Synopsis
Identify life-threatening electrolyte, acid–base, fluid and uraemic complications of acute kidney injury, begin immediate medical treatment, and obtain renal replacement therapy before physiology becomes irreversible.
- Dialysis in AKI is triggered by dangerous physiology and the whole clinical trajectory, not by a single creatinine, urea, potassium value or AKI stage in isolation.
- NICE indications for immediate renal replacement referral, when not responding to medical management, are hyperkalaemia, metabolic acidosis, uraemic symptoms or complications, fluid overload and pulmonary oedema.
- Severe hyperkalaemia or characteristic ECG change is an arrest risk: protect the myocardium, shift potassium into cells, remove potassium from the body and call renal or critical care concurrently.
- Pulmonary oedema in oliguric AKI may deteriorate despite diuretics; provide oxygen or ventilatory support as needed and seek extracorporeal fluid removal when congestion is refractory.
- A low pH alone does not define the dialysis decision. Treat shock, sepsis, ketoacidosis, toxin or respiratory failure while assessing whether acid generation exceeds safe medical correction.
- Uraemic encephalopathy and uraemic pericarditis are clinical diagnoses that should not wait for a predetermined urea threshold; exclude other causes without delaying renal discussion.
- Intermittent haemodialysis can correct potassium or some toxins rapidly, whereas continuous therapy may be better tolerated in haemodynamic instability; the specialist team selects modality and prescription.
- Temporary kidney support is common in severe AKI and does not itself establish end-stage kidney disease; continue cause-directed care and reassess native urine output and solute control.
Key red flags
Potassium at or above 6.5 mmol/L is severe under UKKA guidance, and any compatible ECG toxicity increases urgency. Peaked T waves, PR prolongation, P-wave loss, QRS widening, sine-wave change, bradyarrhythmia or ventricular arrhythmia can evolve rapidly.
Increasing oxygen need, diffuse crackles, radiographic oedema, severe hypertension or exhausting respiratory effort with oliguria suggests fluid cannot be excreted. Failure to improve with appropriate medical and ventilatory therapy is a dialysis indication.
Deep breathing, hypotension, reduced cardiac performance and a falling bicarbonate or pH indicate impaired buffering. Interpret the renal component alongside lactate, ketones, chloride, carbon dioxide and the reversibility of the precipitating process.
New inattention, drowsiness, agitation, asterixis, seizures or coma in advanced AKI may reflect uraemic neurotoxicity. Check glucose, oxygenation, infection, medicines and structural neurology promptly, but do not await a numerical urea cut-off before referral.
Pleuritic or positional central pain, a rub, effusion or unexplained haemodynamic compromise can occur with severe uraemia. Obtain ECG and echocardiography as appropriate and involve renal and cardiology teams urgently because drainage and anticoagulation decisions are specialised.
Some severe poisonings gain clinically important clearance from extracorporeal treatment. Contact the National Poisons Information Service through TOXBASE and renal or critical care early; toxin-specific thresholds and modality lie outside a generic AKI rule.
Investigation priorities
Confirm the electrolyte threat and detect cardiac membrane toxicity requiring immediate calcium.
Management branches
Severe hyperkalaemia, respiratory failure, profound acidaemia, pericardial compromise or altered consciousness is present.
- 1. Use ABCDE, call senior renal and critical-care help, obtain continuous monitoring and place reliable intravenous access while sending urgent bloods and gas.
- 2. Deliver complication-specific immediate care: cardiac calcium for hyperkalaemic ECG toxicity, protocol insulin–glucose, oxygen or non-invasive ventilation, and treatment of shock or sepsis.
- 3. State explicitly whether the problem is refractory, recurrent or predicted to recur because of anuria, ongoing cell breakdown, fluid accumulation or toxin burden.
- 4. Prepare transfer, dialysis access and consent or best-interests decisions without allowing these processes to interrupt resuscitation.