Acute Kidney Injury

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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

The older term is 'acute renal failure' (ARF). Acute kidney injury (AKI) is a rapid deterioration of renal function, resulting in inability to maintain fluid, electrolyte and acid-base balance.

It is detected and monitored by serial serum creatinine readings primarily, which rise acutely. Urine output and eGFR fall, and may also be used for detection and monitoring of the condition.

A 2009 report by the UK National Confidential Enquiry into Patient Outcome and Death (NCEPOD), Acute Kidney Injury, adding insult to injury, found serious deficiencies in patients who died with a diagnosis of AKI.[1] They reported that only 50% of patients received good medical care, and made recommendations for improvements. In the wake of this, and because of a lack of consistent guidelines, the UK National Institute for Health and Care Excellence (NICE) produced guidance for AKI published in August 2013.[2] 

  • Prerenal:
    • Volume depletion (eg, haemorrhage, severe vomiting or diarrhoea, burns, inappropriate diuresis).
    • Oedematous states: cardiac failure, cirrhosis, nephrotic syndrome.
    • Hypotension (eg, cardiogenic shock, sepsis, anaphylaxis).
    • Cardiovascular (eg, severe cardiac failure, arrhythmias).
    • Renal hypoperfusion: non-steroidal anti-inflammatory drugs (NSAIDs) or selective cyclo-oxygenase-2 (COX-2) inhibitors, angiotensin-converting enzyme (ACE) inhibitors or angiotensin-II receptor antagonists (AIIRAs - commonly called angiotensin receptor blockers (ARBs)), abdominal aortic aneurysm, renal artery stenosis or occlusion, hepatorenal syndrome.
  • Intrinsic renal problem:
    • Glomerular disease: glomerulonephritis, thrombosis, haemolytic uraemic syndrome.
    • Tubular injury: acute tubular necrosis (ATN) following prolonged ischaemia; nephrotoxins (eg, aminoglycosides, radiocontrast media, myoglobin, cisplatin, heavy metals, light chains in myeloma kidney).
    • Acute interstitial nephritis due to drugs (eg, NSAIDs), infection or autoimmune diseases.
    • Vascular disease: vasculitis (usually associated with antineutrophil cytoplasmic antibody), cryoglobulinaemia, polyarteritis nodosa, thrombotic microangiopathy, cholesterol emboli, renal artery stenosis, renal vein thrombosis, malignant hypertension.
    • Eclampsia.
  • Postrenal:
    • Calculus.
    • Blood clot.
    • Papillary necrosis.
    • Urethral stricture.
    • Prostatic hypertrophy or malignancy.
    • Bladder tumour.
    • Radiation fibrosis.
    • Pelvic malignancy.
    • Retroperitoneal fibrosis.

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Figures are difficult to establish due to the differing definitions used.

It is estimated that 15% of adults admitted to hospital in developed countries develop AKI.[4] It is particularly common in the elderly.

Population incidence in the UK has been found to be 486-630 per million population, depending on definition.[5] 

The cost to the NHS of AKI in secondary care is estimated to be as high as £630 million per year, which is higher than the combined cost of all lung and skin cancers.[2] 

It has been estimated that improving standards and care could save 12,000 lives in England and save the NHS £150 million per year.[6] 

In people with acute illness
The following increase the risks of developing AKI:

  • Age ≥65 years.
  • Heart failure.
  • Liver disease.
  • Chronic kidney disease (particularly if eGFR <60).
  • Past history of AKI.
  • Diabetes.
  • Neurological impairment or disability, in particular where reliance on a carer may mean reduced access to fluids. Additionally, young age in children for similar reasons.
  • Hypovolaemia.
  • Oliguria (urine output less than 0.5 ml/kg/hour).
  • Haematological malignancy.
  • Symptoms or history of urological obstruction, or a risk factor for it.
  • Sepsis.
  • Use of iodinated contrast agents within the previous week.
  • Current or recent medication with nephrotoxic potential - for example, NSAIDs, ACE inhibitors, AIIRAs, aminoglycosides, diuretics. A recent study concluded that when two antihypertensive agents (such as diuretics plus an ACE inhibitor or AIIRA) are used concurrently with an NSAID, the risk of AKI was increased.[7]
  • Deteriorating early warning scores (see use of track and trigger systems in NICE clinical guideline 50: Acutely ill patients in hospital.)[8] Similarly deteriorating paediatric early warning scores in children.
  • Additionally in children or young adults: severe diarrhoea, symptoms or signs of nephritis (such as oedema or haematuria) and hypotension.

In people having iodinated contrast agents
The following increase the risk of developing AKI:

  • Chronic kidney disease (CKD) (with an eGFR <40).
  • Diabetes if co-existent with CKD.
  • Heart failure.
  • Age ≥75 years.
  • Hypovolaemia.
  • Increasing volume of contrast agent.
  • Intra-arterial administration of contrast agent.

In people having surgery
The following are associated with increased risk of developing AKI:

  • Emergency surgery, particularly in the presence of sepsis or hypovolaemia.
  • Intraperitoneal surgery.
  • CKD (with eGFR <60 in adults).
  • Diabetes.
  • Heart failure.
  • Age ≥65.
  • Nephrotoxic medication.

The presentation will depend on the underlying cause and severity of AKI. There may be no symptoms or signs, but oliguria (urine volume less than 0.5 ml/kg/hour) is common. There is an accumulation of fluid and nitrogenous waste products demonstrated by a rise in blood urea and creatinine.


  • Urine output:
    • AKI is usually accompanied by oliguria or anuria. However polyuria may occur due to either reduced fluid reabsorption by damaged renal tubules, or the osmotic effect of accumulated metabolites.
    • Abrupt anuria suggests an acute obstruction, acute and severe glomerulonephritis, or acute renal artery occlusion.
    • Gradual diminution of urine output may indicate a urethral stricture or bladder outlet obstruction - eg, benign prostatic hyperplasia.
  • Nausea, vomiting.
  • Dehydration.
  • Confusion.


  • Hypertension.
  • Abdomen: may reveal a large, painless bladder typical of chronic urinary retention.
  • Dehydration with postural hypotension and no oedema.
  • Fluid overload with raised jugular venous pressure (JVP), pulmonary oedema and peripheral oedema.
  • Pallor, rash, bruising: petechiae, purpura, and nosebleeds may suggest inflammatory or vascular disease, emboli or disseminated intravascular coagulation.
  • Pericardial rub.

Classification and definitions: a work in progress

Over the past few years, international guideline groups have attempted to establish consistent definitions and staging systems for AKI. Initially the RIFLE (Risk, Injury, Failure, Loss, End stage kidney disease) system was set up in 2004. This was modified by the AKIN (Acute Kidney Injury Network) and further developed in 2012 by KDIGO (Kidney Disease: Improving Global Outcomes).[9] They work on levels of creatinine rise, but use non-SI units. A paediatric version of RIFLE (pRIFLE) is also in use. NICE guidance in 2013 suggests these systems need further development and simplification in order to be useful for clinicians working in the NHS, particularly non-specialists.

Meanwhile NICE recommends that AKI can be detected by using any of the following criteria, in line with pRIFLE, AKIN or KDIGO definitions:

  • Rise in serum creatinine of 26+ µmol/L in 48 hours.
  • A 50% or greater rise in serum creatinine in the past 7 days.
  • A drop in urine output to 0.5 ml/kg/hour for 6 hours in adults or 8 hours in children and young people.
  • In children or young people a fall in eGFR of 25% or more in the past 7 days.

