Acute kidney injury
Acute kidney injury is a measurable fall in kidney filtration or urine output caused by reduced perfusion, intrinsic renal disease or obstruction; identify the cause early, protect the kidneys, monitor complications and escalate for refractory life-threatening physiology.
Definition
Acute kidney injury is an abrupt reduction in kidney function detected by a rise in serum creatinine, reduced urine output or both. It may be caused by reduced perfusion, intrinsic kidney injury or urinary tract obstruction.
Epidemiology
AKI is common in acutely ill, septic, post-operative and older patients and is associated with increased mortality and later chronic kidney disease. Risk is higher with pre-existing CKD, heart failure, liver disease, diabetes, hypovolaemia, obstruction and nephrotoxic medicines.
Pathophysiology
Reduced renal perfusion lowers filtration and may progress to tubular injury. Intrinsic injury can affect glomeruli, tubules, interstitium or vessels, while obstruction raises tubular pressure and reduces filtration. Systemic consequences include potassium and acid retention, uraemia, salt and water retention and drug accumulation.
First principles
AKI is a change from baseline, not a single creatinine value
Detect AKI by a rise in serum creatinine or a sustained fall in urine output, comparing with the best available baseline. A creatinine that looks 'normal' may still represent a major fall in filtration in a person with low muscle mass or a previously lower baseline.1,2
Always look for the reversible triad
Assess perfusion and volume, infection and sepsis, medicines and toxins, intrinsic renal features, and urinary obstruction in parallel. Pre-renal, intrinsic and post-renal mechanisms can coexist, especially in older, septic or post-operative patients.1,2,3
Urine findings can change the diagnosis
Urinalysis for blood, protein, leucocytes, nitrites and glucose is recommended as soon as AKI is suspected. Haematuria with proteinuria without infection or catheter trauma should prompt consideration of acute nephritis and early nephrology discussion.1,2
Dialysis is triggered by physiology and complications
Discuss renal replacement therapy (RRT) urgently for hyperkalaemia, metabolic acidosis, uraemic complications, fluid overload or pulmonary oedema that do not respond to medical treatment. Do not start RRT from an isolated urea, creatinine or potassium value without considering the whole patient.1,2
Presentation
AKI may be detected on routine blood tests or present with oliguria, dehydration, sepsis, breathlessness from fluid overload, confusion, nausea or symptoms of the precipitating illness. Ask about baseline kidney function, fluid losses, infection, medicines, contrast, surgery and urinary symptoms.1,2
Cardinal features
- Rise in serum creatinine compared with baseline
- Urine output below 0.5 ml/kg/hour for more than 6 hours in adults or more than 8 hours in children
- Hypovolaemia, sepsis, hypotension, heart failure, liver disease or recent surgery
- Recent NSAID, ACE inhibitor, ARB, diuretic, aminoglycoside or contrast exposure
- Haematuria, proteinuria, rash, eosinophilia, systemic inflammatory features or urinary obstruction symptoms
Red flags
- Refractory hyperkalaemia, metabolic acidosis, pulmonary oedema or fluid overload
- Uraemic encephalopathy, pericarditis, seizures or severe symptomatic uraemia
- Anuria, rapidly falling urine output, shock or severe sepsis
- Stage 3 AKI, renal transplant, CKD stage 4 or 5, or inadequate response to initial treatment
- Possible glomerulonephritis, vasculitis, interstitial nephritis, myeloma or other disease requiring specialist treatment
- Pyonephrosis, bilateral obstruction or obstruction of a solitary functioning kidney
Investigations
Baseline comparison and AKI staging
Compare serum creatinine with the lowest reliable recent baseline and quantify urine output. NICE criteria include a creatinine rise of at least 26 micromol/litre within 48 hours, a 50% rise within 7 days or sustained oliguria.
Expected finding: The magnitude and rate of creatinine rise, urine output and clinical trajectory determine stage, monitoring frequency and need for specialist discussion; eGFR is unreliable during rapidly changing renal function.
