What is acute kidney injury?
Acute kidney injury (AKI) is a sudden drop in kidney function over hours or days. It is a syndrome rather than one disease, and in hospital it usually happens because the patient is unwell for another reason: sepsis, dehydration, bleeding, heart failure or surgery. The kidneys stop clearing waste, salt, water, potassium, acid and many medicines as well as they should.
AKI matters because it is common, often preventable and linked with longer stays, higher mortality and later chronic kidney disease. Many incident reviews find the same story: a nephrotoxic medicine that nobody stopped, a patient left without fluids, or a blood result that nobody acted on. Most patients with AKI do not need a renal specialist. They need a ward team that notices, finds the cause and gets the basics right.
How is AKI defined?
NICE guideline NG148 detects AKI in adults using any one of the following. You only need one.
- A rise in serum creatinine of 26 micromol/L or more within 48 hours.
- A rise in serum creatinine of 50% or more, known or presumed to have happened within the past 7 days.
- Urine output below 0.5 mL/kg/hour for more than 6 hours.
Children and young people have slightly different criteria, including a fall in eGFR of 25% or more within 7 days and a longer urine output window. In England, laboratories run the national AKI detection algorithm, which compares each creatinine with earlier results and adds an AKI warning stage to the report. Treat that alert as a prompt to go and see the patient, not as a diagnosis. An old baseline or a spurious single result can mislead it.
What are the stages of AKI?
NG148 refers to the established international definitions, and UK practice stages AKI using the KDIGO-based criteria below. Record the highest stage reached by either creatinine or urine output.
| Stage | Serum creatinine | Urine output |
|---|---|---|
| 1 | 1.5 to 1.9 times baseline, or a rise of 26 micromol/L or more within 48 hours | Below 0.5 mL/kg/hour for more than 6 hours |
| 2 | 2.0 to 2.9 times baseline | Below 0.5 mL/kg/hour for more than 12 hours |
| 3 | 3.0 times baseline or more, or a rise to 354 micromol/L or more, or renal replacement therapy started | Below 0.3 mL/kg/hour for 24 hours, or no urine for 12 hours |
Choosing a baseline
Use the most recent stable creatinine from before the illness, ideally within the last few months. If none exists, presume a baseline and repeat the test within 24 hours to see which way it is moving. Be careful in frail, low-weight older adults: their creatinine can sit inside the laboratory range while still representing a large fall in function. The change from the patient's own baseline matters more than the number.
Who is at risk of AKI?
NG148 advises thinking about AKI, and measuring creatinine, in adults with an acute illness who have risk factors. The more risk factors, the closer you should watch.
| Type of risk | Examples |
|---|---|
| Patient factors | Age 65 or over, chronic kidney disease, heart failure, liver disease, diabetes, previous AKI, cognitive impairment or difficulty drinking independently |
| Acute illness | Sepsis, hypovolaemia from vomiting, diarrhoea or bleeding, low urine output, a rising early warning score |
| Medicines | NSAIDs, aminoglycosides, ACE inhibitors, angiotensin II receptor blockers and diuretics, especially within the past week |
| Procedures | Emergency or major surgery; iodinated contrast within the past week in people with risk factors |
| Urinary tract | Known or possible obstruction, such as prostate enlargement, pelvic cancer or stones |
Prevention is mostly good basic care: bloods on admission and repeated while unwell, an accurate fluid balance chart, help with drinking for people who cannot manage alone, and a medicines review as soon as someone becomes unwell.
What should you do first when a patient has AKI?
Start with the patient, not the computer. The steps below follow NG148 and give a structured approach any ward clinician can use. Follow your local AKI care bundle where one exists.
- Check for immediate danger: Assess airway, breathing, circulation, disability and exposure, and look at NEWS2. Is the patient septic, hypotensive, breathless or drowsy? Check potassium straight away and get an ECG if it is high.
- Assess fluid status: Look for hypovolaemia (tachycardia, low blood pressure, slow capillary refill, dry mouth, falling urine output) and for overload (raised JVP, oedema, crackles, rising oxygen needs). Read the fluid chart and weights.
- Take a focused history and read the drug chart: Ask about vomiting, diarrhoea, poor intake, bleeding, urinary symptoms, rashes and joint pains. Check prescribed and over-the-counter medicines, recent contrast and recent surgery.
