Background
Acute kidney injury affects around 1 in 20 hospital admissions in the UK, occurs predominantly in the community, is usually managed by non-specialists, and is associated with high mortality, prolonged hospital stay, and incomplete kidney recovery — even at early stages. (Selby et. al., 2012)
What is acute kidney injury (AKI)?
Acute kidney injury (AKI) refers to a sudden decline in kidney excretory function over hours to days, which can result in impaired regulation of fluid, electrolytes, or acid–base balance (7).
AKI is not a single clinical entity, but instead consists of many overlapping clinical syndromes that arise in different disease contexts (1). AKI commonly develops in association with sepsis, shock, cardiac and obstetric complications, drug and toxin exposure, obstruction, malignancy, and advanced kidney disease. This heterogeneity has made recommending and standardising approaches to AKI prevention and intervention particularly challenging.
As a result, a rise in serum creatinine must always be interpreted in clinical context. For example, a rising creatinine in a dehydrated individual with sepsis has different implications from a rise seen in a patient receiving diuretic therapy to manage significant peripheral oedema.
AKI is often described using a functional framework based on the underlying mechanism:
| Cause | Description | Common causes |
| Pre-renal AKI | Results from decreased blood flow to the kidneys.
Pre-renal AKI is often reversible within days if blood flow is restored promptly; prolonged hypoperfusion may progress to intra-renal injury. |
Volume depletion (e.g. excessive diuresis, haemorrhage, shock, burns, severe trauma), cardiovascular disorders (e.g. heart failure, acute myocardial infarction), and obstruction of the renal arteries (e.g. renal artery stenosis or thrombosis). |
| Intra-renal AKI | Intra-renal injuries refer to anything which damages the cells of the kidney.
Recovery depends on cause, severity, and timeliness of treatment. |
Sustained hypoperfusion, nephrotoxic agents (e.g. aminoglycosides, amphotericin, paracetamol, salicylates, ethylene glycol), autoimmune or inflammatory conditions (e.g. vasculitis, systemic lupus erythematosus, interstitial nephritis, glomerulonephritis). |
| Post-renal AKI | Caused by obstruction to urine flow from the kidneys. This often results in hydronephrosis (“water on the kidneys”).
Post-renal AKI is frequently reversible if obstruction is relieved promptly. |
Causes include urinary tract stones, crystal deposition in the tubules (e.g. uric acid, sulphonamides, aciclovir, cisplatin), and compression of the urinary tract (e.g. prostate enlargement, bladder or bowel tumours). |
How is AKI defined and staged?
The term ‘acute kidney injury’ (AKI) has both subjective and objective definitions.
Subjectively, it is characterised by a sudden decline in kidney excretory function over hours or days that can result in the failure to maintain fluid, electrolyte, or acid-base balance (1). This decline is generally considered to need to have occurred within 7 days for it to be defined an AKI.
Objectively, severity of AKI is defined in stages from 1 to 3. The KDIGO definition of these stages for adults, which take into account biochemical assessment of creatinine as well as urine output criteria, is in widespread accepted use (2):
| AKI stage | Creatinine | Urine output |
|---|---|---|
| 1 | Serum creatinine 1.5–1.9 × baseline or ≥26 μmol/L (≥0.3 mg/dL) | <0.5 mL/kg/hour for 6–12 hours |
| 2 | Creatinine 2.0–2.9 × baseline | <0.5 mL/kg/hour for ≥12 hours |
| 3 | Creatinine ≥3.0 × baseline or ≥354 μmol/L (≥4.0 mg/dL) or initiation of kidney replacement therapy | <0.3 mL/kg/hour for ≥24 hours or anuria for ≥12 hours |
AKI staging and interpretation differ for babies, children, and young people under 18 years of age (BCYP). For BCYP, changes in kidney function are assessed using age- and size-appropriate reference values, and urine output thresholds differ from those used in adults. Baseline kidney function may also be less clearly defined, particularly in younger children.
