Acute Kidney Injury in Children

Topic Overview

Summary

Acute kidney injury (AKI) in children represents a sudden decline in kidney function characterised by rising serum creatinine or reduced urine output. The paediatric AKI population differs substantially from adults in aetiology, with haemolytic uraemic syndrome (HUS), sepsis, congenital heart disease, and nephrotoxic medications being prominent causes. Children demonstrate unique vulnerability due to immature renal function in neonates, different fluid compartments, and age-specific creatinine ranges. Early recognition using validated paediatric criteria (pRIFLE, KDIGO) and prompt intervention addressing fluid balance, electrolyte disturbances, and underlying causes are critical to prevent progression to chronic kidney disease.

Key Facts

• Definition: Diagnosed using pRIFLE or KDIGO criteria (creatinine rise or oliguria based on age-specific thresholds)
• Incidence: Affects 5-10% of PICU admissions; higher in neonates and post-cardiac surgery patients [1,2]
• Common causes: Pre-renal (dehydration, sepsis), intrinsic (HUS, ATN, glomerulonephritis), post-renal (posterior urethral valves, obstruction)
• Key complications: Hyperkalaemia, fluid overload, pulmonary oedema, metabolic acidosis, uraemic encephalopathy
• Treatment: Treat underlying cause, meticulous fluid management, correct electrolytes, renal replacement therapy if indicated
• Prognosis: Most pre-renal AKI recovers fully; HUS carries risk of long-term CKD in 10-30% [3,4]

Clinical Pearls

HUS is the most common cause of AKI requiring dialysis in UK children — typically follows bloody diarrhoea caused by Shiga toxin-producing E. coli (STEC-HUS)

Always interpret creatinine against age-specific normal ranges — adult values (60-120 μmol/L) do not apply to children; neonatal baseline is ~30-40 μmol/L [5]

Fluid overload > 10% at dialysis initiation is associated with increased mortality — daily weights are mandatory [6]

Urine output thresholds differ by age — oliguria defined as less than 1 mL/kg/hr in neonates, less than 0.5 mL/kg/hr in older children

Avoid NSAIDs, ACE inhibitors, and aminoglycosides in at-risk children — nephrotoxin avoidance is critical prevention strategy

Why This Matters Clinically

Paediatric AKI is increasingly recognised as a common complication in critically ill children, with incidence rising from improved detection using standardised criteria. Early AKI (within 48 hours of PICU admission) occurs in 25-30% of critically ill children [7]. Beyond acute morbidity, even transient AKI is associated with long-term risks: children experiencing severe AKI have 3-4 fold increased risk of developing chronic kidney disease, hypertension, and proteinuria over subsequent decades [8,9]. Prompt recognition, fluid resuscitation in pre-renal states, nephrotoxin avoidance, and timely nephrology referral are life-saving interventions that also preserve long-term renal function.

---

Visual Summary

Visual assets to be added:

• pRIFLE and KDIGO criteria comparison table
• Age-specific causes of paediatric AKI diagram (neonate vs infant vs child)
• Hyperkalaemia management algorithm (paediatric doses)
• Fluid assessment and management flowchart
• HUS diagnostic triad (MAHA + thrombocytopenia + AKI)
• Dialysis indications (AEIOU mnemonic)

---

Epidemiology

Incidence and Prevalence

Critical Care Settings:

• PICU: AKI occurs in 10-15% of general PICU admissions; up to 25-30% if AKI defined by any pRIFLE stage [1,7,10]
• Neonatal ICU: 18-40% of critically ill neonates develop AKI; higher rates in extremely preterm infants (less than 28 weeks) and those with perinatal asphyxia [11,12]
• Post-cardiac surgery: 40-50% of children undergoing cardiopulmonary bypass develop AKI; severe AKI (Stage 2-3) in 5-10% [13,14]

Community Settings:

• HUS incidence in UK: approximately 1-2 per 100,000 children less than 5 years annually; seasonal peaks in summer (STEC-HUS) [15]
• Gastroenteritis-associated pre-renal AKI: most common cause of community-acquired AKI in children

Temporal Trends:

• Reported AKI incidence has increased 2-3 fold over past decade, primarily due to improved recognition with standardised criteria rather than true epidemiological rise [10]
• Introduction of pRIFLE (2007) and KDIGO (2012) criteria enabled systematic detection

Age-Specific Risk Factors

Geographical Variations

• STEC-HUS more common in industrialised countries with intensive livestock farming
• Malaria-associated AKI predominates in sub-Saharan Africa and Southeast Asia
• Contrast-induced AKI increasing in Western populations due to rising cardiac catheterisation rates

---

Pathophysiology

Pre-Renal AKI

Mechanism:

• Renal hypoperfusion → reduced glomerular filtration pressure
• Activation of compensatory mechanisms:
  • "RAAS activation: Angiotensin II-mediated efferent arteriolar vasoconstriction maintains GFR"
  • "Tubuloglomerular feedback: Decreased distal tubule sodium delivery → afferent arteriolar dilation"
  • "ADH release: Water retention to restore circulating volume"

Reversibility:

• If perfusion restored promptly (within hours): Full recovery
• If hypoperfusion prolonged (> 24-48 hours): Progression to ischaemic acute tubular necrosis (ATN)

Common Causes:

• Hypovolaemia: gastroenteritis, haemorrhage, burns
• Decreased cardiac output: congenital heart disease, septic shock, myocarditis
• Systemic vasodilation: sepsis, anaphylaxis
• Renal vasoconstriction: NSAIDs, ACE inhibitors, hepatorenal syndrome

Intrinsic Renal AKI

Acute Tubular Necrosis (ATN):

• Ischaemic or nephrotoxic tubular epithelial cell injury
• Pathological features:
  • Loss of brush border
  • Tubular cell apoptosis and necrosis
  • Cast formation obstructing tubular flow
  • Backleak of glomerular filtrate across damaged epithelium

Novel Tubular Injury Biomarkers [16,17]:

• NGAL (Neutrophil Gelatinase-Associated Lipocalin): Rises within 2-4 hours of tubular injury (before creatinine)
• KIM-1 (Kidney Injury Molecule-1): Expressed by proximal tubule cells post-injury
• IL-18: Pro-inflammatory cytokine associated with ischaemic ATN
• Clinical utility: Early detection of AKI before creatinine rise; potential to distinguish ATN from pre-renal azotaemia

Glomerular Disease:

• Post-infectious glomerulonephritis, IgA nephropathy, lupus nephritis, ANCA-associated vasculitis
• Mechanism: Immune-mediated glomerular inflammation → reduced filtration surface area

Interstitial Nephritis:

• Drug-induced (antibiotics, NSAIDs, proton pump inhibitors)
• Mechanism: T-cell mediated hypersensitivity reaction in renal interstitium

