Define Acute Kidney Injury. Describe its classification, clinical features, investigations and management.

Definition

• Acute kidney injury (AKI) is an abrupt (hours to days) decline in kidney function, causing retention of nitrogenous wastes and dysregulation of fluid, electrolyte and acid-base balance.
• It is defined by a rise in serum creatinine and/or a fall in urine output (KDIGO / pRIFLE criteria).

Classification BY Cause

Clinical Features

• Oliguria or anuria (urine output < 0.5–1 mL/kg/hour), though AKI can be non-oliguric.
• Features of the underlying cause (dehydration, sepsis, bloody diarrhoea → HUS, poor stream → obstruction).
• Features of complications — fluid overload (oedema, hypertension, pulmonary oedema), and uraemia (lethargy, vomiting).

Investigations

• Blood — rising urea & creatinine; electrolytes (hyperkalaemia, acidosis), calcium/phosphate.
• Urinalysis — casts (ATN/GN), blood/protein; fractional excretion of sodium (low in pre-renal, high in intrinsic).
• Ultrasound — kidney size and to exclude obstruction (hydronephrosis).
• Cause-specific tests (blood film & platelets for HUS, complement, cultures).

Management — General

• Treat the cause — restore circulation in pre-renal AKI (a fluid challenge if hypovolaemic), treat sepsis, relieve obstruction.
• Fluid balance — careful input/output; in established AKI restrict fluids to insensible losses + urine output.
• Stop/avoid nephrotoxic drugs and adjust drug doses; ensure adequate nutrition.

Management — Complications

• Hyperkalaemia — calcium gluconate (cardioprotection), insulin-dextrose, salbutamol, sodium bicarbonate, and potassium-binding resins.
• Metabolic acidosis — sodium bicarbonate if severe.
• Fluid overload/hypertension — fluid restriction and diuretics.

Indications for Dialysis (mnemonic — Aeiou)

• Acidosis (severe, refractory); Electrolytes (refractory hyperkalaemia).
• Intoxication (dialysable toxins); Overload (refractory fluid overload/pulmonary oedema).
• Uraemia (encephalopathy, pericarditis, severe symptoms).

Pathophysiology & Phases

Sustained hypoperfusion in pre-renal AKI progresses to acute tubular necrosis (ATN). Established ATN classically evolves through three phases:

• Oliguric phase — reduced urine output with rising wastes and the risk of fluid/electrolyte complications.
• Diuretic phase — recovering tubules produce large urine volumes (watch for dehydration and electrolyte loss).
• Recovery phase — gradual return of function.

Monitoring

• Strict input–output charting, daily weight, and serial electrolytes, creatinine and acid-base status.
• ECG monitoring in hyperkalaemia; blood pressure and fluid-status assessment.

Prognosis

• Pre-renal and post-renal AKI recover well if the cause is corrected early.
• Intrinsic AKI (ATN, HUS) may take longer, and severe or prolonged injury can leave residual chronic kidney disease — so follow-up of kidney function is important.

Staging (kdigo — BY Creatinine / Urine Output)

Supportive Care & Nutrition

• Provide adequate calories (limit catabolism); moderate protein, potassium and phosphate as needed.
• Treat infection; review and adjust all renally-excreted drugs.

Prevention

Most childhood AKI is preventable — early, adequate rehydration in diarrhoeal illness, prompt treatment of sepsis, cautious use of nephrotoxic drugs, and timely relief of obstruction.

WHY Hyperkalaemia Is What Kills

• The most urgent priority in a child with acute kidney injury is understanding why hyperkalaemia — not the urea, not the creatinine — is what will kill them in the next hour.
• A rising creatinine is alarming but not immediately dangerous.
• A rising potassium is lethal, because potassium sets the resting membrane potential of the cardiac myocyte: as it rises, the membrane depolarises, conduction slows, and the heart becomes progressively unexcitable — ending in ventricular fibrillation or asystole, often with very little warning.
• And the ECG changes matter far more than the number: tall, tented T waves → a flattened then absent P wave with a lengthening PR → a widening QRS → the sinusoidal pattern → arrest.
• Hence: every child with AKI needs an immediate potassium and an ECG, and any ECG change is an emergency.
• And the treatment follows a strict logic: (1) protect the heart with intravenous calcium (which acts within minutes but does not lower the potassium); (2) shift the potassium into cells with insulin-and-dextrose and nebulised salbutamol (temporary); and (3) remove it — with a resin, or definitively by dialysis.