AKI complications and indications for urgent dialysis

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

As filtration and tubular regulation fail, potassium, acid, water and uraemic solutes accumulate. The resulting arrhythmia, respiratory failure, pericardial inflammation or cerebral dysfunction can kill before the creatinine reaches an impressive number. The bedside approach is therefore syndromic: find the complication, begin its immediate temporising treatment, determine whether it is responding, and organise definitive removal of solute or fluid. The same patient may have several indications, such as hyperkalaemia with pulmonary oedema and worsening acidaemia.

Renal replacement therapy is supportive rather than curative. It buys time while perfusion is restored, infection controlled, obstruction drained or an intrinsic renal process treated. Choice between intermittent haemodialysis, prolonged intermittent treatment and continuous techniques depends on urgency, haemodynamic stability, cerebral considerations, access, staffing and local capability. A technically available dialysis machine does not replace critical-care assessment, reliable vascular access or a prescription tailored to potassium, sodium, fluid and drug clearance.

Medical treatment and dialysis referral proceed together. A patient with toxic hyperkalaemic ECG changes still needs intravenous calcium even if the dialysis team is approaching, because calcium acts on cardiac excitability rather than potassium removal. Conversely, transient biochemical improvement after insulin can rebound as potassium shifts back out of cells, so serial measurement and definitive removal remain essential. Activate the current hospital hyperkalaemia, pulmonary-oedema, critical-care and renal-transfer protocols at presentation.

Key points

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.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Solute and acid retention

Abrupt loss of filtration and tubular secretion allows potassium, hydrogen ions and uraemic solutes to accumulate, particularly when catabolism or tissue breakdown increases their production.

Salt and water retention

Oliguria limits sodium and water excretion, so resuscitation fluids, transfusions and ongoing intake can rapidly convert kidney failure into pulmonary or systemic congestion.

Persistent high-risk insult

Shock, sepsis, major tissue injury and selected poisonings can generate acids, potassium or dialysable toxins faster than compromised kidneys and medical measures can safely clear them.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Potassium accumulation
Reduced excretion, acidosis and cellular release increase extracellular potassium, destabilising cardiac conduction and potentially causing rapidly evolving arrhythmia.
2
Acid-base failure
Impaired net acid excretion combines with ongoing lactate, ketoacid or other acid generation, depressing myocardial function and worsening vasodilatation when severe.
3
Pulmonary congestion
Positive sodium and water balance raises venous and pulmonary capillary pressures, causing interstitial then alveolar oedema and impaired gas exchange.
4
Uraemic organ dysfunction
Retained uraemic solutes can cause encephalopathy or pericarditis; these are clinical syndromes and no single urea concentration defines them.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Electrically dangerous hyperkalaemiaRed flag

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.

Refractory pulmonary oedemaRed flag

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.

Clinically important acidaemiaRed flag

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.

Uraemic encephalopathyRed flag

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.

Uraemic pericardial diseaseRed flag

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.

Dialysable poisoningRed flag

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.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Urgent potassium with 12-lead ECGFirst step
Why
Confirm the electrolyte threat and detect cardiac membrane toxicity requiring immediate calcium.
Interpretation and limitations
UKKA advises urgent ECG for hospitalised potassium at least 6.0 mmol/L and continuous monitoring for severe values or ECG changes. A normal tracing does not make severe hyperkalaemia benign; repeat a possibly haemolysed sample without withholding emergency care when the clinical picture is convincing.
02
Venous or arterial blood gas
Why
Rapidly define pH, bicarbonate, carbon dioxide, lactate, glucose and an immediately available potassium estimate.
Interpretation and limitations
Separate metabolic from respiratory contributions and calculate whether treatment of the cause is likely to reverse the disturbance. Confirm point-of-care electrolytes through the laboratory, but respond to life-threatening results while confirmation is pending.
03
Serial urea, creatinine and electrolytes
Why
Show the rate of solute accumulation and detect rebound after temporary therapy.
Interpretation and limitations
Trend potassium, bicarbonate, sodium, calcium, phosphate and magnesium in context. A rapidly rising value with anuria is more concerning than a stable isolated result, yet no numerical urea or creatinine level alone mandates or rules out dialysis.
04
Cardiorespiratory assessment and chest imaging
Why
Determine the severity and likely mechanism of respiratory compromise and guide fluid removal.
Interpretation and limitations
Combine oxygen requirement, work of breathing, jugular venous pressure, oedema, lung ultrasound or radiograph and cardiac history. Pneumonia or ARDS can coexist with overload, so dialysis may address only part of the respiratory problem.
05
Neurological and pericardial evaluation
Why
Identify uraemic organ dysfunction while excluding immediately treatable mimics.
Interpretation and limitations
Review sedatives and renally accumulated drugs, glucose, sepsis and focal signs. For chest pain or shock, examine for a rub, perform ECG and seek echocardiography; a normal urea threshold cannot exclude a clinical uraemic complication.
06
Fluid balance, weight and urine output
Why
Quantify accumulating volume and establish whether native kidney recovery is emerging.
Interpretation and limitations
Validate catheter patency and include all infusions, nutrition and losses. Increasing weight and positive balance with anuria support the overload mechanism, while an improving spontaneous output can inform—but not single-handedly determine—dialysis discontinuation.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Non-renal hyperkalaemia

