Dr Ivan Benett discusses five key learning points from the recently updated NICE guideline on prevention, detection, and management of acute kidney injury

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Read this article to learn more about:

  • the impact of acute kidney injury (AKI) among people admitted to hospital
  • updated guidance about the risks associated with iodine-based contrast media
  • identifying, preventing, and managing AKI.

 

Between one in five and one in eight people admitted to hospital has, or develops, acute kidney injury (AKI), many of whom are elderly.1 AKI is strongly associated with poor outcomes including higher mortality and increased lengths of stay. Often, AKI results in permanent chronic renal damage, increased frailty, and difficulty managing medication.2–4

The kidney is responsible for removing toxins and water, maintaining electrolyte balance, and excreting drugs, as well as other long-term actions like vitamin D metabolism and haemopoietin production.5

In addition to poorer patient outcomes, the financial cost of AKI to the NHS is estimated at around £500 million a year.1 In an audit of care, only 50% of patients with AKI were considered to have good care.6

AKI is defined by using any of the following criteria:1

  • 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 8 hours in children and young people
  • a 25% or greater fall in estimated glomerular filtration rate (eGFR) in children and young people within the past 7 days.

Impairment of renal function can be caused by reduced perfusion, intrinsic renal disease or toxicity, or renal obstruction.7

In December 2019, NICE Guideline (NG) 148 on Acute kidney injury: prevention, detection and management was published, updating and replacing NICE Clinical Guideline (CG) 169. The updated recommendations in NG148 focus on new evidence relating to the use of iodine-based contrast media in investigations.1 However, it is worth also re-emphasising the other recommendations in the guideline that are relevant to primary care. 

1. Identify and assess AKI

Identify AKI by measuring serum creatinine and comparing with baseline in people with acute illness who are at risk (see Table 1).1

Table 1: Risk factors for acute kidney injury in people with acute illness1
Investigate for acute kidney injury, by measuring serum creatinine and comparing with baseline, in acute illness if any of the following are likely or present:
AdultsChildren and young people

Chronic kidney disease (adults with an eGFR less than 60 ml/min/1.73 m2 are at particular risk)

Chronic kidney disease

Heart failure

Liver disease

Diabetes

History of acute kidney injury

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

Young age, neurological or cognitive impairment or disability, which may mean limited access to fluids because of reliance on a parent or carer

Hypovolaemia

Use of drugs that can cause or exacerbate kidney injury (such as NSAIDs, aminoglycosides, ACE inhibitors, ARBs, and diuretics) within the past week, especially if hypovolaemic

Use of iodine-based contrast media within the past week

Symptoms or history of urological obstruction, or conditions that may lead to obstruction

Sepsis

Deteriorating early warning scores

A deteriorating paediatric early warning score

Age 65 years or over

­—

 

Severe diarrhoea (children and young people with bloody diarrhoea are at particular risk)

 

Symptoms or signs of nephritis (such as oedema or haematuria)

 

Haematological malignancy

 

Hypotension

eGFR=estimated glomerular filtration rate; NSAIDs=non-steroidal anti-inflammatory drugs; ACE=angiotensin-converting enzyme; ARBs=angiotensin II receptor antagonists

Table created from NG148, recommendations 1.1.1 and 1.1.2.

© NICE 2019. Acute kidney injury: prevention, detection and management. Available from: www.nice.org.uk/guidance/ng148 All rights reserved. Subject to Notice of rights. NICE guidance is prepared for the National Health Service in England. All NICE guidance is subject to regular review and may be updated or withdrawn. NICE accepts no responsibility for the use of its content in this product/publication. See www.nice.org.uk/re-using-our-content/uk-open-content-licence for further details.

NG148 offers further detail on assessment of AKI. There is no need to routinely perform an ultrasound of the urinary tract when the cause of AKI has been identified.1 When pyonephrosis (infected and obstructed kidney[s]) is suspected with AKI, it is recommended that ultrasound of the urinary tract be performed within 6 hours of assessment.1

If there is no identified cause of AKI or the patient is at risk of urinary tract obstruction, offer an urgent ultrasound of the urinary tract, which should be performed within 24 hours of assessment.1

Urine dipstick testing for blood, protein, leucocytes, nitrites, and glucose should be performed for all people as soon as AKI is suspected or detected.1 If the results are abnormal they must be acted upon, for example by checking for infection.

