Acute Kidney Injury (AKI)


Acute Kidney Injury (AKI) was previously known as acute renal failure, and means a sudden reduction in renal function. It is associated with increased mortality, can have many different underlying causes, and is not a result of traumatic injury.

Significance in Primary Care

  • AKI is a marker of the sick patient who requires prompt treatment
  • Episodes of AKI cause and increase progression of Chronic Kidney Disease (CKD)
  • Up to two-thirds of patients who sustain AKI leading to hospital admission do so in the community
  • Clear management plans are required after recovery from AKI

Related Clinical Referral Guidelines:


Risk Groups

Patient factors:

  • Elderly
  • CKD
  • Diabetes
  • Heart failure
  • Liver disease

Clinical factors:

  • Dehydration
  • Hypotension
  • Sepsis
  • Post-operative


  • Increase in serum creatinine by greater than 26micromol/L within 48 hours; or
  • Increase in serum creatinine by greater than or equal to 1.5 x baseline which is known or presumed to have occurred within the prior 7 days; or
  • Urine volume less than 0.5 ml/kg/h for 6 hours

It is common to see patents with an increase in serum creatinine and a long gap between current value and baseline. In this situation consider:

  • Is the patient acutely unwell? If so AKI is more likely to be present and need action
  • Repeating the creatinine within 48-72 hours. This will help to determine whether the changes are stable (suggestive of CKD)

Stages of AKI

  1. Increase in serum Creatinine of 1.5 - 1.9 times x baseline level or creatinine rise greater than 26 micromol/L within 48 hours
  2. Increase in serum Creatinine to 2.0 - 2.9 times baseline level
  3. Increase in serum Creatinine greater than or equal to 3 or more times baseline level or has risen greater than 1.5 x baseline to greater than 354 micromol/L

Red Flag

Red Flags - discuss with nephrology

  • Blood and Protein (≥2+) on urinalysis in the absence of infection / traumatic catheterisation
  • Vasculitic rash, arthralgia, epistaxis or haemoptysis
  • Following introduction of a new drug (PPI, NSAID, antibiotic, diuretic, allopurinol) without other explanation for AKI and where cessation of the drug has not led to resolution
  • Hypercalcaemia
  • CKD stage 4 or 5 at baseline
  • Prior renal transplant
  • AKI Stage 3 should usually be managed by Nephrology


  • Most cases occur in conjunction with an acute illness and are a result of sepsis, dehydration, hypotension or medication effects. This is commonly seen in patients with long term conditions or the frail / elderly
  • 5-10% of AKI is due to obstruction
  • Intrinsic renal disease is rare but early referral is important. This includes drug induced nephritis, vasculitis, glomerulonephritis and myeloma


Is this definitely AKI?

Not every patient with a rise in creatinine will have a recent baseline to compare. The result has to be taken in clinical context, and if the situation allows a repeat creatinine (after 48-72 hours) may help distinguish dynamic changes in serum creatinine from a more stable CKD picture.

Is the patient acutely unwell?

If so this should increase clinical concern.

How severe?

Increasing severity correlates with worse outcomes. AKI stage 3 should be managed in secondary care.


Is there obstruction / intrinsic renal disease. Dip the urine.

  • Negative urinalysis – usually pre renal but consider drug causes including iodinated contrast media within the past week
  • ≥2+ blood and protein consider intrinsic renal disease if no UTI / recent traumatic catheterisation

Avoid / correct dehydration

Medication review, consider stopping

  • ACEi / ARB, and diuretics
  • Metformin (to reduce risk of lactic acidosis)
  • NSAIDs
  • new drugs such as antibiotics / PPIs may be responsible for AKI

See here for a more comprehensive list regarding optimising medication in patients with AKI

Early review with repeat Renal Biochemistry (Na, K, Creatinine but don't routinely measure Urea)

Following an episode of AKI

Assess degree of recovery
  • Even after hospital discharge with resolved AKI, Renal Biochemistry and proteinuria should be checked 3-6 months later
  • For patients who haven't returned to their normal baseline renal function, consider checking Renal Biochemistry until the creatinine level stabilises
  • If patient has new onset CKD assess proteinuria and Renal Biochemistry at 3 months
  • Contact Nephrology if concerned about a significant reduction in renal function
Review medications
  • Restart antihypertensives as BP rises during recovery, check Renal Biochemistry 1-2 weeks after restarting ACEi / ARB
  • If aspirin (75mg once daily) was stopped then restart. This dose is not nephrotoxic
  • If a drug was implicated as causing AKI, then record an adverse reaction in the medical record

Code the occurrence of an AKI episode and if secondary to medication then code as a Drug sensitivity

Reducing the risk of AKI

  • Patients at risk of AKI should temporarily stop certain medication during acute illness, especially when at risk of dehydration. ACEi/ARB can be temporarily stopped without risk even in heart failure. Greater care is needed in stopping diuretics in patients with moderate / severe heart failure
  • Consider checking renal function in patients at increased risk of AKI with intercurrent illness
  • Avoid long term prescription of NSAIDs, especially in patients at risk of AKI
  • Avoid prescribing triple combination of ACEi/ARB, NSAIDS and spironolactone
  • Check Renal Biochemistry one week after starting
    • Loop diuretics in patients with CKD
    • Spironolactone
    • ACEi/ARB (could be delayed to two weeks in patients at lower risk of AKI, to allow hypotensive effect to be measured at the same time)


Referral Instructions

e-Referral Service Selection

  • Specialty: Nephrology
  • Clinic Type: Nephrology
  • Service: DRSS-Northern-Nephrology-Devon CCG- 15N

Supporting Information

Patient Information

At risk of AKI

Following AKI


NHS England AKI Programme (Think Kidneys)

NICE Acute kidney injury: prevention, detection and management

Clinical guideline [CG169] Published 2013

Pathway Group

This guideline has been signed off by the Pathology Optimisation Clinical Group on behalf of NEW Devon CCG.

Publication date: April 2017


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