1,2Fluid status, physiology and cause-focused examination
Assess blood pressure, perfusion, mucous membranes, JVP, oedema, weight, lung findings, temperature, sepsis features and bladder distension. Review fluid balance and urine output rather than relying on creatinine alone.
Expected finding: Hypovolaemia, sepsis, congestion, pulmonary oedema or obstruction directs the initial treatment; mixed causes are common.
1,2Urine dipstick and microscopy when indicated
Perform urine dipstick testing for blood, protein, leucocytes, nitrites and glucose as soon as AKI is suspected. Haematuria with proteinuria without UTI or catheter trauma suggests glomerular or interstitial disease and needs nephrology discussion.
Expected finding: Blood and protein may indicate glomerulonephritis, vasculitis or interstitial disease; nitrites and leucocytes support infection but do not define the cause of AKI.
1,2Blood tests for complications and systemic cause
Check electrolytes, bicarbonate or blood gas, urea, creatinine, full blood count, glucose and liver tests; add cultures, inflammatory markers, CK, haemolysis or immunological tests when the clinical question requires them.
Expected finding: Hyperkalaemia, acidosis, uraemia, anaemia, thrombocytopenia, rhabdomyolysis or sepsis may explain the AKI or require immediate treatment.
1,2Urgent urinary-tract ultrasound when obstruction is possible
Do not scan every patient if the cause is clear. Perform immediate ultrasound within 6 hours when pyonephrosis is suspected and urgent ultrasound within 24 hours when the cause is unclear or obstruction is possible.
Expected finding: Hydronephrosis, an obstructed solitary kidney, bilateral obstruction or an infected obstructed system requires urgent urology intervention.
1,2Review medicines and nephrotoxic exposures
Reconcile prescribed, over-the-counter and recently stopped medicines, including NSAIDs, ACE inhibitors, ARBs, diuretics, aminoglycosides, contrast and renally cleared medicines. Seek pharmacist advice for dose adjustment and safer alternatives.
Expected finding: A reversible medicine-related contributor, accumulation or interaction is identified; drug dosing is changed using current BNF and local pharmacy guidance.
1,3,4,5,6Management
| Step | Detail | Source |
|---|---|---|
| Recognise AKI and stabilise immediately | Use ABCDE, treat shock and sepsis promptly, monitor urine output and fluid balance, and manage hyperkalaemia, acidosis, hypoglycaemia and pulmonary oedema according to the relevant emergency pathway. Escalate early if physiology is deteriorating.1,2 | NICE NG148 prevention, detection and management of AKI |
| Find and reverse the cause | Assess perfusion and volume, infection, nephrotoxic medicines, intrinsic renal disease and obstruction in parallel. Give isotonic fluid only when hypovolaemia is present and reassess after each intervention; avoid both persistent under-resuscitation and fluid overload.1,2 | NICE NG148; UK Kidney Association AKI guidance |
| Optimise medicines and renal dosing | Review all medicines with a pharmacist. NICE advises considering temporary cessation of ACE inhibitors and ARBs during diarrhoea, vomiting or sepsis until the condition improves and stabilises; stop or replace nephrotoxic medicines where possible and adjust renally cleared drugs using current BNF guidance. Do not use unstructured blanket sick-day rules without individual risk assessment and a restart plan.1,3,4,5,2 | NICE NG148 recommendation 1.2.14; BNF renal prescribing guidance; individualised local medicines guidance |
| Monitor response and complications | Repeat creatinine and electrolytes according to clinical need, with daily measurement typical in hospital, and record urine output, weight, fluid balance and observations. Avoid routine potassium-containing fluids or medicines when potassium is high, and seek senior advice for worsening renal function or new complications.1,2 | NICE NG148; UK Kidney Association AKI guidance |