The stage of AKI affects both management recommendations and prognosis, hence the importance of defining consistent stages. KDIGO defines stage 1, 2 and 3 through increasing rises in creatinine levels and drop in urinary output. For children the pRIFLE, stages 1 (risk), 2 (injury), and 3 (failure) are defined at specific falling levels of eGFR and falling urinary output.[4] 

It is important to first identify the cause of AKI, as this will affect management, particularly where there is a potentially treatable cause (for example obstruction, hypovolaemia, nephrotoxic drugs or glomerulonephritis). Often, however, there are multiple causes, and finding the cause will not always dictate specific management.

Cause established by:


  • Drugs - nephrotoxic drugs, remembering recreational drugs, over-the-counter drugs and herbal remedies.
  • Occupational or recreational history - exposure to sewer systems, tropical diseases, rodents.
  • Urinary symptoms.
  • Past medical history.


  • Signs of infection or sepsis.
  • Signs of acute or chronic heart failure.
  • Fluid status (dehydration or fluid overload).
  • Palpable bladder or abdominal/pelvic mass.
  • Features of underlying systemic disease (rashes, arthralgia).


  • Dipstick urine for blood, nitrates, leukocytes, glucose and protein in all patients with suspected AKI. (Consider acute nephritis and referral to a nephrologist if there is blood or protein on the dipstick in the absence of urinary infection or trauma due to catheterisation, and no obvious cause for AKI.)
  • Urine osmolality.

Blood tests

As appropriate to find cause as dictated by history. This could involve:

  • FBC, blood film. (Eosinophilia may be present in acute interstitial nephritis, cholesterol embolisation, vasculitis. Thrombocytopenia and red cell fragments suggest thrombotic microangiopathy.)
  • U&Es and creatinine.
  • Coagulation studies: disseminated intravascular coagulation associated with sepsis.
  • Creatine kinase, myoglobinuria: markedly elevated creatine kinase and myoglobinuria suggest rhabdomyolysis.
  • C-reactive protein (CRP): nonspecific marker of infection or inflammation.
  • Immunology:
    • Serum immunoglobulins, serum protein electrophoresis, Bence Jones' proteinuria: immune paresis, monoclonal band on serum protein electrophoresis, and Bence Jones' proteinuria suggest myeloma.
    • Antinuclear antibody (ANA): ANA positive in systemic lupus erythematosus (SLE) and other autoimmune disorders; anti-double-stranded DNA (anti-dsDNA) antibodies more specific for SLE; anti-dsDNA antibodies; antineutrophil cytoplasmic antibody (ANCA) (associated with systemic vasculitis; classical antineutrophil cytoplasmic antibodies (c-ANCA) and antiproteinase 3 (anti-PR3) antibodies associated with Wegener's granulomatosis; protoplasmic-staining antineutrophil cytoplasmic antibodies (p-ANCA) and antimyeloperoxidase (anti-MPO) antibodies present in microscopic polyangiitis), anti-PR3 antibodies, anti-MPO antibodies.
    • Complement concentrations: low in SLE, acute postinfectious glomerulonephritis, cryoglobulinaemia.
    • Antiglomerular basement membrane (anti-GBM) antibodies: present in Goodpasture's syndrome.
    • Antistreptolysin O and anti-DNase B titres: high after streptococcal infection.
  • Virology: hepatitis B and C; HIV: (important implications for infection control within dialysis area).
  • New biomarkers: creatinine is a poor indicator of renal function, and there have been many studies trying to find a more sensitive biomarker. These include cystatin C, neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1) and interleukin-18 (IL-18). None have yet been recommended for routine use.


When obstruction is suspected or no cause has been identified.

Other radiology

Where appropriate. For example:

  • CXR (pulmonary oedema).
  • Abdominal X-ray if renal calculi are suspected.
  • Contrast studies such as intravenous urogram (IVU) and renal angiography should be avoided because of the risk of contrast nephropathy.
  • Doppler ultrasound of the renal artery and veins: assessment of possible occlusion of the renal artery and veins.
  • Magnetic resonance angiography: for more accurate assessment of renal vascular occlusion.