- Dip the urine: NG148 recommends a dipstick for blood, protein, leucocytes, nitrites and glucose in everyone with suspected or confirmed AKI, ideally before catheterisation. Blood and protein without an obvious cause may suggest acute nephritis and needs a prompt renal discussion.
- Look for obstruction: Feel for a bladder, use a bladder scanner and check any catheter is draining. NG148 recommends urgent ultrasound within 24 hours if no cause is found or obstruction is possible, and immediately (within 6 hours) if an infected obstructed kidney is suspected.
- Send the right bloods: Repeat urea, creatinine and electrolytes, and consider a full blood count, bone and liver profile and a venous gas if acidosis is likely.
- Write a plan and escalate: Record the stage and likely cause, the fluid and medicines plan, monitoring, and clear triggers for calling a doctor. Inform a senior.
Causes are often grouped as pre-renal (poor blood flow to the kidneys, by far the commonest in hospital), intrinsic (damage within the kidney, such as acute tubular injury, drugs or inflammation) and post-renal (obstruction). A patient can have more than one at once.
Which medicines should be stopped or adjusted in AKI?
Medicines can cause AKI, worsen it, or build up to toxic levels during it. Every patient with AKI needs a structured review, ideally with a pharmacist. Think in three parts: stop what is harming the kidney, adjust the dose of what is still needed, and plan when to restart.
| Medicine group | Why it matters | Usual action (follow local guidance) |
|---|---|---|
| NSAIDs | Reduce blood flow within the kidney | Stop; ask about over-the-counter use |
| ACE inhibitors and ARBs | Reduce filtration pressure, especially when dry | Usually withhold while acutely unwell; plan restart |
| Diuretics | Worsen dehydration | Withhold if dry; seek senior advice if overloaded |
| Gentamicin, vancomycin | Directly toxic to the kidney | Review need, use alternatives if possible, monitor levels |
| Metformin | Accumulates; linked with lactic acidosis | Usually withhold until recovery |
| SGLT2 inhibitors | Volume depletion and ketoacidosis in acute illness | Usually withhold while acutely unwell |
| Renally cleared drugs (some LMWHs, morphine, some antibiotics) | Accumulate and cause side effects | Check dose in BNF and local renal guidance |
The restart plan is easy to forget. An ACE inhibitor withheld during AKI and never restarted can leave someone with heart failure undertreated for months. Write the restart criteria on the chart and in the discharge summary.
Do not withhold an urgent scan because of worries about contrast. Discuss the risk with radiology, make sure the patient is adequately hydrated and follow local policy.
Fluids, potassium and when to call the renal team
If the patient is hypovolaemic, NICE guidance on intravenous fluids in adults (CG174) describes a 500 mL crystalloid bolus over less than 15 minutes, followed by reassessment, with further boluses of 250 to 500 mL if needed and expert help if 2,000 mL has been given. Use smaller volumes and more caution in heart failure, frailty and low body weight. If the patient is overloaded, more fluid is the wrong answer: they need senior review, oxygen if hypoxic and possibly a careful diuretic trial.
Hyperkalaemia is the most dangerous early complication because it can cause fatal arrhythmias. Get an ECG and cardiac monitoring for a high result, and do not delay treatment in an unwell patient while waiting for a repeat sample. Treatment (intravenous calcium, insulin with glucose and other measures) must follow your local protocol, with close glucose monitoring after insulin.
Worked example: the quiet deterioration
At 4pm a nurse, Daniel, tells the foundation doctor, Amira, that a 68-year-old man has passed 60 mL of urine in five hours. His heart rate is 108, blood pressure 98/60 and his NEWS2 has risen. His morning creatinine was 165, up from 82 before surgery, and nobody had acted on it. He is on regular ibuprofen and ramipril, and his IV fluids were stopped that morning. Amira finds him dry with cool peripheries; the bladder scan shows little urine. She gives a fluid bolus, reassesses and repeats it, stops ibuprofen, withholds ramipril, dips the urine, rechecks potassium, documents stage 2 AKI and agrees an hourly urine output trigger with Daniel. She informs her registrar. By evening his output has improved.
AKI. Creatinine up. Push fluids. Repeat bloods tomorrow.