Haemolysis, acidosis, insulin deficiency, tissue breakdown and potassium-shifting medicines can raise potassium independently; repeat sampling helps when safe, but ECG danger requires immediate action.

Cardiogenic pulmonary oedema

Primary myocardial ischaemia, arrhythmia or valve disease may drive congestion; cardiac findings and imaging help, although cardiac and renal failure frequently reinforce one another.

Alternative metabolic acidosis

Sepsis, ketoacidosis, lactic acidosis, diarrhoeal bicarbonate loss and toxins may dominate the low pH, so treating the generator remains essential alongside renal support.

Non-uraemic encephalopathy

Sepsis, hypoxia, glucose disturbance, medicines and intracranial disease can mimic uraemic confusion; parallel assessment should not postpone renal escalation when the overall physiology is dangerous.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First minutesStabilise a dialysis-level complicationFirst stepSevere hyperkalaemia, respiratory failure, profound acidaemia, pericardial compromise or altered consciousness is present.

11. Use ABCDE, call senior renal and critical-care help, obtain continuous monitoring and place reliable intravenous access while sending urgent bloods and gas.
22. 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.
33. State explicitly whether the problem is refractory, recurrent or predicted to recur because of anuria, ongoing cell breakdown, fluid accumulation or toxin burden.
44. Prepare transfer, dialysis access and consent or best-interests decisions without allowing these processes to interrupt resuscitation.

02RRT decisionEscalate on physiology, not a laboratory thresholdEscalationA complication is not responding adequately to medical management or the trajectory makes deterioration imminent.

11. Summarise AKI cause and stage, haemodynamics, potassium and pH trends, respiratory status, cognition, urine output, balance and treatments already given.
22. Apply the NICE complication set—hyperkalaemia, acidosis, uraemia, overload or pulmonary oedema—and consider toxin-specific extracorporeal advice when relevant.
33. Agree the urgency, location and modality with nephrology and critical care, considering how rapidly solute must fall and whether the circulation will tolerate intermittent therapy.
44. Review goals of care and proportionality with the patient or representative, but provide emergency life-saving treatment under the appropriate legal framework when immediate consent is impossible.

03During supportDeliver safe renal replacement and reassess recoveryIntermittent or continuous extracorporeal kidney support has started for AKI.

11. Check prescribed and delivered clearance, ultrafiltration, anticoagulation and vascular-access performance with the renal or critical-care team each treatment period.
22. Monitor blood pressure, rhythm, temperature, electrolytes and acid–base response; adjust fluid removal if perfusion deteriorates or disequilibrium is a concern.
33. Re-dose antimicrobials and other medicines for the actual modality and schedule, using pharmacy support because continuous and intermittent clearance differ substantially.
44. Continue treating the renal insult and assess spontaneous urine output, interdialytic potassium, bicarbonate and volume control before pausing support to test recovery.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Stabilises the cardiac membrane during toxic hyperkalaemia; it acts within minutes but does not lower serum potassium, so shifting and removal treatments remain mandatory.

Intravenous calcium for hyperkalaemic ECG toxicity

Follow the current UKKA and local emergency algorithm: an equivalent 6.8 mmol calcium dose is 30 mL calcium gluconate 10% over 10 minutes, or 10 mL calcium chloride 10% over 5 minutes in resuscitation settings.

Use calcium chloride preferentially in arrest or peri-arrest with secure access because extravasation is damaging; otherwise gluconate is generally used. Reassess the ECG and repeat only according to the emergency algorithm and senior advice.

