Acute kidney injury (AKI), previously termed acute renal failure, describes a reduction in renal function following an insult to the kidneys. In years gone by the kidneys were very much a neglected organ in acute medicine - the recognition of decreasing renal function was often slow and action limited. Around 15% of patients admitted to hospital develop AKI.


Causes of AKI are traditionally divided into prerenal, intrinsic and postrenal causes


One of the major causes of AKI is ischaemia, or lack of blood flowing to the kidneys.

  • Hypovolaemia secondary to diarrhoea/vomiting
  • Renal artery stenosis


The second group of causes relate to intrinsic damage to the glomeruli, renal tubules or interstitium of the kidneys themselves. This may be due to toxins (drugs, contrast etc) or immune-mediated glomuleronephritis.

  • Glomerulonephritis
  • Acute tubular necrosis (ATN)
  • Acute interstitial nephritis (AIN), respectively
  • Rhabdomyolysis
  • Tumour lysis syndrome


The third group relates to problems after the kidneys. This is where there is an obstruction to the urine coming from the kidneys resulting in things 'backing-up' and affecting the normal renal function. An example could be a unilateral ureteric stone or bilateral hydroneprosis secondary to acute urinary retention caused by benign prostatic hyperplasia.

  • Kidney stone in ureter or bladder
  • Benign prostatic hyperplasia
  • External compression of the ureter

Who is at an increased risk of AKI?

One of the keys to reducing the incidence of AKI is identifying patient who are at increased risk. NICE support this approach and have published guidelines suggesting which patients are at greater risk.

Risk factors for AKI include:
  • Chronic kidney disease
  • Other organ failure/chronic disease e.g. heart failure, liver disease, diabetes mellitus
  • History of acute kidney injury
  • Use of drugs with nephrotoxic potential (e.g. NSAIDs, aminoglycosides, ACE inhibitors, angiotensin II receptor antagonists [ARBs] and diuretics) within the past week
  • Use of iodinated contrast agents within the past week
  • Age 65 years or over
oliguria (urine output less than 0.5 ml/kg/hour)
  • Neurological or cognitive impairment or disability, which may mean limited access to fluids because of reliance on a carer


Basic steps
  • Final pathway is tubular cell death.
  • Renal medulla is a relatively hypoxic environment making it susceptible to renal tubular hypoxia.
  • Renovascular autoregulation maintains renal blood flow across a range of arterial pressures.
  • Estimates of GFR are the best indices of renal function. Useful clinical estimates can be obtained by considering serum creatinine, age, race, gender and body size. eGFR calculations such as the Cockcroft and Gault equation are less reliable in populations with high GFRs.
  • Nephrotoxic stimuli such as aminoglycosides and radiological contrast media induce apoptosis. Myoglobinuria and haemolysis result in necrosis. Overlap exists and proinflammatory cytokines play and important role in potentiating ongoing damage.
  • Post-operative renal failure is more likely to occur in patients who are elderly, have peripheral vascular disease, high BMI, have COPD, receive vasopressors, are on nephrotoxic medication or undergo emergency surgery.
  • Avoiding hypotension will reduce the risk of renal tubular damage.
  • There is no evidence that administration of ACE inhibitors or dopamine reduces the incidence of post-operative renal failure.

Clinical features



Urine analysis
  • urine dipstick
    • urinary tract infection: leucocytes +/- nitrites
    • glomerulonephritis: haematuria + leucocytes
    • acute interstitial nephritis: leucocytes by themselves
  • microscopy, culture and sensitivity
    • if any evidence of UTI on the urine dipstick
  • protein:creatinine ratio if glomerulonephritis is suspected

  • urea and electrolytes
    • important to detect hyperkalaemia as this may require urgent treatment
  • as a minimum a FBC, CRP and bone profile should also be performed
  • if the cause is not known further blood tests should be considered including:
    • creatinine kinase
  • ANA
  • ANCA
  • anti-GBM
  • complement levels
  • immunoglobulin levels
  • antistreptolysin O titre
  • HIV

  • an ultrasound scan should be performed in new cases of AKI
  • if obstructive uropathy or pyelonephritis is suspected this should be performed urgently
    • UK guidelines suggest this should be performed within 24 hours if obstruction is suspected or there is no identifiable cause.

Prerenal uraemia - kidneys hold on to sodium to preserve volume

Pre-renal uraemiaAcute tubular necrosis
Urine sodium < 20 mmol/L> 30 mmol/L
Fractional sodium excretion*< 1% > 1%
Fractional urea excretion**< 35% >35%
Urine:plasma osmolality> 1.5 < 1.1
Urine:plasma urea> 10:1 < 8:1
Specific gravity> 1020< 1010
Urine 'bland' sedimentbrown granular casts
Response to fluid challengeYes No

*fractional sodium excretion = (urine sodium/plasma sodium) / (urine creatinine/plasma creatinine) x 100

**fractional urea excretion = (urine urea /blood urea ) / (urine creatinine/plasma creatinine) x 100


NICE recommends that we can use a variety of different criteria to make an official diagnosis of AKI. They state:

Detect acute kidney injury, in line with the (p)RIFLE, AKIN or KDIGO definitions, by using any of the following criteria:
  • A rise in serum creatinine of 26 micromol/litre or greater within 48 hours
  • A 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
  • A fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than

Once diagnosed, AKI can be staged using the KDIGO classification:

StageSerum creatinineUrine output
11.5-1.9 * baseline creatine or
> 26 umol/L within 24 hours
< 0.5 mL/kg/hour for 6 hours
22.0-2.9 * baseline creatine< 0.5 mL/kg/hour for 12 hours
3> 3.0 * baseline creatine or
> 353.6 umol/L or
initiation of renal replacement therapy or
decrease of eGFR to < 35 mL/min
< 0.3 mL/kg/hour for 24 hours or
anuria for 12 hours


The management of AKI is largely supportive. This means patients require careful fluid balance to ensure that the kidneys are properly perfused but not excessively to avoid fluid overload. It is also important to review a patient's medication list to see what treatments may either be exacerbating their renal dysfunction or may be dangerous as a consequence of renal dysfunction. The table below gives some examples of common drugs:

Usually safe to continue in AKIShould be stopped in AKI as may worsen renal functionMay have to be stopped in AKI as increased risk of toxicity (but doesn't usually worsen AKI itself)
• Paracetamol
• Warfarin
• Statins
• Aspirin (at a cardioprotective dose of 75mg od)
• Clopidogrel
• Beta-blockers
• Aminoglycosides
• ACE inhibitors
• Angiotensin II receptor antagonists
• Diuretics
• Metformin
• Lithium
• Digoxin

Treatments which are not recommend include the routine use of loop diuretics (to artificially boost urine output) and low-dose dopamine (in an attempt to increase renal perfusion). There is however a role for loop diuretics in patients who experience significant fluid overload.

Specialist input from a nephrologist is required for cases where the cause is not known or where the AKI is severe.

All patients with suspected AKI secondary to urinary obstruction require prompt review by a urologist.

Renal replacement therapy (e.g. haemodialysis) is used when a patient is not responding to medical treatment of complications, for example hyperkalaemia, acidosis or uraemia.


Whilst most patients with AKI recover their renal function there are many patients who will have long term impaired kidney function due to AKI. As well as long-term morbidity, AKI may also result in acute complications including death. Whilst exact figures are difficult to calculate NICE estimate that inpatient mortality of AKI in the UK might typically be 25-30% or more.