Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Acute kidney injury and fluid balance
Paediatrics and child health · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
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Hyperkalaemia, pulmonary oedema or anuria
ECG change, severe potassium elevation, pulmonary oedema, refractory acidosis, uraemic encephalopathy or pericarditis, anuria and rapidly increasing fluid overload can become fatal before the cause of AKI is fully defined.
Action: Call paediatric critical care and nephrology, stop potassium and nephrotoxins, obtain ECG and urgent repeat venous potassium without delaying treatment of credible ECG-positive hyperkalaemia, and manage through the local paediatric emergency protocol. Support ventilation and arrange kidney replacement therapy when complications do not respond promptly to medical management.
Overview
Detect paediatric AKI from creatinine change and urine output, distinguish perfusion, intrinsic and obstructive causes, prescribe fluids from repeated weight-based assessment, stop nephrotoxins and escalate complications promptly.
Serum creatinine is a lagging marker influenced by age, muscle mass and dilution. A small rise can be proportionally important in a young child, and severe injury may exist before the value reaches an adult laboratory upper limit.
NICE accepts pRIFLE, AKIN or KDIGO definitions. Accurate urine measurement provides an earlier signal in many children, but nappies, diarrhoea, catheter blockage and undocumented voids can create false impressions.
Pre-renal AKI results from inadequate effective renal perfusion due to dehydration, haemorrhage, sepsis, vasodilatation, heart failure or capillary leak. Prompt restoration before structural injury may reverse it.
Intrinsic causes include acute tubular injury, nephritis, HUS, nephrotoxins, rhabdomyolysis, interstitial nephritis and vascular disease. Urine pattern, systemic features and exposure history guide targeted tests.
Post-renal AKI results from bilateral obstruction, obstruction in a solitary kidney or bladder outlet disease. In infants and boys consider posterior urethral valves; at any age consider stones, neurogenic bladder, tumour, clots and catheter obstruction.
Practice
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Paediatrics and child healthOriginal SBA
Paediatric AKI criterion
A child has urine output of 0.4 mL/kg/hour for 10 hours, while creatinine is still within the laboratory reference range. What is the correct interpretation?
Sources and review status4 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 27 Aug 2026; clinical approval remains outstanding.
History covers exact intake and losses, fever, diarrhoea, blood, urine frequency and colour, oedema, breathlessness, rash, joints, recent throat infection, muscle injury, congenital urinary disease and every prescribed or non-prescribed medicine.
Volume examination combines pulse, capillary refill, mucosa, fontanelle in infants, blood pressure, jugular or liver signs where useful, peripheral oedema, lung findings and serial weight. No single sign defines intravascular state.
Fluid balance is a prescription, not bookkeeping. Weigh nappies, document oral, enteral and intravenous input, include drug carrier volumes, drains, vomit and stool estimates, and reconcile totals against serial weight.
A 10-kg child gaining 1 kg has accumulated roughly 1 litre, approximately 10% of body weight, even if the chart appears balanced. Cumulative percentage fluid overload helps explain respiratory and blood-pressure deterioration.
Urinalysis separates patterns: blood plus protein suggests nephritis, haem pigment with few red cells suggests haemolysis or rhabdomyolysis, leucocytes may suggest infection or interstitial nephritis, and glycosuria can indicate proximal tubular injury or hyperglycaemia.
Ultrasound is not automatic when a clear reversible cause responds. It becomes urgent when the cause is uncertain or obstruction is possible and immediate when infected obstruction is suspected.
AKI is not fully over at discharge. Document the episode, medication changes and current creatinine, arrange reassessment based on severity, and refer persistent hypertension, impaired function or at least 1+ early-morning proteinuria to paediatric nephrology.
Key points
Paediatric AKI is an abrupt fall in kidney function detected by change from the child's baseline, not by an adult creatinine reference range.
NICE criteria include creatinine rise of at least 26 micromol/L within 48 hours, at least 50% within 7 days, eGFR fall of at least 25% within 7 days, or urine below 0.5 mL/kg/hour for more than 8 hours.