Haemolytic Uraemic Syndrome (HUS)

STEC-HUS Pathophysiology [18,19]:

1. Shiga Toxin Production: E. coli O157:H7 or other STEC serotypes produce Shiga toxin (Stx)
2. Toxin Binding: Stx binds to globotriaosylceramide (Gb3) receptors on renal glomerular endothelial cells, podocytes, and tubular epithelium
3. Endothelial Injury: Toxin inhibits protein synthesis → endothelial cell apoptosis
4. Thrombotic Microangiopathy:
   • Exposed subendothelial collagen → platelet adhesion and aggregation
   • Formation of platelet-fibrin thrombi in glomerular capillaries
   • Microangiopathic haemolytic anaemia (MAHA) from mechanical RBC fragmentation (schistocytes)
   • Thrombocytopenia from platelet consumption
   • Glomerular ischaemia → acute kidney injury

Atypical HUS (aHUS):

• Complement dysregulation: Mutations in complement regulatory proteins (Factor H, Factor I, MCP, C3)
• Uncontrolled alternative pathway activation → endothelial damage
• Often requires eculizumab (C5 inhibitor) therapy

Clinical Triad:

• Microangiopathic haemolytic anaemia (MAHA)
• Thrombocytopenia (less than 150 × 10⁹/L)
• Acute kidney injury

Post-Renal (Obstructive) AKI

Mechanism:

• Bilateral ureteric obstruction OR unilateral obstruction in solitary kidney
• Increased intratubular pressure → decreased net filtration pressure
• If prolonged: tubular atrophy and interstitial fibrosis

Common Causes:

• Neonates: Posterior urethral valves (PUV), bilateral PUJO, ureteroceles
• Older children: Renal calculi, tumour compression (neuroblastoma, rhabdomyosarcoma)

Age-Specific Vulnerabilities

Neonatal Kidneys:

• Glomerulogenesis complete only by 34-36 weeks gestation
• Low GFR at birth (~20 mL/min/1.73m²); rises to ~60 mL/min/1.73m² by 1 year [5]
• Immature tubular function: Limited ability to concentrate urine or excrete sodium/acid loads
• Increased susceptibility to nephrotoxins (aminoglycosides, NSAIDs)

Fluid Compartments in Children:

• Total body water decreases with age: 75-80% in neonates → 60% in adults
• Higher percentage of extracellular fluid in young children → greater vulnerability to dehydration

---

Clinical Presentation

Diagnostic Criteria

pRIFLE Criteria (Paediatric RIFLE)

Notes:

• Baseline creatinine: Use previous known value; if unavailable, assume eCCl of 100 mL/min/1.73m²
• eCCl calculated using Schwartz formula: eCCl = k × Height (cm) / Serum Creatinine (μmol/L)
  • k = 0.33 (preterm infants), 0.45 (term infants), 0.55 (children and adolescent girls), 0.70 (adolescent boys)

KDIGO Criteria (2012)

Comparison:

• KDIGO more sensitive for early AKI detection (Stage 1 captures smaller creatinine rises)
• pRIFLE uses eCCl (functional measure); KDIGO uses absolute creatinine
• Both validated in paediatric populations; choice depends on institutional practice [1,10,20]

Age-Specific Serum Creatinine Normal Ranges [5]

Clinical Pearl: A creatinine of 80 μmol/L is normal in an adult but represents significant renal impairment in an infant.

Symptoms and Signs

Symptoms:

• Oliguria: Urine output less than 0.5 mL/kg/hr (> 6 months) or less than 1 mL/kg/hr (neonates)
• Anuria: Urine output less than 0.3 mL/kg/hr for 24 hours
• Oedema: Periorbital (most sensitive), peripheral, sacral, scrotal
• Lethargy, irritability
• Nausea, vomiting
• Symptoms of underlying cause:
  • Bloody diarrhoea → suspect HUS
  • Fever, rash → sepsis or drug reaction (interstitial nephritis)
  • Cola-coloured urine → glomerulonephritis

Signs:

• Fluid overload:
  • Hypertension (> 95th percentile for age/height)
  • Tachypnoea, crackles (pulmonary oedema)
  • Raised JVP (older children)
  • Hepatomegaly
  • Gallop rhythm (S3)
• Dehydration (pre-renal):
  • Tachycardia, prolonged CRT > 2 seconds
  • Dry mucous membranes
  • Reduced skin turgor
  • Sunken fontanelle (infants)
• Uraemia:
  • Altered consciousness, seizures (uraemic encephalopathy)
  • Pericardial friction rub (uraemic pericarditis)
  • Uraemic frost (rare; severe uraemia)
• HUS-specific:
  • Pallor (anaemia)
  • Petechiae, bruising (thrombocytopenia)
  • Jaundice (haemolysis)
  • "Neurological signs in 20-30%: seizures, altered consciousness, focal deficits [15]"

Red Flags Requiring Immediate Action

Cause-Specific Presentations

HUS Presentation (Classical STEC-HUS) [15,18]

Prodrome (3-10 days before AKI):

• Bloody diarrhoea (90-95% of cases)
• Abdominal pain, vomiting
• Fever (may be low-grade or absent)

Acute Phase:

• Pallor (onset over 24-48 hours)
• Oliguria or anuria (60-70%)
• Oedema
• Hypertension (60%)
• Petechiae (thrombocytopenia)
• Neurological involvement (20-30%): irritability, seizures, stroke, encephalopathy

Laboratory Triad:

• Anaemia (Hb typically 60-90 g/L)
• Thrombocytopenia (less than 150 × 10⁹/L; often less than 50)
• Elevated creatinine

Neonatal AKI

Common Causes:

• Perinatal asphyxia: Hypoxic-ischaemic tubular injury
• Sepsis: Especially late-onset sepsis with E. coli, Klebsiella
• Congenital anomalies: Bilateral renal agenesis, dysplasia, posterior urethral valves
• Nephrotoxic drugs: Gentamicin, indomethacin, ibuprofen (for PDA closure)

Clinical Features:

• May be non-oliguric initially
• Electrolyte disturbances common (hyperkalaemia, hyponatraemia, hypocalcaemia)
• Anuria → suspect PUV or bilateral obstruction

Cardiac Surgery-Associated AKI [13,14]

Risk Factors:

• Prolonged cardiopulmonary bypass time (> 120 minutes)
• Younger age (less than 6 months)
• Cyanotic heart disease
• Use of inotropes, vasopressors
• Complex procedures (e.g., Norwood, arterial switch)

Mechanism:

• Cardiopulmonary bypass → systemic inflammatory response
• Renal hypoperfusion during surgery
• Haemolysis from bypass circuit
• Nephrotoxic drug exposure (aminoglycosides, vancomycin)

Timing:

• Typically develops within 48-72 hours post-surgery
• Early detection using biomarkers (NGAL) allows preventive strategies

---

Clinical Examination

Focused Examination for AKI Assessment

Vital Signs:

• Blood pressure: Use age- and height-appropriate percentile charts; hypertension common in fluid overload and intrinsic AKI
• Heart rate: Tachycardia in dehydration, sepsis; bradycardia if severe hyperkalaemia
• Respiratory rate: Tachypnoea suggests acidosis or pulmonary oedema
• Temperature: Fever in sepsis, pyelonephritis, drug-induced interstitial nephritis

Fluid Status Assessment:

Daily Weight Monitoring:

• Most sensitive marker of fluid balance
• Weight gain > 5% above baseline indicates fluid overload
• Weight gain > 10% associated with worse outcomes and increased mortality [6]

Abdominal Examination:

• Palpable bladder: Suggests urinary retention or obstruction (posterior urethral valves)
• Flank masses: Bilateral enlarged kidneys in ADPKD, bilateral hydronephrosis
• Hepatomegaly: Fluid overload, congestive heart failure
• Abdominal distension: Ascites in nephrotic syndrome, peritoneal dialysis

Neurological Examination:

• Altered consciousness: Uraemic encephalopathy, hyponatraemia, HUS CNS involvement
• Seizures: HUS, severe electrolyte disturbances, posterior reversible encephalopathy syndrome (PRES)
• Focal deficits: HUS-associated stroke (rare but important complication)

Skin Examination:

• Petechiae, purpura: Thrombocytopenia (HUS, vasculitis)
• Rash: Drug-induced interstitial nephritis, SLE, Henoch-Schönlein purpura
• Pallor: Anaemia (HUS, chronic kidney disease)
• Uraemic frost: Severe uraemia (very rare)

---

Investigations

Blood Tests

Novel Biomarkers [16,17]

Clinical Note: Biomarkers not yet routinely available in most UK centres; research tools with promise for future clinical application.

Urine Tests

Note: FeNa less reliable in neonates (physiologically unable to conserve sodium); use FeUrea instead.

HUS-Specific Investigations [15,18]

Diagnostic Workup:

1. Blood film: Schistocytes confirm MAHA
2. LDH: Elevated (haemolysis)
3. Haptoglobin: Reduced (haemolysis)
4. Direct Coombs test: Negative (distinguishes from autoimmune haemolytic anaemia)
5. Stool culture: E. coli O157:H7 or other STEC (positive in ~80% if sent early)
6. Stool PCR for Shiga toxin: More sensitive than culture

Atypical HUS (if suspected):

• Complement studies: C3, C4, CH50, Factor H, Factor I levels
• ADAMTS13 activity: If TTP considered (very rare in young children)
• Genetic testing: Complement gene mutations (Factor H, MCP, Factor I)

Indications to Suspect aHUS (vs STEC-HUS):

• No diarrhoeal prodrome
• Age less than 6 months or > 10 years
• Family history of HUS
• Recurrent episodes
• Normal stool culture/Shiga toxin testing

Imaging

Renal Ultrasound (First-Line):

• Indications: All children with AKI to exclude obstruction and assess renal structure
• Findings:
  • "Normal kidneys: Pre-renal AKI, early ATN"
  • "Echogenic kidneys: ATN, HUS, acute interstitial nephritis"
  • "Hydronephrosis: Obstruction (PUV, stones, tumour compression)"
  • "Small kidneys (less than 10th percentile for age): Chronic kidney disease or congenital dysplasia"
  • "Absent kidney(s): Renal agenesis, unilateral kidney at risk"

Doppler Ultrasound:

• Assess renal artery and vein patency
• Renal vein thrombosis: Common in dehydrated neonates, nephrotic syndrome

Chest X-Ray:

• Indications: Suspected fluid overload, pulmonary oedema
• Findings: Bilateral perihilar opacification, Kerley B lines, cardiomegaly, pleural effusions

MCUG (Micturating Cystourethrogram):

• Indications: Male neonate with bilateral hydronephrosis (suspect PUV)
• Perform after acute phase resolved

DMSA Scan:

• Indications: Assess differential renal function, detect scarring (post-pyelonephritis)
• Delayed until after AKI recovery

Specialist Tests

Renal Biopsy:

• Reserved for unclear diagnosis after non-invasive workup
• Contraindications: Bleeding diathesis (thrombocytopenia), small kidneys, uncontrolled hypertension, single kidney

---

Classification & Staging

AKI Stages and Clinical Implications

Outcome Associations:

• Stage 1 AKI: 90% renal recovery; less than 5% require RRT
• Stage 2-3 AKI: 60-70% renal recovery; 10-20% require RRT; increased CKD risk [1,9]

---

Management

General Principles

1. Treat underlying cause
2. Optimise fluid balance
3. Correct life-threatening electrolyte abnormalities
4. Avoid nephrotoxins
5. Adjust drug doses for renal function
6. Nutritional support
7. Initiate renal replacement therapy (RRT) if indicated

Fluid Management

Initial Resuscitation (Pre-Renal AKI / Sepsis)

Hypovolaemic Shock:

• Fluid bolus: 10-20 mL/kg 0.9% sodium chloride over 10-20 minutes
• Reassess after each bolus (BP, CRT, HR, UO)
• Repeat up to 40-60 mL/kg total in first hour if ongoing shock
• If persistent shock after 40-60 mL/kg: Consider inotropes, senior escalation

Caution in Cardiac Disease:

• Use smaller boluses (5-10 mL/kg) in congenital heart disease, heart failure

Maintenance Fluids (Euvolaemic / Oliguric AKI)

Holliday-Segar Formula (Normal Maintenance):

• 100 mL/kg/day for first 10 kg
• 50 mL/kg/day for next 10 kg (10-20 kg)
• 20 mL/kg/day for each kg above 20 kg
• Example: 25 kg child = (100×10) + (50×10) + (20×5) = 1000 + 500 + 100 = 1600 mL/day

Oliguric AKI:

• Restrict to insensible losses + urine output:
  • "Insensible losses: 300-400 mL/m²/day (higher if febrile: add 12% per °C > 37°C)"
  • Plus measured urine output
• Sodium restriction: 1-2 mmol/kg/day
• Potassium restriction: Avoid potassium in IV fluids if K⁺ > 4.5 mmol/L

Fluid Overload Management

Fluid Overload Calculation:

• % Fluid Overload = [(Current Weight - Dry Weight) / Dry Weight] × 100

Diuretics in AKI:

• Furosemide:
  • "Initial dose: 1-2 mg/kg IV bolus"
  • "If no response: Double dose (up to 5 mg/kg)"
  • "Continuous infusion: 0.1-0.4 mg/kg/hr"
  • "Evidence: Does not prevent AKI or improve renal recovery; used only for fluid overload management [21]"
• Metolazone: 0.1-0.2 mg/kg PO (synergistic with furosemide in diuretic resistance)

