Paediatric Acute Kidney Injury (AKI) 

Lesson Objectives

By the end of this lesson, learners should be able to:

1. Define acute kidney injury and describe its diagnostic criteria in children.

2. Identify pre-renal, renal, and post-renal causes of AKI.

3. Recognize the clinical signs and symptoms of AKI.

4. Interpret laboratory and imaging investigations for diagnosis and monitoring.

5. Understand supportive management, pharmacologic interventions, and indications for renal replacement therapy.

6. Identify complications such as hyperkalaemia, metabolic acidosis, and fluid overload.

Description

Acute Kidney Injury (AKI) is a potentially reversible deterioration in kidney function that prevents the maintenance of normal physiological homeostasis. It is characterized by elevated blood urea and serum creatinine, often accompanied by hyperkalaemia, metabolic acidosis, and hypertension. Oliguria (<0.5 mL/kg/hour in children or <1 mL/kg/hour in neonates) may be present, though some forms (e.g., aminoglycoside toxicity) may present with polyuria.

Causes of AKI:

Clinical Features

• Fluid overload: hypertension, oedema

• Heart failure: hepatomegaly, gallop rhythm, pulmonary oedema

• Intravascular depletion: tachycardia, hypotension, dry mucous membranes, poor skin turgor, altered sensorium

• Oliguria or anuria

• Rash or arthritis (SLE, HSP)

• Flank masses (renal vein thrombosis, tumors, urinary tract obstruction)

Investigations

Treatment

Supportive Care

• Urinary catheterization for monitoring or in suspected obstruction

• Fluid management:

  • Hypovolaemia → isotonic saline 20 mL/kg over 30 min

  • Normovolaemic → replace insensible losses + urine output + extra-renal losses

• Daily monitoring: urine/stool output, body weight, electrolytes

• Renal dosing of medications (use Schwartz formula for eGFR)

• Nutritional support with dietician input

Renal Replacement Therapy (Dialysis)

Indications for peritoneal dialysis or haemodialysis:

• Fluid overload / hypertension

• Severe acidosis unresponsive to medical therapy

• Persistent hyperkalaemia

• Symptomatic uraemia or urea > 35.7–53.6 mmol/L

• Dialyzable toxins

• Anuria

Pharmacologic Management of Hyperkalaemia

• Stop exogenous potassium

• Kayexalate (sodium polystyrene sulfonate) 1 g/kg

• If K⁺ > 7 mmol/L with ECG changes:

  • Nebulised salbutamol or IV salbutamol

  • IV calcium gluconate 0.5 mL/kg

  • IV sodium bicarbonate 1–2 mmol/kg

  • Insulin 0.1 U/kg + 50% glucose 1 mL/kg over 1 hr

  • Furosemide 1 mg/kg BD

Note: These are temporary measures; urgent nephrology consultation is essential for dialysis.

Other Electrolyte/Metabolic Corrections

• Hypocalcaemia: oral calcium carbonate 45–65 mg/kg/day or IV calcium gluconate if symptomatic

• Hyponatraemia: correct cautiously if <120 mmol/L or symptomatic using 3% hypertonic saline

• Severe metabolic acidosis (pH ≤7.15, HCO₃⁻ <8 mmol/L) → partial correction with IV sodium bicarbonate; dialysis preferred

• Hypertension and anaemia managed per standard protocols

Complications

• Hyperkalaemia (>6 mmol/L) → life-threatening arrhythmias

• Pulmonary oedema / fluid overload

• Severe metabolic acidosis

• Uraemia and electrolyte imbalances

Key Summary

• AKI = rapid deterioration in renal function → impaired homeostasis

• Causes: pre-renal (hypoperfusion), renal (parenchymal), post-renal (obstruction)

• Presenting features: oliguria/anuria, oedema, hypertension, heart failure, electrolyte disturbances

• Investigations: urinalysis, blood chemistry, imaging, renal biopsy if unclear

• Management: supportive care, correct fluids/electrolytes, renal replacement therapy when indicated

• Hyperkalaemia and severe acidosis require urgent attention

• Early nephrology involvement is critical