Which tests are relevant will vary considerably with the individual. Urinalysis is done in all, and ultrasound is often indicated.

There is no specific treatment for AKI so management is largely supportive. It consists of treating the cause where possible, monitoring fluid and electrolyte balance closely, and optimising haemodynamic status with appropriate fluid therapy.

Stop nephrotoxic drugs where possible
Nephrotoxic drugs account for some part of the aetiology of AKI in 20-30% of cases, but because the patient already may be ill when they are started, or because there are other factors, it may be difficult to know exactly how much of the problem they have caused.[9] It makes sense, however, to limit exposure to these drugs as much as possible.

Monitor creatinine, sodium, potassium, calcium, phosphate, glucose
Frequency of monitoring should be tailored to the individual and the stage of AKI as appropriate.

Oral potassium and sodium may need restricting, and abnormal levels correcting. Watch for, and avoid hyperglycaemia. Insulin therapy may be required in critically ill patients to maintain blood glucose levels. Insulin also has the effect of driving potassium into the cells, thus reducing blood levels, which may be of benefit. 

Hypoglycaemia is also a potential risk in AKI, either with or without insulin therapy.

Identify and treat infection
Infection is a significant cause of mortality. Therefore, strict sepsis control is essential; avoidance of intravenous lines, bladder catheters, and respirators is recommended.

Optimise fluid balance
Accurate measurement of urine output is essential to prevent volume overload or depletion.

Refer to a urologist where appropriate
A urologist's advice may be required where there is an obstructive cause. Situations include renal calculi, papillary necrosis, tumours, strictures or prostatic enlargement.

Refer to a nephrologist for specific treatment of underlying intrinsic renal disease where appropriate

  • Acute renal artery thrombosis (of a single functioning kidney) may be treated surgically, or by angioplasty and stenting.
  • In rhabdomyolysis with myoglobulinuria, alkaline diuresis may prevent the development of severe renal failure, but must be undertaken with care in oliguric patients.
  • Acute tubulo-interstitial nephritis may respond to a short course of high-dose corticosteroids, though no controlled trials have been undertaken to support this approach.
  • AKI due to crescentic glomerulonephritis may respond to treatment with prednisolone and cyclophosphamide, together with the addition of plasma exchange.
  • Haemolytic uraemic syndrome may respond to plasma exchange with fresh frozen plasma.

Identify and treat acute complications
These include:

  • Hyperkalaemia.
  • Acidosis.
  • Pulmonary oedema.
  • Bleeding.

Drug options

  • There are no drugs which have been shown to limit progression of, or speed up recovery from, AKI.
  • Treatment as appropriate for complications.
  • Loop diuretics are not routinely used. They may be considered for treatment of fluid overload or oedema while awaiting renal replacement therapy or when renal function is recovering.

Referral for renal replacement therapy (RRT)
This should be considered if any of the following are not responding to medical management:

  • Hyperkalaemia.
  • Metabolic acidosis.
  • Symptoms or complications of uraemia such as pericarditis or encephalopathy.
  • Fluid overload.
  • Pulmonary oedema.

This decision should be made on the basis of the overall condition of the patient, and should be discussed with the patient and/or relatives in accordance with shared decision-making guidelines.[10] Referral to a nephrologist or critical care specialist should be made immediately if the above criteria are met.

All patients receiving RRT should have an assessment by a dietician and advice about nutritional support. Choice of modality of RRT will be guided by local availability and patient status.