Hyperkalaemia Management [22]

Classification:

Treatment Algorithm (Severe Hyperkalaemia > 6.5 mmol/L):

Step 1: Cardiac Protection (Immediate - within 5 minutes)

• Calcium gluconate 10%: 0.5 mL/kg IV over 5-10 minutes (maximum 20 mL)
  • Stabilises cardiac membrane; no effect on K⁺ level
  • "Onset: 1-3 minutes; duration: 30-60 minutes"
  • Repeat if ECG changes persist
  • "Caution: Give slowly in patients on digoxin (risk of arrhythmia)"

Step 2: Shift K⁺ into Cells (within 15-30 minutes)

Step 3: Remove K⁺ from Body (within 2-4 hours)

Monitoring:

• Continuous ECG monitoring
• Repeat K⁺ every 1-2 hours initially
• Glucose monitoring if insulin given (risk of hypoglycaemia)

Caution: Calcium resonium may cause bowel necrosis (rare); avoid in ileus or post-operative state.

Metabolic Acidosis Management

Indications for Sodium Bicarbonate:

• pH less than 7.20 with HCO₃⁻ less than 15 mmol/L
• Symptomatic acidosis (Kussmaul breathing, cardiovascular instability)

Dosing:

• Calculate bicarbonate deficit: Deficit (mmol) = 0.3 × Weight (kg) × Base Deficit
• Give 1-2 mmol/kg IV over 30-60 minutes (8.4% NaHCO₃ contains 1 mmol/mL)
• Caution: Risk of fluid overload, hypocalcaemia, paradoxical CNS acidosis

Preferred Approach:

• Correct underlying cause (restore perfusion in pre-renal AKI)
• Initiate RRT if severe refractory acidosis

Hypertension Management

Target BP: less than 95th percentile for age, sex, and height

Acute Severe Hypertension (> 99th percentile + symptoms):

Chronic Hypertension in AKI:

• ACE inhibitors / ARBs: Contraindicated in AKI (worsen renal perfusion)
• Prefer calcium channel blockers, beta-blockers

Nephrotoxin Avoidance

High-Risk Drugs to Avoid:

• NSAIDs: Reduce renal perfusion (prostaglandin inhibition)
• ACE inhibitors / ARBs: Reduce GFR (efferent arteriolar dilation)
• Aminoglycosides: Direct tubular toxicity (if essential, monitor levels closely)
• Vancomycin: Dose-adjust for GFR; monitor trough levels
• Contrast media: Avoid unless essential; use lowest dose + IV hydration prophylaxis

Drug Dose Adjustment:

• Adjust renally-cleared drugs (aminoglycosides, vancomycin, gentamicin, aciclovir, low-molecular-weight heparin) for GFR
• Consult pharmacy / BNF for Children

HUS-Specific Management [15,18,19]

General Principles (STEC-HUS):

1. Supportive care: Mainstay of treatment
2. Fluid and electrolyte management: As per AKI protocols
3. Blood transfusion:
   • Transfuse packed RBCs if Hb less than 60-70 g/L or symptomatic anaemia
   • Avoid platelet transfusion unless active bleeding or invasive procedure required (theoretical risk of worsening thrombosis)
4. Dialysis: Required in 50-70% of STEC-HUS cases
5. Avoid antibiotics in early diarrhoeal phase: May increase Shiga toxin release (controversial; observational data suggest harm) [23]
6. Avoid anti-motility agents (loperamide): Prolonged gut exposure to toxin

Eculizumab in STEC-HUS:

• Evidence: Randomised trial showed NO benefit in STEC-HUS [19]
• Recommendation: Do NOT use eculizumab for STEC-HUS

Atypical HUS (aHUS):

• Eculizumab (C5 inhibitor):
  • "Dose: 300-900 mg IV weekly (weight-based dosing)"
  • Vaccinate against Neisseria meningitidis before starting (or cover with prophylactic antibiotics)
  • Dramatically improves outcomes in aHUS; > 80% achieve renal recovery
• Plasma exchange: Historical treatment (before eculizumab era); less effective than eculizumab

Nutritional Support

Protein Intake:

• Maintain adequate protein (1-2 g/kg/day) to prevent catabolism
• Restrict only if severe uraemia and RRT unavailable

Calories:

• Provide adequate calories (80-100 kcal/kg/day in infants; age-appropriate in older children) to prevent protein breakdown

Phosphate Restriction:

• Limit dietary phosphate; use phosphate binders (calcium carbonate, sevelamer) if hyperphosphataemia

Enteral vs Parenteral Nutrition:

• Prefer enteral nutrition (NG/NJ feeding) if gut functional
• Parenteral nutrition if prolonged ileus, severe fluid overload (adjust volumes for fluid restriction)

Renal Replacement Therapy (RRT)

Indications (AEIOU Mnemonic):

• A: Acidosis (severe, refractory; pH less than 7.1)
• E: Electrolyte disturbances (hyperkalaemia > 7 mmol/L refractory to medical management)
• I: Intoxication (dialysable toxins: methanol, ethylene glycol, lithium, salicylates)
• O: Fluid overload (refractory to diuretics; > 10-15% overload with pulmonary oedema)
• U: Uraemia (symptomatic: encephalopathy, pericarditis, bleeding)

Modalities:

Choice in Paediatric AKI:

• PICU patients: CVVH preferred (better tolerated haemodynamically)
• Stable ward patients: IHD or PD
• Neonates: PD often preferred (easier vascular access challenges)

Vascular Access for HD/CVVH:

• Temporary dialysis catheter (internal jugular or femoral vein)
• Size: 7-8 Fr (infants), 10-12 Fr (older children)

Duration:

• Continue RRT until renal function recovers (creatinine falling, urine output improving)
• Median duration: 5-10 days in AKI

Referral to Paediatric Nephrology

Indications for Urgent Referral:

• All Stage 2-3 AKI (pRIFLE Injury/Failure; KDIGO 2-3)
• Suspected intrinsic renal disease (glomerulonephritis, HUS, vasculitis)
• Hyperkalaemia > 6.5 mmol/L
• Severe acidosis (pH less than 7.2)
• Fluid overload > 10%
• Anuria > 12 hours
• Need for RRT

Early Involvement:

• Contact nephrology within 24 hours of AKI diagnosis even if Stage 1 (for advice and follow-up planning)

---

Complications

Acute Complications

Long-Term Complications (Post-AKI) [8,9,24]

Chronic Kidney Disease (CKD):

• Risk: 10-30% of children with severe AKI (Stage 2-3) develop CKD over 10-20 years [8,9]
• HUS-associated CKD: 10-30% have reduced GFR, proteinuria, or hypertension at long-term follow-up [3,4]
• Mechanism: Maladaptive repair → tubulointerstitial fibrosis, glomerulosclerosis