Infant creatinine changes rapidly after birth and initially reflects maternal creatinine; neonatal age, gestation, postnatal day and urine output require neonatal interpretation.
Classify causes as reduced renal perfusion, intrinsic renal injury or post-renal obstruction, while recognising that sepsis and critical illness often combine mechanisms.
First-line assessment is ABCDE, perfusion, volume status, blood pressure, weight change, measured intake and output, bladder examination and complete medication review.
First-line tests are serial creatinine, urea and electrolytes, bicarbonate or blood gas, glucose, calcium, phosphate, FBC and urine dipstick for blood, protein, leucocytes, nitrite and glucose.
Stop or withhold avoidable nephrotoxins and renal-haemodynamic medicines during acute hypovolaemia, including NSAIDs, ACE inhibitors, ARBs and unnecessary aminoglycosides; dose essential medicines to current kidney function.
For true hypovolaemia, give a cautious isotonic crystalloid bolus under paediatric assessment and reassess pulse, perfusion, pressure, lungs, weight and urine response after each aliquot.
Aetiology
01
Reduced renal perfusion
Dehydration, sepsis, haemorrhage, cardiac dysfunction or vasodilatation lowers glomerular blood flow before structural kidney damage develops.
NSAIDs, aminoglycosides, ACE inhibitors, ARBs, contrast and other agents can reduce perfusion or cause direct toxicity.
Pathophysiology
1
Falling filtration
Reduced glomerular filtration retains urea, creatinine, potassium, hydrogen ions, salt and water abnormally within the circulation.
2
Tubular dysfunction
Injured tubules cannot concentrate urine, regulate electrolytes or reabsorb filtered solutes normally, sometimes causing polyuric recovery.
3
Fluid accumulation
Oliguria with continued input increases body water, blood pressure and pulmonary interstitial fluid, progressively impairing respiratory oxygenation.
4
Electrolyte toxicity
Potassium and acid retention destabilises cardiac membranes, while sodium, calcium and phosphate disturbances affect neurological and muscular function.
5
Recovery hyperdiuresis
Filtration may recover before tubular concentration, producing large ongoing urine losses, recurrent dehydration and clinically important potassium depletion.
Clinical features and red flags
Creatinine change
Compare every result with age, gestation, muscle mass and a known or estimated baseline instead of adult limits.
Urine-output threshold
Measure mL/kg/hour over time; below 0.5 for more than 8 hours meets a child AKI criterion.
Volume phenotype
Combine perfusion, mucosa, pressure, oedema, lung signs and serial weight before choosing fluid, restriction or diuresis.
Cause pattern
Separate perfusion loss, parenchymal urine findings and obstruction clues while allowing overlapping causes in sepsis.
Complication screen
Look repeatedly for ECG change, weakness, breathlessness, hypertension, confusion, seizure, bleeding or pericardial pain.
Medicine exposure
List NSAIDs, antimicrobials, ACE inhibitors, ARBs, diuretics, contrast, herbal products and recent dose changes.
Red flags requiring action
Urine output below 0.5 mL/kg/hour for more than 8 hours in a child meets a NICE AKI detection criterion and requires investigation.
A creatinine rise of at least 26 micromol/L within 48 hours or at least 50% within 7 days meets an AKI criterion even when the absolute value appears age-normal.
Hyperkalaemic ECG changes, pulmonary oedema, severe acidosis, uraemic symptoms or refractory fluid overload requires immediate nephrology and critical-care referral.
Investigations
01First-line: serial creatinine and urine outputFirst stepFirst line
Why
Detect AKI and stage change using NICE-approved biochemical and output criteria.
Interpretation and limitations
Use change from baseline and mL/kg/hour duration; creatinine can lag, so either criterion independently matters.
02Renal profile, blood gas and ECG
Why
Detect potassium, acid-base and electrical complications needing immediate treatment.
Interpretation and limitations
Repeat a haemolysed potassium urgently, but do not delay emergency treatment when credible hyperkalaemia has ECG effects.