| Treat obstruction urgently | Refer upper-tract obstruction to urology. Pyonephrosis, bilateral obstruction, obstruction of a solitary kidney or obstruction-related AKI with complications requires immediate specialist intervention; nephrostomy or stenting should be performed as soon as possible and within 12 hours when indicated.1 | NICE NG148 recommendations 1.5.1 and 1.5.2 |
| Use diuretics only for the right indication | Do not routinely use loop diuretics to treat AKI or to force urine production. Consider them for fluid overload or oedema while awaiting RRT, or during recovery when the patient is not receiving RRT, with close monitoring of perfusion and electrolytes. Do not use low-dose dopamine to treat AKI.1,6 | NICE NG148 recommendations 1.5.3 to 1.5.5 |
| Escalate immediately for possible RRT | Discuss RRT with nephrology and/or critical care immediately when hyperkalaemia, metabolic acidosis, uraemic complications, fluid overload or pulmonary oedema is not responding to medical treatment. Decide using the whole clinical picture, not an isolated biochemical value.1,2 | NICE NG148 recommendations 1.5.6 to 1.5.10 |
| Refer and plan post-AKI follow-up | Discuss with nephrology within 24 hours when AKI is stage 3, has no clear cause, responds inadequately, has complications, may represent vasculitis/glomerulonephritis/interstitial nephritis/myeloma, occurs in a transplant or coexists with CKD stage 4 or 5. After discharge monitor creatinine and renal recovery; NICE CKD guidance recommends monitoring for at least 3 years after AKI, longer after stage 3, even if eGFR returns to baseline.1,7,2 | NICE NG148 recommendation 1.5.15 to 1.5.16; NICE NG203 |
Illustrations
Differentials
Pre-renal AKI
Hypovolaemia, sepsis, hypotension or reduced effective circulating volume, often with a potentially reversible trigger.
Intrinsic renal AKI
Glomerulonephritis, vasculitis, acute tubular injury, interstitial nephritis, rhabdomyolysis or vascular disease, with urine or systemic clues.
Post-renal AKI
Urinary obstruction, hydronephrosis, retention, bilateral or solitary-kidney obstruction, sometimes with little pain.
Chronic kidney disease
Longstanding stable reduction in renal function or small echogenic kidneys, although CKD and AKI can coexist.
Complications
- Hyperkalaemia and cardiac arrhythmia
- Metabolic acidosis
- Fluid overload and pulmonary oedema
- Uraemic encephalopathy, pericarditis or seizures
- Drug toxicity from reduced clearance
- Incomplete recovery, CKD and recurrent AKI
Prognosis
Many patients recover, but recovery may be incomplete and an episode of AKI increases later CKD and cardiovascular risk. Prognosis depends on the cause, severity, duration, complications and the speed of restoring perfusion, treating infection or obstruction and stopping harmful exposures.
Guidelines
- Acute kidney injury: prevention, detection and management (NG148) (NICE, 2024)
- Acute kidney injury clinical guideline (UK Kidney Association, 2024)
- Chronic kidney disease: assessment and management (NG203) (NICE, 2021)
References
- NICE NG148: Acute kidney injury, recommendations (NG148, last updated 16 October 2024)
- UK Kidney Association: Acute kidney injury guideline (UKKA AKI guideline, published 2019 and reviewed 1 August 2024)
- BNF: Ibuprofen (BNF medicine monograph for NSAID renal cautions)
- BNF: Ramipril (BNF medicine monograph for ACE-inhibitor cautions and renal monitoring)
- BNF: Losartan (BNF medicine monograph for ARB cautions and renal monitoring)
- BNF: Furosemide (BNF medicine monograph for loop-diuretic use and monitoring)
- NICE NG203: Chronic kidney disease, recommendations (NG203 recommendations for monitoring after AKI)
Evidence checked: 2026-08-03
This page is exam revision material, not medical advice, and must not be used for patient care. Always check drug doses against the BNF and current guidance. Full disclaimer.