Hypertension:

• Prevalence: 10-20% at 5-10 year follow-up
• Mechanism: Nephron loss → glomerular hyperfiltration, RAAS activation, sodium retention

Proteinuria:

• Marker of ongoing glomerular injury
• Predictor of progressive CKD

Cardiovascular Risk:

• Emerging evidence links childhood AKI to increased cardiovascular morbidity in adulthood (similar to adult AKI data)

Neurodevelopmental Outcomes (HUS):

• 5-10% have long-term neurological sequelae: cognitive impairment, motor deficits, epilepsy [15]

---

Prognosis & Outcomes

Renal Recovery

Overall Outcomes:

• Pre-renal AKI: 95-100% full renal recovery if perfusion restored promptly
• ATN: 70-80% full recovery; 10-20% incomplete recovery with residual CKD
• HUS: 70-80% recover renal function; 10-15% progress to ESKD; 10-15% have residual CKD [3,4]
• Glomerulonephritis: Variable (depends on type); post-infectious GN has excellent prognosis; RPGN poor without treatment

Predictors of Poor Renal Outcome:

• Prolonged oliguria/anuria (> 2 weeks)
• Need for RRT
• Underlying chronic kidney disease
• Recurrent AKI episodes

Mortality

PICU-Associated AKI:

• AKI presence increases mortality 2-5 fold [1,7]
• Stage 3 AKI: 20-30% mortality (largely driven by multiorgan failure, sepsis)
• Isolated AKI (without multiorgan failure): less than 5% mortality

HUS:

• Acute mortality: 3-5% in STEC-HUS (with modern supportive care)
• Deaths due to: CNS complications (stroke, seizures), multiorgan failure, severe colitis

Cardiac Surgery-Associated AKI:

• Mild AKI: Minimal mortality impact
• Severe AKI requiring RRT: 30-50% mortality [13,14]

Follow-Up Protocols

All Children with AKI (≥Stage 2) Require Long-Term Follow-Up:

Schedule:

• 1 month post-discharge
• 3 months
• 6 months
• 12 months
• Annually thereafter until adulthood

Monitoring:

• U&E, creatinine: Assess GFR (eGFR using Schwartz equation)
• Urinalysis: Proteinuria, haematuria
• Blood pressure: Detect hypertension early
• Growth parameters: Height, weight (CKD impairs growth)
• Renal ultrasound: If structural abnormality suspected or progressive CKD

Criteria for Discharge from Follow-Up:

• Normal BP, no proteinuria, normal GFR for ≥2 years
• Counsel about lifelong nephrotoxin avoidance (NSAIDs, dehydration)

---

Special Populations

Neonatal AKI [11,12]

Epidemiology:

• 8-24% of NICU admissions (higher in extremely preterm, perinatal asphyxia)

Common Causes:

• Perinatal asphyxia: Hypoxic-ischaemic injury
• Sepsis: E. coli, Klebsiella, Candida
• Congenital anomalies: Bilateral renal agenesis/dysplasia, PUV, CAKUT
• Nephrotoxic drugs: Gentamicin, indomethacin, ibuprofen (for PDA closure)
• Renal vein thrombosis: Dehydration, polycythaemia, maternal diabetes

Diagnostic Challenges:

• Serum creatinine reflects maternal levels for first 48-72 hours
• Use of urine output more reliable initially
• Novel biomarkers (NGAL, Cystatin C) may improve early detection [16,17]

Management:

• Conservative fluid management (avoid fluid overload)
• Peritoneal dialysis preferred RRT modality (vascular access difficult in neonates)
• Address underlying cause (treat sepsis, relieve obstruction)

Prognosis:

• Asphyxia-associated AKI: 50-70% full recovery
• CAKUT: Depends on severity; bilateral renal dysplasia → ESKD
• Long-term CKD risk higher than older children

Cardiac Surgery-Associated AKI [13,14]

Epidemiology:

• 40-50% develop AKI post-cardiopulmonary bypass
• 5-10% develop severe AKI (Stage 2-3)

Risk Factors:

• Young age (less than 6 months)
• Cyanotic heart disease
• Prolonged bypass time (> 120 minutes)
• Deep hypothermic circulatory arrest
• Complex surgeries (Norwood, arterial switch)
• Use of high-dose inotropes

Pathophysiology:

• Cardiopulmonary bypass → systemic inflammatory response (cytokine release)
• Renal hypoperfusion during surgery
• Haemolysis from bypass circuit
• Nephrotoxic drugs (aminoglycosides, vancomycin, diuretics)

Prevention Strategies:

• Minimise bypass time
• Avoid nephrotoxins: Adjust aminoglycoside dosing; avoid NSAIDs
• NGAL monitoring: Early biomarker rise (2-4 hours post-bypass) predicts AKI; allows early intervention [16]
• Fenoldopam: Investigational (no proven benefit in paediatric RCTs)

Management:

• Restrictive fluid strategy (avoid fluid overload; associated with worse outcomes)
• Early diuretics (furosemide) if oliguria develops
• Early RRT if fluid overload > 10%

Prognosis:

• Most recover renal function within 1-2 weeks
• Persistent AKI → increased PICU length of stay, mortality

Oncology-Associated AKI

Tumour Lysis Syndrome (TLS):

• High-risk malignancies: Burkitt lymphoma, T-cell ALL, stage 3-4 lymphoma
• Mechanism: Massive cell lysis → release of intracellular contents:
  • Hyperuricaemia → uric acid crystal deposition in tubules
  • Hyperphosphataemia → calcium-phosphate crystal deposition
  • Hyperkalaemia → arrhythmia risk

Prevention (High-Risk Patients):

• Aggressive IV hydration: 3 L/m²/day (twice maintenance)
• Rasburicase: 0.2 mg/kg IV (recombinant urate oxidase; converts uric acid → allantoin)
• Allopurinol: 10 mg/kg/day PO (xanthine oxidase inhibitor; prevents uric acid formation) — less effective than rasburicase
• Avoid phosphate in IV fluids
• Monitor U&E, uric acid, phosphate, calcium every 6-8 hours

Management of Established TLS:

• Continue aggressive hydration
• Rasburicase
• RRT if refractory hyperkalaemia, severe hyperphosphataemia, or AKI

Chemotherapy Nephrotoxicity:

• Cisplatin, ifosfamide, methotrexate: Direct tubular toxicity
• Ifosfamide: Fanconi syndrome (proximal tubule dysfunction)
• Prevention: Hydration, mesna (for ifosfamide), leucovorin rescue (for methotrexate)

Post-Bone Marrow Transplant AKI

Causes:

• Sinusoidal obstruction syndrome (SOS): Hepatorenal syndrome-like picture
• Calcineurin inhibitor toxicity: Ciclosporin, tacrolimus
• Infection: Viral (CMV, BK virus), fungal, bacterial sepsis
• Graft-versus-host disease (GVHD)

Management:

• Supportive care
• Adjust calcineurin inhibitor dosing
• Treat infections
• RRT if severe

---

Examination Focus (MRCPCH)

Viva Questions

Question 1: "A 3-year-old presents with bloody diarrhoea for 3 days, now pale and passing little urine. What is your differential diagnosis and initial management?"