03Urine dipstick and microscopy
Why
Identify blood, protein, infection, glucose, pigment and sediment patterns that direct cause.
Interpretation and limitations
Blood plus protein without infection suggests nephritis; granular casts suggest tubular injury and haem pigment needs CK or haemolysis assessment.
04Urgent renal and bladder ultrasound
Why
Detect obstruction, pyonephrosis or congenital urinary abnormality when cause is unclear.
Interpretation and limitations
Perform within 6 hours for suspected pyonephrosis and within 24 hours for unexplained AKI or obstruction risk.
Differential diagnosis
01
Chronic kidney disease
Poor growth, anaemia, longstanding hypertension, small echogenic kidneys or prior abnormal creatinine suggests chronic rather than purely acute dysfunction.
02
Laboratory or dilution effect
Haemolysis can falsely elevate potassium, while fluid loading can dilute creatinine; repeat credible samples and interpret the trajectory.
03
Physiological neonatal transition
Early newborn creatinine reflects maternal level and gestational physiology, requiring neonatal reference trends rather than older-child criteria alone.
04
Urine-measurement error
Unweighed nappies, stool mixing, missed voids or a blocked catheter can create apparent oliguria without true filtration decline.
05
Syndrome of inappropriate antidiuresis
Hyponatraemia with concentrated urine and preserved renal filtration causes water retention but not the full AKI biochemical pattern.
Management
01DetectionConfirm AKI and severityFirst stepCreatinine rises, urine falls or an at-risk child deteriorates.+
1Compare creatinine with baseline, calculate weight-based urine output and assess paediatric early-warning physiology.
2Check renal profile, gas, glucose, calcium, phosphate, urinalysis and a current measured weight.
3Stop nephrotoxins, adjust essential medicines and call nephrology immediately for stage 3 disease or life-threatening complications.
02HypovolaemiaRestore perfusion cautiouslyExamination and history support true intravascular depletion without overload.+
1Give an age-appropriate isotonic crystalloid aliquot under senior paediatric direction.
2Reassess perfusion, pressure, lungs, liver, weight and urine response after each aliquot rather than prescribing repeated automatic boluses.
Complications
01
Hyperkalaemic arrhythmia
Potassium retention can cause conduction delay, broad complexes, ventricular arrhythmia and cardiac arrest with little warning.
02
Pulmonary oedema
Salt and water accumulation produces hypoxaemia, respiratory distress and need for ventilatory or kidney replacement support.
03
Uraemic organ dysfunction
Accumulated uraemic toxins can cause encephalopathy, seizures, pericarditis, bleeding tendency, nausea and progressive nutritional decline in children.
04
Chronic kidney impairment
Severe or recurrent injury increases later hypertension, proteinuria, reduced renal reserve and chronic kidney disease risk.
05
Polyuric recovery losses
Excess urine during tubular recovery can cause recurrent hypovolaemia, hypokalaemia and hypernatraemia unless measured losses receive appropriate replacement.
Monitoring and follow-up
Measure urine output accurately in mL/kg/hour and document catheter, nappy or collection limitations.
Obtain a current weight at least daily and twice daily when fluid balance is unstable, as NICE recommends for at-risk children.
Trend creatinine and electrolytes daily in hospital as a typical minimum, increasing frequency for potassium or rapid change.
Record all oral, enteral and intravenous input, including flushes and drug carriers, and every measurable output.
Repeat blood pressure, respiratory and neurological assessment according to severity and the paediatric early-warning response.
During recovery, monitor polyuria, thirst, weight, sodium and potassium to avoid a second perfusion injury.
After discharge, reassess creatinine based on recovery stability and refer hypertension, impaired eGFR or at least 1+ early-morning proteinuria.
Special situations
A normal value may be abnormal
A child's creatinine can double yet remain inside an adult reference interval, still meeting a major AKI criterion.
Weight audits the chart
Unexpected weight gain often exposes missed intravenous carriers, unmeasured intake or inaccurate output recording.