Temporarily transfers potassium into cells while definitive potassium removal, renal recovery or urgent dialysis is arranged.

Soluble insulin with intravenous glucose

UKKA recommends 10 units soluble insulin with 25 g glucose intravenously for severe hyperkalaemia; use the approved prescription and add the specified glucose infusion when pretreatment glucose is below 7 mmol/L.

Hypoglycaemia may occur hours later, especially in kidney failure. Use the full local glucose-monitoring schedule, check response and rebound potassium, and never regard a transient fall as potassium removal.

Promotes intracellular potassium shift through beta-2 stimulation and can add to insulin–glucose while dialysis is mobilised.

Nebulised salbutamol

UKKA uses 10–20 mg nebulised as an adjunct in severe hyperkalaemia and allows consideration in moderate hyperkalaemia; confirm the local emergency protocol.

Do not use as monotherapy for severe hyperkalaemia because response is variable. Monitor tachycardia, tremor, ischaemia and rhythm, particularly in frail patients or those with coronary disease.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Cardiac arrest

Progressive hyperkalaemia can produce conduction block, ventricular arrhythmia or asystole, sometimes before the creatinine or overall AKI stage appears extreme.

Respiratory failure

Refractory pulmonary oedema impairs oxygenation and may require ventilatory support and extracorporeal fluid removal when diuretic response is inadequate.

Pericardial and neurological injury

Uraemic pericarditis can progress to effusion and haemodynamic compromise, while encephalopathy may advance to seizures, reduced consciousness or loss of airway protection.

Multiorgan deterioration

Persistent acidosis, overload and toxin accumulation worsen haemodynamics, medication handling and tissue oxygenation, reducing the opportunity for recovery from the precipitating illness.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

For moderate or severe hyperkalaemia, follow the current UKKA serial potassium schedule and watch for rebound after intracellular-shift treatment; arrange continuous rhythm monitoring when severity or ECG findings require it.
After insulin–glucose, perform protocol blood-glucose checks through the full delayed hypoglycaemia window rather than stopping when the first result is normal.
Track pH, bicarbonate, lactate and respiratory compensation alongside blood pressure and perfusion, because a numerically improved pH can conceal worsening shock or carbon dioxide retention.
Record oxygen delivery, work of breathing, weight, cumulative balance and achieved ultrafiltration; pause or adjust removal if intravascular depletion compromises organ perfusion.
Inspect the dialysis catheter and dressing, observe for bleeding or infection, and preserve upper-limb veins where future kidney access may become relevant.
Review daily whether each dialysis indication persists and whether native urine and interdialytic solute control support a supervised trial without treatment.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Calcium buys electrical safety

Intravenous calcium antagonises the myocardial effect of potassium but leaves total body potassium unchanged. Its use and dialysis referral are complementary rather than competing interventions.

Insulin improvement can rebound

Intracellular shifting lowers the measured serum concentration temporarily. In anuric AKI the excess remains in the body, so repeat potassium and a removal strategy are indispensable.

Urea has no magic line

NICE directs clinicians to judge the whole patient rather than an isolated urea, creatinine or potassium. Pericarditis, encephalopathy and fluid failure make the decision clinical and time-sensitive.

Modality follows the problem

Rapid intermittent clearance can be valuable for a stable patient with severe potassium or a dialysable toxin; continuous removal may better suit shock and gradual fluid control. Expertise and local capacity shape the final prescription.

Dialysis is not the endpoint

Extracorporeal support cannot drain an obstructed kidney, reverse sepsis or stop muscle necrosis. Causal therapy continues throughout, and its success determines whether kidney support can be withdrawn.

11Common pitfallsFrequent interpretation and management errors.

01
Waiting for creatinine or urea to cross a remembered threshold delays treatment of pulmonary oedema, encephalopathy or life-threatening potassium that already justifies urgent referral.
02
Sending for dialysis without giving calcium when hyperkalaemic ECG toxicity is present leaves the myocardium unprotected during a dangerous transfer and setup period.
03
Assuming potassium is solved after insulin ignores redistribution and rebound, particularly when ongoing tissue breakdown or anuria prevents removal from the body.
04
Using bicarbonate routinely as a potassium treatment disregards UKKA guidance and may add harmful sodium or volume; acidosis therapy must address cause and physiology.
05
Prescribing medicines by a generic ‘renal dose’ without naming the dialysis modality and timing can under-treat sepsis or cause accumulation as delivered clearance changes.