Model Answer:

• Differential: Haemolytic uraemic syndrome (HUS) is most likely given bloody diarrhoea prodrome and triad of pallor (anaemia), oliguria (AKI), and likely thrombocytopenia. Differentials include severe gastroenteritis with pre-renal AKI, sepsis, or intussusception.
• Immediate investigations: FBC (Hb, platelets), blood film (schistocytes), U&E (creatinine, K⁺), LDH, haptoglobin, blood gas (acidosis), stool culture for STEC.
• Initial management:
  • "Fluid status assessment: Examine for dehydration vs fluid overload; daily weights"
  • "Cautious fluid resuscitation: 10 mL/kg bolus if dehydrated; avoid over-resuscitation (risk of fluid overload in oliguric AKI)"
  • "Electrolyte management: Urgent K⁺ check; treat hyperkalaemia if > 6.5 mmol/L (calcium gluconate, salbutamol, insulin-dextrose)"
  • Avoid antibiotics in early diarrhoeal phase (may worsen Shiga toxin release)
  • Transfuse RBCs if Hb less than 60-70 g/L or symptomatic; avoid platelets unless active bleeding
  • "Urgent paediatric nephrology referral: High likelihood of needing dialysis (50-70% of HUS cases)"

---

Question 2: "What are the pRIFLE criteria for AKI in children?"

Model Answer: pRIFLE defines AKI stages based on reduction in estimated creatinine clearance (eCCl) OR urine output:

• Risk: eCCl decreased by 25% OR urine output less than 0.5 mL/kg/hr for 8 hours
• Injury: eCCl decreased by 50% OR urine output less than 0.5 mL/kg/hr for 16 hours
• Failure: eCCl decreased by 75% OR eCCl less than 35 mL/min/1.73m² OR urine output less than 0.3 mL/kg/hr for 24 hours OR anuria for 12 hours
• Loss: Persistent failure > 4 weeks
• ESKD: Persistent failure > 3 months

eCCl calculated using Schwartz formula: k × Height (cm) / Creatinine (μmol/L), where k varies by age/sex.

---

Question 3: "How would you manage severe hyperkalaemia (K⁺ 7.2 mmol/L) with ECG changes in a child with AKI?"

Model Answer:

• Immediate cardiac protection: IV calcium gluconate 10% 0.5 mL/kg over 5-10 minutes (stabilises cardiac membrane; repeat if ECG changes persist)
• Shift K⁺ into cells:
  • Nebulised salbutamol 2.5-5 mg (depending on weight)
  • IV insulin 0.05-0.1 unit/kg + 25% dextrose 2 mL/kg over 30-60 minutes (monitor glucose)
  • Sodium bicarbonate 1-2 mmol/kg IV if acidotic
• Remove K⁺ from body:
  • Calcium resonium 1 g/kg PO or PR
  • Prepare for renal replacement therapy (definitive treatment)
• Monitoring: Continuous ECG, repeat K⁺ every 1-2 hours, glucose monitoring
• Treat underlying cause: Optimise renal perfusion, avoid further K⁺ intake

---

Question 4: "What are the indications for dialysis in paediatric AKI?"

Model Answer: Use AEIOU mnemonic:

• A: Acidosis — severe, refractory (pH less than 7.1 despite medical management)
• E: Electrolyte disturbances — hyperkalaemia > 7 mmol/L refractory to medical therapy
• I: Intoxication — dialysable poisons (methanol, ethylene glycol, lithium, salicylates)
• O: Fluid overload — refractory to diuretics, > 10-15% overload with pulmonary oedema
• U: Uraemia — symptomatic (encephalopathy, pericarditis, seizures, bleeding)

Additional indication: Severe hyperphosphataemia or hypocalcaemia (tumour lysis syndrome)

---

Clinical Scenario (OSCE Station)

Scenario: "You are the paediatric SHO called to see a 6-year-old boy admitted with gastroenteritis. He has passed 50 mL urine in the last 12 hours. His weight on admission was 20 kg; today it is 21.5 kg. BP 130/90 mmHg (> 99th percentile). U&E: Na 135, K 6.2, Urea 18, Creatinine 180 μmol/L (baseline 40 μmol/L). Discuss your assessment and management."

Model Answer:

Assessment:

• Diagnosis: Acute kidney injury (Stage 3 by KDIGO: creatinine > 3× baseline)
• Oliguria: 50 mL/12 hr = ~0.2 mL/kg/hr (severe oliguria)
• Fluid overload: Weight gain 1.5 kg = 7.5% fluid overload
• Hypertension: Likely secondary to fluid overload
• Hyperkalaemia: K⁺ 6.2 mmol/L (moderate; approaching severe)

Immediate Actions:

1. ECG: Assess for hyperkalaemia changes (peaked T waves)
2. Hyperkalaemia management:
   • If ECG changes: IV calcium gluconate 10% (10 mL = 0.5 mL/kg)
   • Nebulised salbutamol 2.5 mg
   • Consider insulin-dextrose if K⁺ rising or > 6.5 mmol/L
3. Fluid restriction: Stop IV fluids; restrict to insensible losses + urine output (~600 mL/day for 20 kg child)
4. Hypertension management: IV furosemide 1-2 mg/kg (attempt to offload fluid); if refractory, consider labetalol or nifedipine
5. Urgent paediatric nephrology referral: High risk of needing dialysis given severe AKI, fluid overload, hyperkalaemia

Further Investigations:

• Repeat U&E, K⁺ in 2-4 hours
• Blood gas (assess acidosis)
• Urine dipstick, microscopy (blood/protein suggests glomerulonephritis)
• Renal ultrasound (exclude obstruction)
• If post-infectious GN suspected: ASO titre, C3/C4

Ongoing Management:

• Daily weights (monitor fluid balance)
• Strict fluid balance chart
• Avoid nephrotoxins (NSAIDs, ACE inhibitors)
• Nutritional support (adequate calories, protein 1-2 g/kg/day)
• Consider dialysis if fluid overload worsens, hyperkalaemia refractory, or develops severe acidosis

---

Data Interpretation (Written Exam Question)

Question: A 4-year-old child (weight 16 kg) in PICU has the following results:

• Na 138 mmol/L, K 5.8 mmol/L, Urea 22 mmol/L, Creatinine 150 μmol/L (baseline 35 μmol/L)
• pH 7.22, HCO₃⁻ 12 mmol/L, PaCO₂ 4.2 kPa
• Urine output: 80 mL in last 12 hours
• Weight today: 17.2 kg (admission weight 16 kg)

Questions:

1. What stage of AKI is this?
2. Calculate the fluid overload percentage.
3. What are the three most urgent management priorities?