Fluid is a repeated decision
The correct bolus for early dehydration can become harmful hours later after filtration falls and urine stops.
Diuretics change volume, not injury
Producing urine does not prove renal recovery and an absent response should accelerate dialysis assessment, not repeated dosing.
Recovery can cause dehydration
Polyuria after tubular or obstructive recovery may lose water and electrolytes faster than a child can drink.
Common pitfalls
01
Do not use an adult creatinine upper limit to exclude paediatric AKI.
02
Do not accept undocumented nappies as evidence of adequate urine output.
03
Do not repeat fluid boluses without reassessing perfusion and overload.
04
Do not continue NSAIDs, ACE inhibitors or other avoidable nephrotoxins during hypovolaemic AKI.
05
Do not prescribe potassium-containing maintenance fluid before reviewing urine output and serum potassium.
06
Do not use loop diuretics as routine treatment for kidney injury.
07
Do not wait for a creatinine threshold when pulmonary oedema or ECG-positive hyperkalaemia requires dialysis assessment.
08
Do not discharge without a documented creatinine and renal follow-up plan.
Do not give repeated fluid boluses to an oedematous, hypertensive or oliguric child without evidence of fluid responsiveness; overload worsens respiratory and renal outcomes.
Once euvolaemic or overloaded, prescribe daily input from insensible needs plus measured urine and other losses, with adjustments for fever, ventilation, drains and ongoing diarrhoea.
Loop diuretics do not treat renal injury and are not routine. They may be used for fluid overload while awaiting or during renal replacement therapy if residual urine output exists.
Kidney replacement therapy is indicated by refractory hyperkalaemia, acidosis, uraemic complications, pulmonary oedema or fluid overload; do not wait for a fixed creatinine threshold.
Haematuria plus proteinuria without UTI or catheter trauma suggests acute nephritis and needs urgent nephrology consideration.
Pyonephrosis requires ultrasound within 6 hours; unexplained AKI or obstruction risk requires urinary ultrasound within 24 hours under NICE NG148.
Stage 3 AKI, no clear cause, inadequate response, transplant status or suspected vasculitis, glomerulonephritis or interstitial nephritis warrants early specialist discussion.
05
Cause-specific tests
Why
Investigate sepsis, HUS, glomerulonephritis, rhabdomyolysis, vasculitis or toxin exposure.
Interpretation and limitations
Select FBC and film, cultures, complement, autoantibodies, CK or toxicology from the phenotype rather than ordering indiscriminately.
3
EscalationTreat ongoing cause such as sepsis or diarrhoea and stop fluid escalation when euvolaemia, overload or non-responsiveness appears.
03Euvolaemia or overloadPrescribe measured daily inputThe child is no longer fluid responsive or has oedema, hypertension or pulmonary signs.+
1Set input from insensible requirement plus measured urine and other losses, subtracting enteral feeds and medicine-carrier volumes.
2Restrict salt and potassium as biochemistry indicates, obtain daily or twice-daily weight and reconcile charted balance against weight change.
3Use loop diuretic only for overload with specialist oversight and arrange kidney replacement therapy if complications remain refractory.
04ObstructionImage and decompress promptlyThere is anuria, poor stream, palpable bladder, hydronephrosis risk or unexplained AKI.+
1Check catheter patency or bladder retention immediately and obtain urinary ultrasound within the NICE time frame.
2Refer infected obstruction, bilateral upper-tract obstruction or obstruction in a solitary kidney immediately to urology.
3Arrange nephrostomy, stent or bladder drainage promptly and monitor for post-obstructive polyuria and electrolyte loss.
05RecoveryPrevent relapse after AKICreatinine and urine output begin improving.+
1Watch for polyuria and replace measured losses proportionately while monitoring sodium and potassium.
2Restart withheld medicines only after renal function, hydration and clinical indication are reviewed.
3Document the episode and arrange creatinine, pressure and urine protein follow-up; refer persistent abnormality to paediatric nephrology.