Consider a diagnosis of acute nephritis and refer to the nephrology team when patients with no obvious cause of acute kidney injury have urine dipstick results showing haematuria and proteinuria, without urinary tract infection or trauma due to catheterisation.1

2. Consider AKI in people with illness and no acute component

Consider AKI in anyone who presents with an illness but with no clear acute component. This applies to those with chronic kidney disease (CKD), especially stage 3B or worse, or with pre-existing urological disease. Also new or significantly worsening urological symptoms, or symptoms suggesting complications of AKI. Symptoms or signs of a multi-system disease affecting the kidneys and other organ systems (for example, signs or symptoms of AKI, plus a purpuric rash) may also indicate or lead to AKI.1

In people with CKD and no obvious acute illness, a rise in serum creatinine may indicate AKI rather than a worsening of their chronic disease.1

3. Assess risk factors in adults having iodine-based contrast media

Before offering iodine-based contrast media to adults for non-emergency imaging, investigate for CKD by measuring eGFR or by checking an eGFR result obtained within the past 3 months.1

Assess their risk of AKI but do not delay emergency imaging. Increased risk is particularly associated with:1

  • CKD (adults with an eGFR less than 40 ml/min/1.73 m2 are at particular risk)
  • diabetes but only with CKD (adults with an eGFR less than 40 ml/min/1.73 m2 are at particular risk)
  • heart failure
  • renal transplant
  • age 75 years or over
  • hypovolaemia
  • increasing volume of contrast agent
  • intra-arterial administration of contrast medium with first-pass renal exposure.

4. Preventing AKI

Much of the advice in NG148 refers to adults and children in hospital, but in primary care we should also think of people at risk of AKI. Consider electronic clinical decision support systems (CDSS) to support clinical decision making and prescribing, but ensure they do not replace clinical judgement.1 Modern clinical systems provide an alert if there is evidence of a significant acute rise in creatinine.

If necessary, seek advice from a pharmacist about optimising medicines and drug dosing in patients with or at risk of AKI.1 Many drugs are known to be nephrotoxic, notably non-steroidal anti-inflammatory drugs (NSAIDs), and other common drugs such as angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor antagonists (ARBs), and diuretics.7

Consider temporarily stopping ACE inhibitors and ARBs in patients with diarrhoea, vomiting, or sepsis until their clinical condition has improved and stabilised.1

Preventing AKI in adults having iodine-based contrast media will normally be the responsibility of the clinician requesting the investigation. The guideline recommends encouraging oral hydration before and after procedures that use intravenous iodine-based contrast media in people at increased risk of contrast-induced AKI. Intravenous volume expansion with either isotonic sodium bicarbonate or 0.9% sodium chloride should be considered for inpatients having iodine-based contrast media if they are at particularly high risk, for example, if:1

  • they have an eGFR less than 30 ml/min/1.73 m2
  • they have had a renal transplant
  • a large volume of contrast medium is being used (for example, higher than the standard diagnostic dose or repeat administration within 24 hours)
  • intra-arterial administration of contrast medium with first-pass renal exposure is being used.

If patients have CKD with an eGFR lower than 40 ml/min/1.73 m2, they may be asked to temporarily stop ACE inhibitors and ARBs.1

5. Manage AKI and know when to refer

Refer everyone with upper tract urological obstruction to a urologist.1 AKI in those awaiting renal replacement therapy will usually be managed by the renal team.

There is no need to refer people to a nephrologist or paediatric nephrologist when there is a clear cause for AKI and the condition is responding promptly to medical management. The exception is if they have had a renal transplant.1

In patients who may be nearing the end of life, consider discussing management with a nephrologist or paediatric nephrologist if they have severe illness that might benefit from treatment.1

NG148 suggests discussing the management of AKI with a nephrologist or paediatric nephrologist as soon as possible and within 24 hours of detection when one or more of the following is present:1

  • a possible diagnosis that may need specialist treatment (for example, vasculitis, glomerulonephritis, tubulointerstitial nephritis, or myeloma)
  • AKI with no clear cause
  • inadequate response to treatment
  • complications associated with AKI
  • stage 3 AKI (according to (p)RIFLE, AKIN or KDIGO criteria [see Table 2])
  • a renal transplant
  • CKD stage 4 or 5.
Table 2: Staging of acute kidney injury8
StageSerum creatinineUrine output

1

1.5–1.9 times baseline or

≥0.3 mg/dl (≥26.5 micromol/l) increase

<0.5 ml/kg/h for 6–12 hours

2

2.0–2.9 times baseline

<0.5 ml/kg/h for ≥12 hours

3

3.0 times baseline or

Increase in serum creatinine to ≥4.0 mg/dl (≥353.6 micromol/l) or

Initiation of renal replacement therapy or

In patients <18 years, decrease in eGFR to <35 ml/min/1.73 m2

<0.3 ml/kg/h for ≥24 hours or

Anuria for ≥12 hours

 

Kidney Disease: Improving Global Outcomes. Clinical practice guideline for acute kidney injury. International Society of Nephrology, 2012. Available at: kdigo.org/wp-content/uploads/2016/10/KDIGO-2012-AKI-Guideline-English.pdf
Reproduced with permission.

Consider referral to a nephrologist or paediatric nephrologist when eGFR remains 30 ml/min/ 1.73 m2 or less in adults, children, and young people who have recovered from an episode of AKI.1 Also consider referral to a paediatric nephrologist for children and young people who have recovered from an episode of AKI but have hypertension, impaired renal function or 1+ or greater proteinuria on dipstick testing of an early morning urine sample.1

As always, it is important to involve patients and carers in sharing ideas, concerns, and expectations, and in decision making. If appropriate, provide information about long-term treatment options, monitoring, self-management, and support to people who have had AKI (and/or their parent or carer, if appropriate) in collaboration with a multidisciplinary team appropriate to the person’s individual needs.1

Discuss the risk of developing AKI, particularly the risk associated with conditions leading to dehydration (for example, diarrhoea and vomiting) and drugs that can cause or exacerbate kidney injury (including over-the-counter NSAIDs), with people who are at risk.1

Summary

Acute kidney injury is associated with poor outcomes. It is important to reduce the risk of AKI, identify it as soon as possible, and manage the clinical situation to minimise the damage to kidney function and improve outcomes.