Answers:

1. Stage 3 AKI (KDIGO): Creatinine > 3× baseline (150/35 = 4.3×); urine output 0.4 mL/kg/hr for 12 hours (less than 0.5 mL/kg/hr threshold)
2. Fluid overload: (17.2 - 16) / 16 × 100 = 7.5%
3. Urgent management priorities:
   • Hyperkalaemia: K⁺ 5.8 mmol/L approaching severe; check ECG; prepare salbutamol, calcium gluconate
   • Metabolic acidosis: pH 7.22, HCO₃⁻ 12 mmol/L; give IV sodium bicarbonate 1-2 mmol/kg or prepare for RRT
   • Fluid overload: 7.5% overload with oliguria; strict fluid restriction, IV furosemide; if no response, prepare for RRT

---

Patient & Family Information

What is Acute Kidney Injury?

For Parents: Acute kidney injury (AKI) means your child's kidneys have suddenly stopped working as well as they should. The kidneys normally filter waste and extra water from the blood to make urine. When the kidneys aren't working properly, waste builds up in the body and your child may make less urine than usual.

Causes: AKI can happen for many reasons:

• Dehydration from vomiting and diarrhoea (most common)
• Infections (sepsis)
• A condition called HUS (haemolytic uraemic syndrome), which can happen after bloody diarrhoea
• Blockage in the urinary tract
• Medicines that can harm the kidneys

Symptoms

Your child may have:

• Less wee than usual (or no wee at all)
• Swelling in the face, hands, or feet
• Feeling very tired and unwell
• Nausea or vomiting
• High blood pressure

Treatment in Hospital

What we will do:

1. Find the cause: Blood tests, urine tests, and an ultrasound scan of the kidneys
2. Give fluids carefully: Through a drip in the vein (if dehydrated) OR restrict fluids (if too much fluid in the body)
3. Correct salt levels: The kidneys control salts like potassium; we may give medicines to keep these safe
4. Monitor closely: Daily weight, urine output, blood pressure
5. Dialysis (if needed): A machine that does the kidney's job temporarily

Dialysis:

• Used if the kidneys can't remove waste or extra fluid on their own
• Types:
  • "Haemodialysis: Blood goes through a filter machine (a tube goes into a vein)"
  • "Peritoneal dialysis: Fluid goes into the tummy through a small tube; the tummy lining filters the blood"
• Most children only need dialysis for a few days to weeks while the kidneys recover

What Happens Next?

Recovery:

• Most children recover fully within a few weeks
• Some children (especially those with HUS) may have long-term kidney problems

Follow-Up:

• Your child will need regular check-ups for months or years after AKI
• We will check:
  • Blood pressure
  • Urine tests (for protein)
  • Blood tests (kidney function)
• This helps us make sure the kidneys have recovered completely

At Home

Things to avoid:

• NSAIDs (ibuprofen, diclofenac): These can harm the kidneys. Use paracetamol instead for pain/fever.
• Dehydration: Make sure your child drinks enough fluids, especially if unwell
• Certain medicines: Always tell doctors/pharmacists about your child's kidney history before starting new medicines

Questions to Ask Your Doctor

• What caused my child's AKI?
• Will the kidneys recover fully?
• How long will my child need to stay in hospital?
• Will my child need dialysis?
• How often will we need follow-up appointments?

Resources

• Kidney Care UK: www.kidneycareuk.org — Information and support for families
• NHS: www.nhs.uk — Search "acute kidney injury in children"
• Great Ormond Street Hospital: Patient information leaflets on AKI, dialysis, HUS

---

Evidence & Guidelines

Key Guidelines

1. KDIGO Clinical Practice Guideline for Acute Kidney Injury (2012)

   • Kidney Disease: Improving Global Outcomes (KDIGO) Work Group. Kidney Int Suppl. 2012;2(1):1-138.
   • Defines KDIGO AKI criteria (applicable to children and adults); evidence-based recommendations for prevention, diagnosis, and management

2. NICE Guideline NG148: Acute Kidney Injury — Prevention, Detection and Management (2019)

   • National Institute for Health and Care Excellence (NICE). Available: nice.org.uk/guidance/ng148
   • UK-focused guideline; includes paediatric considerations; emphasises early detection and nephrotoxin avoidance

3. Kidney Disease: Improving Global Outcomes (KDIGO) — AKI in Children (Consensus Statement, 2024)

   • Addresses paediatric-specific aspects: age-adjusted creatinine, neonatal AKI, long-term follow-up

Key Evidence

pRIFLE and KDIGO Criteria Validation:

• pRIFLE criteria validated in multiple paediatric cohorts; predicts mortality and need for RRT [1,10,20]
• KDIGO more sensitive for early AKI detection than pRIFLE [20]

Epidemiology:

• PICU AKI incidence: 10-25% depending on definition; associated with 2-5 fold increased mortality [1,7]
• Cardiac surgery-associated AKI: 40-50% incidence; severe AKI in 5-10% [13,14]

HUS Pathophysiology and Management:

• STEC-HUS: Shiga toxin binds Gb3 receptors → endothelial injury → thrombotic microangiopathy [18]
• Eculizumab NOT beneficial in STEC-HUS (RCT evidence) [19]; supportive care is mainstay
• Atypical HUS: Eculizumab dramatically improves outcomes in complement-mediated aHUS

Novel Biomarkers:

• NGAL rises 2-4 hours post-tubular injury; predicts AKI before creatinine rise [16,17]
• Potential for early intervention strategies (e.g., post-cardiac surgery)

Fluid Overload and Outcomes:

• Fluid overload > 10% at dialysis initiation associated with increased mortality [6]
• Restrictive fluid strategies post-cardiac surgery may reduce AKI severity

Long-Term Outcomes:

• Children with severe AKI have 3-4 fold increased risk of CKD, hypertension, proteinuria over 10-20 years [8,9,24]
• Highlights need for lifelong follow-up

---

References

1. 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;8(10):1661-1669. doi:10.2215/CJN.00270113

2. Naeem M, Alarishi S, Othman F, et al. Acute Kidney Injury in Critically Ill Children: Prevalence, Progression, Recovery Mortality, and Impact of Severity. J Clin Med. 2025;14(2):548. PMID: 39941556