Referral to a nephrologist where indicated[2] 

  • If the criteria for RRT are met as above.
  • When there is uncertainty about cause, management or prognosis.
  • Where there is a likely diagnosis that will need specialist treatment (glomerulonephritis, vasculitis, tubulo-interstitial nephritis, myeloma).
  • Inadequate response to treatment.
  • Complications.
  • History of renal transplant or CKD stage 4 or 5.
  • Stage 3 AKI according to pRIFLE, AKIN or KDIGO.
  • Doctors and patients can use Decision Aids together to help choose the best course of action to take.
  • Compare the options  

Life-threatening complications include:

  • Inpatient mortality varies greatly depending on the severity, setting, and many patient-related factors. In the UK it may be 20-30% or even higher.[2] 
  • Indicators of poor prognosis include older age, multiple organ failure, oliguria, hypotension, number of transfusions and acute on chronic renal failure. Prognosis is closely related to the underlying cause.
  • Patients who need dialysis have a higher mortality but this is a reflection of the condition rather than a result of the treatment.
  • The risk of mortality increases with the stage of AKI.
  • Patients who have had AKI are at increased risk of developing CKD.[11] 
  • There may be an ongoing requirement for RRT.[12] 

The best "treatment" of acute kidney injury (AKI) is prevention.[13] NICE guidance of 2013 reflects this, with the emphasis being on identification of patients at risk. Close monitoring of urinary output and creatinine levels for these patients allows early detection. Avoidance of nephrotoxic drugs and iodinated contrast agents in these patients reduces the risk of them developing AKI. All acutely ill patients in hospital should be closely monitored for signs of developing AKI.

At-risk patients who need iodinated contrast agents should be offered intravenous volume expansion with isotonic sodium bicarbonate or 0.9% sodium chloride to reduce the risks of developing AKI.[2]

Further reading & references

  1. Acute Kidney Injury: Adding insult to injury; National Confidential Enquiry into Patient Outcome and Death (NCEPOD) 2009
  2. Acute kidney injury - Prevention, detection and management of acute kidney injury up to the point of renal replacement therapy; NICE Guidelines (Aug 2013)
  3. Hilton R; Acute renal failure. BMJ. 2006 Oct 14;333(7572):786-90.
  4. Ftouh S, Thomas M; Acute kidney injury: summary of NICE guidance. BMJ. 2013 Aug 28;347:f4930. doi: 10.1136/bmj.f4930.
  5. Acute Kidney Injury; Renal Association (2011)
  6. Calculating the cost, interview with Marion Kerr; Health Service Journal 2011, June 23 supplement
  7. Lapi F, Azoulay L, Yin H, et al; Concurrent use of diuretics, angiotensin converting enzyme inhibitors, and angiotensin receptor blockers with non-steroidal anti-inflammatory drugs and risk of acute kidney injury: nested case-control study. BMJ. 2013 Jan 8;346:e8525. doi: 10.1136/bmj.e8525.
  8. Acutely ill patients in hospital , NICE Clinical Guidance (2007)
  9. Clinical practice guideline for acute kidney injury; KDIGO (Kidney Disease: Improving Global Outcome), 2012
  10. Patient experience in adult NHS services: improving the experience of care for people using adult NHS services (CG138); NICE (Feb 2012)
  11. Bellomo R, Kellum JA, Ronco C; Acute kidney injury. Lancet. 2012 Aug 25;380(9843):756-66. doi: 10.1016/S0140-6736(11)61454-2. Epub 2012 May 21.
  12. Murugan R, Kellum JA; Acute kidney injury: what's the prognosis? Nat Rev Nephrol. 2011 Apr;7(4):209-17. doi: 10.1038/nrneph.2011.13. Epub 2011 Feb 22.
  13. Fliser D, Laville M, Covic A, et al; A European Renal Best Practice (ERBP) position statement on the Kidney Disease Improving Global Outcomes (KDIGO) clinical practice guidelines on acute kidney injury: part 1: definitions, conservative management and contrast-induced nephropathy. Nephrol Dial Transplant. 2012 Dec;27(12):4263-72. doi: 10.1093/ndt/gfs375. Epub 2012 Oct 8.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Colin Tidy
Current Version:
Peer Reviewer:
Dr Hayley Willacy
Document ID:
1772 (v23)
Last Checked:
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