Overview
Acute Kidney Injury in Children
Topic Overview
Summary
Acute kidney injury (AKI) in children is a sudden decline in kidney function, defined by rising creatinine or reduced urine output. Causes differ from adults — haemolytic uraemic syndrome (HUS), sepsis, and nephrotoxic drugs are common. Children are at higher risk of fluid and electrolyte imbalances. Management focuses on treating the underlying cause, managing complications (hyperkalaemia, fluid overload), and supporting renal function. Dialysis may be required in severe cases.
Key Facts
- Definition: pRIFLE or KDIGO criteria (creatinine rise or oliguria)
- Common causes: Pre-renal (dehydration, sepsis), intrinsic (HUS, ATN, GN), post-renal (obstruction)
- Key complications: Hyperkalaemia, fluid overload, metabolic acidosis
- Treatment: Treat cause, manage fluid balance, correct electrolytes, dialysis if needed
- Prognosis: Good in most non-HUS causes; depends on aetiology
Clinical Pearls
HUS is the most common cause of AKI requiring dialysis in children in the UK
Check creatinine against normal for age — adult values don't apply to children
Fluid overload is common and dangerous — monitor weight daily
Why This Matters Clinically
AKI in children can progress rapidly. Early recognition, fluid management, and treatment of hyperkalaemia are life-saving. Referral to paediatric nephrology is essential for severe cases.
Visual Summary
Visual assets to be added:
- pRIFLE criteria table
- Causes of paediatric AKI diagram
- Hyperkalaemia management algorithm (paediatric)
- Fluid balance chart
Epidemiology
Incidence
- 5-10% of PICU admissions have AKI
- Increasing due to improved recognition
- More common in neonates and critically ill children
Demographics
- All ages including neonates
- Higher in critical illness
Causes
| Category | Examples |
|---|---|
| Pre-renal | Dehydration (gastroenteritis), sepsis, haemorrhage, cardiac failure |
| Intrinsic renal | HUS (most common for dialysis), ATN, glomerulonephritis, interstitial nephritis |
| Post-renal | Posterior urethral valves (neonates), stones, tumour |
| Nephrotoxic drugs | NSAIDs, aminoglycosides, contrast, chemotherapy |
Pathophysiology
Pre-Renal AKI
- Reduced renal perfusion
- Reversible if perfusion restored
- If prolonged → acute tubular necrosis (ATN)
Intrinsic AKI
- Direct kidney parenchymal damage
- Tubular (ATN), glomerular (GN), vascular (HUS), interstitial
Post-Renal AKI
- Urinary tract obstruction
- Bilateral obstruction or obstruction of single kidney
HUS — Common in Children
- Shiga toxin-producing E. coli (STEC)
- Triad: MAHA + thrombocytopenia + AKI
- Most common cause of AKI requiring dialysis in children
Clinical Presentation
Symptoms
Signs
Red Flags
| Finding | Significance |
|---|---|
| Anuria | Severe AKI — urgent intervention |
| Hyperkalaemia | Cardiac risk — treat immediately |
| Fluid overload | Pulmonary oedema risk |
| Altered consciousness | Uraemic encephalopathy |
Reduced urine output
Common presentation.
Swelling (oedema)
Common presentation.
Lethargy
Common presentation.
Nausea, vomiting
Common presentation.
Symptoms of underlying cause (diarrhoea in HUS, fever in sepsis)
Common presentation.