For guidance on recognising and staging AKI in BCYP, refer to the Paediatric section of this guide.
The KDIGO criteria offer standardised definitions to allow reporting, triaging and research & improvement work, however at the individual level it should be noted that they must be viewed in the context of which AKI clinical syndrome is at play.
A rising creatinine takes on a different meaning in the context of a dehydrated individual with sepsis compared to an individual who is receiving diuretic therapy to target marked peripheral oedema.
Creatinine based criteria also suffer from the limitations of the creatinine assays themselves. For instance, at extremes of body mass or in pregnant individuals, baseline or changes in creatinine can be more difficult to interpret. Biochemical or urine output definitions are part of, but not a complete substitute for wholistic clinical assessment.
A note on terminology
- AKI vs acute renal failure (ARF): Acute kidney injury has replaced the outdated term acute renal failure. While ARF emphasised severity, AKI is considered a better descriptor of the spectrum of structural and functional kidney damage that can occur (9).
- AKI vs acute tubular necrosis (ATN): ATN is a histological description of tubular injury seen on microscopy. It is not interchangeable with AKI, does not occur in all AKI syndromes, and is not a diagnosis in itself unless supported by kidney biopsy and appropriate clinical context.
- Acute kidney disease (AKD): AKD is an increasingly used term that describes the continuum between the initial establishment of AKI within hours to days and either partial or complete recovery, or persistence of kidney dysfunction beyond the acute phase. Chronic kidney disease is defined by abnormalities present for more than 90 days (7).
Why does AKI matter?
AKI is a common, serious, and costly patient safety issue across healthcare systems:
- Common: Approximately 600,000 patients experiencing an episode in England in 2022 alone (2).
- Increasing: Incidence in England in 2022 was 12,651 per million population compared to 11,660 in 2018 (1).
- Deadly: AKI has an unadjusted 30-day mortality rate of 19% and an estimated 100,000 in-hospital deaths associated with an AKI episode each year (1,3).
- Costly: The annual cost of related inpatient care in England is estimated at £1.02 billion (4).
- Largely community-acquired: Around 3 in 5 AKI episodes begin in the community, often before hospital admission (10).
- Frequently encountered in secondary care: AKI is identified in 1 in 5 emergency hospital admissions whilst roughly a third of episodes occur after hospitalisation. (1,5)
- Often predictable and preventable: 20% of AKI episodes are thought to be predictable and preventable (2).
Lessons from national reviews
The findings from the National Confidential Enquiry into Patient Outcome and Death (NCEPOD) report Acute kidney injury: adding insult to injury (2009) were a catalyst in improvement in the field, with shortcomings identified particularly in the recognition and treatment of post-hospitalisation AKI. Key findings from this report are summarised in Table 1.
| Design | Key Findings |
|---|---|
| Multi-centre questionnaire and casenote review of AKI events by multidisciplinary panel | Poor assessment of risk factors for AKI |
| 1518 patients from 215 hospitals selected | Unacceptable delay in recognising post-admission AKI in 43% |
| ~700 had either questionnaire or casenotes available for review | A fifth of post-admission AKI was both predictable and avoidable |
| Complications of AKI missed in 13% of cases | |
| 33% had basic clinical exam or simple tests omitted | |
| Recognition of acute illness, hypovolaemia and sepsis was poor | |
| Only 50% of patients received a standard of care considered good |
Table 1: NCEPOD Report 2009: AKI: Adding Insult to Injury (3)
Disappointingly, a national audit by the NEPHwork team in 2021, in conjunction with Kidney Care UK and the UKKA, showed that after more than 10 years since the NCEPOD report, significant variation remains between organisations in AKI care-quality measures (6).
Groups at higher risk of AKI
Some people are at higher risk of developing AKI, particularly during intercurrent illness or physiological stress. Risk is shaped not only by underlying kidney disease, but also by comorbidity, medicines, dependency, and access to fluids and care.
