producing Escherichia coli (STEC). UK Health Security Agency, Jan 2023.
  11. Shiga toxin-producing Escherichia coli: complications. Guidance – Public Health England, Dec 2017.
  12. National Institute for Health and Care Excellence (NICE). Intravenous fluid therapy in children and young people in hospital. [NG29], 2015. Last updated: 11 June 2020.