3. Alconcher LF, Lucarelli LI, Bronfen S, et al. Dynamic evolution of kidney function in patients with STEC-hemolytic uremic syndrome followed for more than 15 years: unexpected changes. Pediatr Nephrol. 2024;39(9):2827-2835. PMID: 38602519

4. Gülhan B, Özaltın F, Fidan K. Management of pediatric hemolytic uremic syndrome. Turk J Pediatr. 2024;66(1):1-19. PMID: 38523374

5. Schwartz GJ, Muñoz A, Schneider MF, et al. New equations to estimate GFR in children with CKD. J Am Soc Nephrol. 2009;20(3):629-637. doi:10.1681/ASN.2008030287

6. Goldstein SL, Currier H, Graf JM, et al. Outcome in children receiving continuous venovenous hemofiltration. Pediatrics. 2001;107(6):1309-1312. doi:10.1542/peds.107.6.1309

7. Kaddourah A, Basu RK, Bagshaw SM, Goldstein SL; AWARE Investigators. Epidemiology of Acute Kidney Injury in Critically Ill Children and Young Adults. N Engl J Med. 2017;376(1):11-20. doi:10.1056/NEJMoa1611391

8. Ulrich EH, Yordanova M, Morgan C, et al. Kidney and blood pressure outcomes 11 years after pediatric critical illness and longitudinal impact of AKI: a prospective cohort study. Pediatr Nephrol. 2024;39(5):1627-1638. PMID: 39585355

9. Mammen C, Al Abbas A, Skippen P, 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;59(4):523-530. doi:10.1053/j.ajkd.2011.10.048

10. Akcan-Arikan A, Zappitelli M, Loftis LL, et al. Modified RIFLE criteria in critically ill children with acute kidney injury. Kidney Int. 2007;71(10):1028-1035. doi:10.1038/sj.ki.5002231

11. Jetton JG, Boohaker LJ, Sethi SK, et al. Incidence and outcomes of neonatal acute kidney injury (AWAKEN): a multicentre, multinational, observational cohort study. Lancet Child Adolesc Health. 2017;1(3):184-194. doi:10.1016/S2352-4642(17)30069-X

12. Askenazi DJ, Ambalavanan N, Goldstein SL. Acute kidney injury in critically ill newborns: what do we know? What do we need to learn? Pediatr Nephrol. 2009;24(2):265-274. doi:10.1007/s00467-008-1060-2

13. Li S, Krawczeski CD, Zappitelli M, et al. Incidence, risk factors, and outcomes of acute kidney injury after pediatric cardiac surgery: a prospective multicenter study. Crit Care Med. 2011;39(6):1493-1499. doi:10.1097/CCM.0b013e31821201d3

14. Blinder JJ, Goldstein SL, Lee VV, et al. Congenital heart surgery in infants: effects of acute kidney injury on outcomes. J Thorac Cardiovasc Surg. 2012;143(2):368-374. doi:10.1016/j.jtcvs.2011.06.021

15. Gülhan B, Özaltın F. Hemolytic Uremic Syndrome in Children. Turk Arch Pediatr. 2022;57(1):1-13. doi:10.5152/TurkArchPediatr.2021.21214. PMID: 35110108

16. Devarajan P. Neutrophil gelatinase-associated lipocalin (NGAL): a new marker of kidney disease. Scand J Clin Lab Invest Suppl. 2008;241:89-94. doi:10.1080/00365510802150158

17. Parikh CR, Devarajan P. New biomarkers of acute kidney injury. Crit Care Med. 2008;36(4 Suppl):S159-S165. doi:10.1097/CCM.0b013e318168c652

18. Mayer CL, Leibowitz CS, Kurosawa S, Stearns-Kurosawa DJ. Shiga toxins and renal disease. Toxins (Basel). 2012;4(11):1228-1254. doi:10.3390/toxins4111228

19. Garnier A, Brochard K, Kwon T, et al. Efficacy and Safety of Eculizumab in Pediatric Patients Affected by Shiga Toxin-Related Hemolytic and Uremic Syndrome: A Randomized, Placebo-Controlled Trial. J Am Soc Nephrol. 2023;34(9):1608-1621. doi:10.1681/ASN.0000000000000178. PMID: 37303085

20. Zappitelli M, Parikh CR, Akcan-Arikan A, et al. Ascertainment and epidemiology of acute kidney injury varies with definition interpretation. Clin J Am Soc Nephrol. 2008;3(4):948-954. doi:10.2215/CJN.05431207

21. Bagshaw SM, Delaney A, Haase M, et al. Loop diuretics in the management of acute renal failure: a systematic review and meta-analysis. Crit Care Resusc. 2007;9(1):60-68. PMID: 17352670

22. Weisberg LS. Management of severe hyperkalemia. Crit Care Med. 2008;36(12):3246-3251. doi:10.1097/CCM.0b013e31818f222b

23. Wong CS, Jelacic S, Habeeb RL, et al. The risk of the hemolytic-uremic syndrome after antibiotic treatment of Escherichia coli O157:H7 infections. N Engl J Med. 2000;342(26):1930-1936. doi:10.1056/NEJM200006293422601

24. Askenazi DJ, Feig DI, Graham NM, et al. 3-5 year longitudinal follow-up of pediatric patients after acute renal failure. Kidney Int. 2006;69(1):184-189. doi:10.1038/sj.ki.5000032

---

Summary Card (Quick Reference)

Acute Kidney Injury in Children — MRCPCH Essentials

Definition: Rise in creatinine OR reduced urine output (pRIFLE / KDIGO criteria)

Key Causes:

• Pre-renal: Dehydration, sepsis
• Intrinsic: HUS (most common for dialysis), ATN, GN
• Post-renal: PUV (neonates), stones

Red Flags:

• Anuria, K⁺ > 6.5 mmol/L, fluid overload > 10%, pH less than 7.1, altered consciousness

Investigations:

• U&E (creatinine vs age norms), K⁺, blood gas, FBC, blood film (schistocytes in HUS)
• Urine: dipstick, microscopy, FeNa
• Renal ultrasound (exclude obstruction)

Management:

• Pre-renal: Fluid boluses 10-20 mL/kg
• Oliguric AKI: Restrict fluids (insensible + UO), daily weights
• Hyperkalaemia: Calcium gluconate, salbutamol, insulin-dextrose, calcium resonium, RRT
• Dialysis indications (AEIOU): Acidosis, Electrolytes, Intoxication, Overload, Uraemia

HUS: Supportive care, RBC transfusion (not platelets), dialysis (50-70%), NO eculizumab for STEC-HUS

Prognosis:

• Pre-renal: 95% full recovery
• HUS: 70-80% recovery; 10-30% CKD risk
• All AKI: Lifelong follow-up (BP, proteinuria, GFR)

Long-Term Risks: CKD, hypertension, proteinuria (especially Stage 2-3 AKI)

---