Groups at higher risk include:
- Older adults, particularly those with frailty, multimorbidity, or cognitive impairment
- People with chronic kidney disease, a history of AKI, or a kidney transplant
- People with long-term conditions such as heart failure, diabetes, liver disease, or vascular disease
- People with cancer, especially those receiving chemotherapy, experiencing volume depletion, obstruction, sepsis, or metabolic complications
- People with severe mental illness, substance misuse, or self-neglect, including those prescribed medicines such as lithium
- People who are dependent on others for hydration or care, including those in residential settings
- Babies and children, particularly during episodes of dehydration, sepsis, gastroenteritis, or when exposed to nephrotoxic agents
Awareness of these higher-risk groups supports earlier recognition of AKI, more proactive monitoring during acute illness, and timely action to reduce avoidable harm.
Key resources
- NICE guideline NG148: Acute kidney injury—prevention, detection and management
- NICE quality standard QS76 (AKI), including timeliness expectations for response and post-discharge review
- NHS England AKI detection algorithm
- UKKA AKI National Summit Report and Recommendations
- RCP Acute Care Toolkit 12: Acute kidney injury and intravenous fluid therapy
- NICE Clinical Knowledge Summary: AKI
- UKKA Acute Kidney Injury Guideline
- UKKA Acute Kidney Injury Data Portal
- UK Kidney Association – AKI: The Essentials (free, login required)
- BMJ Learning – Acute kidney injury: diagnosis and management in primary care (membership required)
People who have had an episode of AKI or are more vulnerable to AKI may benefit from clear, plain-language information about the role of the kidneys, how acute illness and medicines can affect kidney function, and when to seek advice if their health changes.
- Kidney Care UK: Acute kidney injury information page
- Kidney Care UK: AKI patient booklet (downloadable)
- Kidney care UK: AKI patient booklet – easy read version (downloadable)
- InfoKID information for parents and carers about AKI in BCYP
- NHS AKI Patient Information
- Keeping kidneys safe – Know how medicines affect the kidneys video from the US National Institute of Health’s National Institute of Diabetes and Digestive and Kidney Diseases
- Your kidneys and what they do video from Leicester’s Hospitals
- How to keep your kidneys healthy video from Leicester’s Hospitals
References
- Ronco C, Bellomo R, Kellum JA. Acute kidney injury. Lancet. 2019;394(10212):1949–1964. doi:10.1016/S0140-6736(19)32563-2.
- UK Kidney Association. Acute kidney injury summit report. Bristol: UK Kidney Association; 2023.
- Stewart J, Findlay G, Smith N, et al. Acute kidney injury: adding insult to injury. London: National Confidential Enquiry into Patient Outcome and Death; 2009.
- Kerr M, Bedford M, Matthews B, O’Donoghue D. The economic impact of acute kidney injury in England. Nephrol Dial Transplant. 2014;29(7):1362–1368. doi:10.1093/ndt/gfu016.
- Wang HE, Muntner P, Chertow GM, Warnock DG. Acute kidney injury and mortality in hospitalized patients. Am J Nephrol. 2012;35(4):349–355. doi:10.1159/000337487.
- UK Kidney Association. NEPHwork National AKI Audit. Bristol: UK Kidney Association; 2019.
- National Institute for Health and Care Excellence (NICE). Acute kidney injury: definition. London: NICE; 2023.
- Kidney Disease: Improving Global Outcomes (KDIGO). KDIGO clinical practice guideline for acute kidney injury. Kidney Int Suppl. 2012;2(1):1–138.
- Makris K, Spanou L. Acute kidney injury: definition, pathophysiology and clinical phenotypes. Clin Biochem Rev. 2016;37(2):85–98.
- Selby NM, Crowley L, Fluck RJ, McIntyre CW, Monaghan J, Lawson N, Kolhe NV. Use of electronic results reporting to diagnose and monitor acute kidney injury in hospitalized patients. Clin J Am Soc Nephrol. 2012;7(4):533–540. doi:10.2215/CJN.08970911.