The main change in the update is that the committee agreed that intravenous fluids are not necessary for outpatients who are at a lower risk of contrast-induced AKI. The committee also agreed that only inpatients at particularly high risk need intravenous fluids.

In general practice, dehydration, drug toxicity and interactions, and co-morbidities such as infections are common. There are frequent opportunities to minimise the risk of AKI and improve outcomes for patients.

Dr Ivan Benett

GP, Didsbury, Manchester

Member of the guideline development group for NG148

The guideline referred to in this article was produced by the Guideline Updates Team at the National Institute for Health and Care Excellence (NICE). The views expressed in this article are those of the author and not necessarily those of NICE.

National Institute for Health and Care Excellence (2019) Acute kidney injury: prevention, detection and management. Available from www.nice.org.uk/guidance/ng148

Key points

  • Identify AKI in people with acute illness by measuring serum creatinine and comparing with baseline, in people with acute illness who are at risk (see Table 1)
  • Consider AKI in anyone who presents with an illness but with no clear acute component
  • Assess risk factors in adults having iodine-based contrast media, especially people with an eGFR <40 ml/min/1.73 m2, people with heart failure, renal transplant, age 75 years or over, hypovolaemia, when using increasing volume of contrast agent or intra-arterial administration of contrast medium with first-pass renal exposure
  • Prevent AKI by ensuring hydration and avoidance of nephrotoxic drugs. Consider temporarily stopping ACE inhibitors and ARBs in people with diarrhoea, vomiting, or sepsis
  • Manage AKI by correcting dehydration, identifying urinary tract obstruction, treating intrinsic renal disease, and minimising nephrotoxicity; know when to refer to a urology or nephrologist.

AKI=acute kidney injury; ACE=angiotensin-converting enzyme; ARBs=angiotensin II receptor antagonists; eGFR= estimated glomerular filtration rate

Implementation actions for STPs and ICSs

The following implementation actions are designed to support STPs and ICSs with the challenges involved with implementing new guidance at a system level. Our aim is to help you consider how to deliver improvements to healthcare within the available resources.

  • Consider establishing a multi-professional clinical forum to review NICE guideline 148 and coordinate a local system action plan to help prevent, identify, and manage AKI
  • Encourage primary care and community pharmacy to issue ‘sick day guidance’ for people to follow if they are taking potentially nephrotoxic medication and experience acute illness, especially diarrhoea and vomiting
  • Identify, through medication reviews and practice registers, those more at risk of AKI and look to reduce the use of nephrotoxic medication where possible
  • Establish and implement protocols for the use of contrast media in radiological practice
  • Raise awareness with first contact services of the possibility of AKI presenting as non-specific illness: include GP, out-of-hours, and community pharmacy services
  • Ensure rapid identification of AKI in patients presenting to hospital and rapid access to specialist nephrological clinical opinion.

STP=sustainability and transformation partnership; ICS=integrated care system; AKI=acute kidney injury

References

  1. NICE. Acute kidney injury: prevention, detection and management. NICE Guideline 148. NICE, 2019. Available at: www.nice.org.uk/ng148
  2. Ortiz-Soriano V and Neyra J. The impact of acute kidney injury on frailty status in critical illness survivors—is there enough evidence? J Emerg Crit Care Med 2018; 2: 93.
  3. Parr S and Siew E. Delayed consequences of acute kidney injury. Adv Chronic Kidney Dis 2016; 23 (3): 186–194.
  4. Ostermann M, Chawla L, Forni L et al, ADQI 16 workgroup. Drug management in acute kidney disease – report of the acute disease quality initiative XVI meeting. Br J Clin Pharmacol 2018; 84: 396–403.
  5. National Kidney Foundation. How your kidneys work. www.kidney.org/kidneydisease/howkidneyswrk (accessed 10 February 2020).
  6. National Confidential Inquiry into Patient Outcome and Death. Adding insult to injury—a review of the care of patients who died in hospital with a primary diagnosis of acute kidney injury (acute renal failure). NCEPOD, 2009. Available at: www.ncepod.org.uk/2009report1/Downloads/AKI_report.pdf
  7. NICE. Acute kidney injury. NICE Clinical Knowledge Summary, 2018. Available at: cks.nice.org.uk/acute-kidney-injury
  8. Kidney Disease: Improving Global Outcomes. Clinical practice guideline for acute kidney injury. International Society of Nephrology, 2012. Available at: kdigo.org/wp-content/uploads/2016/10/KDIGO-2012-AKI-Guideline-English.pdf