Stage 2 AKI (creatinine 165, baseline 82), likely pre-renal: post-op hypovolaemia, IV fluids stopped, on ibuprofen and ramipril. Dip: trace protein. Bladder scan 40 mL. K 5.1. Two 500 mL crystalloid boluses with reassessment. Stop ibuprofen; withhold ramipril, restart when creatinine back to baseline. Hourly urine output; call if below 30 mL/hour for 2 hours or NEWS2 rises. U and E at 8am. Registrar informed. Ultrasound if no improvement in 24 hours.
Every warning sign was present that morning. The learning is not about blame but about systems: a result-acknowledgement process, a fluid chart people read, and a habit of reviewing medicines when someone becomes unwell.
Discharge and learning more
AKI does not end at discharge. The summary should state the stage and likely cause, the creatinine at discharge, which medicines were stopped or changed, when to restart them, and who will recheck the creatinine and when. Tell the patient in plain words what happened and which medicines, such as over-the-counter anti-inflammatories, to avoid.
This guide is educational; follow NICE NG148, your local AKI pathway and senior advice. The Acute Kidney Injury: Recognition and Management course works through staging, assessment, medicines review and fluids with ward scenarios and a reflective exercise for your CPD record. Severe hyperkalaemia can cause cardiac arrest, so keeping resuscitation skills current through accredited hands-on training also matters.
Frequently asked questions
What creatinine level is AKI stage 3?
Stage 3 is a creatinine of three times baseline or more, a rise to 354 micromol/L or more, or the start of renal replacement therapy. Urine output below 0.3 mL/kg/hour for 24 hours, or no urine for 12 hours, also counts. NG148 advises discussing stage 3 AKI with nephrology or critical care within 24 hours.
What is the difference between AKI stage 1 and stage 2?
Stage 1 is a creatinine of 1.5 to 1.9 times baseline, or a rise of 26 micromol/L or more within 48 hours, or low urine output for more than 6 hours. Stage 2 is 2.0 to 2.9 times baseline, or low urine output for more than 12 hours. Initial management principles are the same; higher stages need closer monitoring and earlier senior input.
What does an AKI warning stage on a blood result mean?
In England, laboratories use a national algorithm that compares the new creatinine with the patient's previous results and flags a warning stage. It is a prompt to assess the patient promptly, check the baseline and look for a cause. It can be wrong if the baseline is old or a result is spurious, so clinical judgement still applies.
Which medicines should be stopped in acute kidney injury?
Commonly reviewed medicines include NSAIDs (usually stopped), ACE inhibitors, ARBs and diuretics (often withheld while the patient is dry), metformin and SGLT2 inhibitors (usually withheld), and nephrotoxic antibiotics such as gentamicin. Renally cleared drugs need dose checks. Decisions depend on the patient, so follow local guidance, involve a pharmacist and document a restart plan.
Does every patient with AKI need a renal ultrasound?
No. NG148 recommends urgent ultrasound within 24 hours when no cause has been found or obstruction is possible, and immediately if an infected obstructed kidney is suspected. If there is a clear cause, such as dehydration with a prompt response to fluids, routine ultrasound is not needed.
How often should creatinine be checked in AKI?
There is no single rule. Many teams check urea, creatinine and electrolytes daily while the patient is unwell, and sooner if potassium is high or the patient is deteriorating. Agree the frequency with your team, write it in the plan and make sure someone is responsible for acting on the result.
Can a normal creatinine still mean AKI?
Yes. In frail older adults with low muscle mass, a creatinine inside the laboratory reference range can still be a large rise from their own baseline. Creatinine also lags behind the injury, so low urine output may show AKI first. Always compare with the patient's baseline and look at the fluid chart.
Sources and further reading
- Acute kidney injury: prevention, detection and management (NG148). National Institute for Health and Care Excellence.
- Intravenous fluid therapy in over 16s in hospital (CG174). National Institute for Health and Care Excellence.
- Clinical practice guideline: treatment of acute hyperkalaemia in adults. UK Kidney Association.
- Think Kidneys: acute kidney injury resources. UK Kidney Association.
- National Early Warning Score (NEWS) 2. Royal College of Physicians.
- British National Formulary. BMJ Group and Royal Pharmaceutical Society.
Practitioner Insight is an independent education provider. It is not affiliated with or endorsed by the GMC, MPTS, NMC, HCPC, GPhC or any NHS organisation, and this information is not legal advice. If you have been referred to a regulator, speak to your defence organisation, trade union or legal representative.