Clinical Examination
Vital Signs
- Blood pressure (hypertension common)
- Heart rate
- Respiratory rate (acidosis)
Fluid Status
- Weight (daily)
- Oedema
- JVP (older children)
- Lung crackles
Abdominal
- Palpable bladder (obstruction)
- Flank masses
Investigations
Blood Tests
| Test | Purpose |
|---|---|
| U&E, creatinine | Diagnosis and staging |
| K+ | Hyperkalaemia risk |
| Bicarbonate | Acidosis |
| FBC | Anaemia (HUS) |
| Blood film | Schistocytes (HUS) |
| LDH | Haemolysis |
| CRP | Infection |
| Blood gas | Acidosis |
Urine
| Test | Purpose |
|---|---|
| Urinalysis | Blood, protein (GN) |
| Microscopy | Red cell casts (GN) |
| Sodium | FeNa (under 1% = pre-renal) |
Imaging
| Modality | Indication |
|---|---|
| Renal USS | Size, obstruction, structural abnormality |
| CXR | Fluid overload |
Specialist Tests
- Complement (C3, C4) — if GN or aHUS suspected
- ANCA, ANA — if vasculitis suspected
- Stool culture — STEC in HUS
Classification & Staging
pRIFLE Criteria
| Stage | Creatinine Clearance | Urine Output |
|---|---|---|
| Risk | Decreased by 25% | Under 0.5 mL/kg/hr for 8h |
| Injury | Decreased by 50% | Under 0.5 mL/kg/hr for 16h |
| Failure | Decreased by 75% or under 35 mL/min/1.73m² | Under 0.3 mL/kg/hr for 24h or anuric 12h |
| Loss | Persistent failure over 4 weeks | |
| ESKD | Persistent failure over 3 months |
KDIGO Criteria (Also Used)
- Stage 1-3 based on creatinine rise and urine output
Management
General Principles
- Treat underlying cause
- Manage fluid balance
- Correct electrolyte abnormalities
- Dialysis if indicated
Fluid Management
| Situation | Approach |
|---|---|
| Hypovolaemic | Cautious fluid resuscitation (10-20 mL/kg boluses) |
| Euvolaemic | Maintenance only (insensible losses + urine output) |
| Fluid overloaded | Fluid restriction; diuretics (furosemide); dialysis if refractory |
Hyperkalaemia Management (Paediatric)
| Treatment | Dose |
|---|---|
| Calcium gluconate | 0.5 mL/kg 10% IV (cardiac protection) |
| Salbutamol | Nebulised 2.5-5 mg (shifts K+ into cells) |
| Insulin + glucose | 0.1 unit/kg insulin + 0.5 g/kg glucose IV |
| Sodium bicarbonate | If acidotic |
| Calcium resonium | 1 g/kg PO/PR (removes K+) |
| Dialysis | Definitive if refractory |
Dialysis Indications
- Refractory hyperkalaemia
- Refractory fluid overload
- Uraemic symptoms (encephalopathy, pericarditis)
- Severe acidosis
- Toxin removal (some drugs)
Referral
- Early involvement of paediatric nephrology
- PICU if unstable
Complications
Acute
- Hyperkalaemia (arrhythmias)
- Fluid overload (pulmonary oedema)
- Metabolic acidosis
- Uraemic encephalopathy
- Hypertension
- Infection
Long-Term
- Chronic kidney disease
- Hypertension
- Proteinuria
Prognosis & Outcomes
Prognosis
- Most pre-renal AKI recovers fully
- HUS: Most recover renal function; some develop CKD
- Depends on aetiology and severity
Follow-Up
- All children with AKI need renal follow-up
- Monitor BP, proteinuria, renal function
Evidence & Guidelines
Key Guidelines
- NICE AKI Guideline (NG148) — Applicable to Children
- KDIGO AKI Guidelines
Key Evidence
- Early recognition and intervention improves outcomes
- Fluid overload is associated with worse prognosis
Patient & Family Information
What is AKI?
Acute kidney injury means the kidneys suddenly stop working properly. This can happen for many reasons including dehydration, infection, or a condition that damages the kidneys.
Symptoms
- Making less wee than usual
- Swelling (face, hands, feet)
- Feeling tired and unwell
Treatment
- Treating the cause
- Careful fluids through a drip
- Sometimes dialysis (a machine that does the kidney's job)
What Happens Next?
- Most children recover fully
- Some need follow-up to check kidney function
Resources
References
Primary Guidelines
- NICE. Acute Kidney Injury: Prevention, Detection and Management (NG148). 2019. nice.org.uk
- KDIGO. Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl. 2012;2(1):1-138.
Key Reviews
- Basu RK, et al. Acute kidney injury in pediatric cardiac surgery. Pediatr Crit Care Med. 2016;17(8):753-763. PMID: 27464761