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Detection and Management of Acute Kidney Injury:A Guide for Primary Care

Publication date March 2016

Detection and Management of Acute Kidney Injury: A Guide for Primary Care

Review Date June 2016

Table of Contents

Subject Page No1. An Overview of Acute Kidney Injury 22. Testing for AKI in Primary Care 43. Responding to AKI Warning Stage Test Results in Primary Care 84. Managing Patients with AKI in Primary Care 145. Post-AKI Management in Primary Care 156. Acknowledgements 17

AppendicesA. Thinking Sepsis and Acute Kidney Injury in Primary Care 18B. Timeliness in response AKI warning stage test results in primary care 19C. Flow diagram to support post AKI management in primary care 20D. Useful resources 21E. National AKI algorithm 22F. Think Safety ensuring safe and reliable systems for managing tests 23G. Audit measures 24H. Reflective template for AKI case studies 25

References 26

DisclaimerTo the best of our knowledge, the contents of this publication are in line with National Institute for Health and Care Excellence guidance relating to the management and treatment of acute kidney injury. Professional advice should be sought before taking, or refraining from taking, any action on the basis of the content of this publication. We cannot be held responsible for any errors or omissions therein, nor for the consequences of these or for any loss or damage suffered by readers or any third party informed of its contents. The UK Renal Registry disclaims all liability and responsibility arising from any reliance placed on the information contained in this publication by you or any third party who may be informed of its contents.

Detection and Management of Acute Kidney Injury: A Handy Guide for Primary Care1

Detection and Management of Acute Kidney Injury: A Handy Guide for Primary Care 2

1. An Overview of Acute Kidney Injury

What is AKI? Acute kidney injury (AKI) simply means a sudden reduction in renal function resulting in a difficulty to maintain fluid, electrolyte and acid-base balance. The term has replaced ‘acute renal failure’ and includes earlier stages of kidney damage other than just ‘failure’. 1 The diagnosis of AKI and its staging is based on acute changes in serum creatinine and/or a reduction in urine output (see Box 2 on page 9).1 2 It is not a traumatic injury to the kidney as the name may imply, rather a clinical syndrome with many different underlying causes.1

What Causes AKI? There are many causes of AKI. However, it usually occurs within the context of other serious illness (e.g. sepsis) on a background of increased risk.1-3 Most cases occur in conjunction with co-existing acute illness and are a result of sepsis, hypovolaemia, hypotension or medication effects; these causes, often in combination, account for up to 80% of cases. 4 This scenario is commonly associated with frailty and is seen in patients with co-morbidities including diabetes, chronic kidney disease (CKD), chronic liver disease and heart failure. Post renal urinary tract obstruction (e.g. bladder outflow obstruction) accounts for between 5 to 10% of cases of AKI. 4 Intrinsic renal diseases are less common, but are important not to miss because it is crucial that specialised management of these cases is accessed early. This category includes a variety of less common conditions such as: drug induced tubulo-interstitial nephritis, vasculitis/rapidly progressive glomerulonephritis and myeloma.

Medications also impact on AKI. Some, such as NSAIDs, will directly increase the risk of AKI. Diuretics may worsen hypovolaemia. ACE inhibitors (ACEi) and angiotensin receptor blockers (ARB) reduce the ability of the kidney to adapt to changes in perfusion pressure. One of the actions of ACEi and ARBs that account for their reno-protective effects in diabetic nephropathy and proteinuric CKD is the reduction in efferent glomerular arteriolar tone. However this action also reduces the ability to maintain glomerular filtration pressure in the face of hypovolaemia/hypotension. However, all anti-hypertensive medication should be reviewed as low blood pressure is a major contributor to AKI.

Why is AKI Important?AKI is extremely common in hospitalised patients, occurring in 10-20% of emergency hospital admissions, and is associated with extremely poor outcomes.5 However, AKI is not just a secondary care problem – primary care has a crucial role to play, particularly in prevention, early detection and management as well as post-AKI care.

Poor outcomes associated with AKI include:Extremely high mortality rates (more than 20% of patients with AKI will die during hospital admission, rising to >35% in those with AKI stage 3)5

Increased length of hospital stay and higher healthcare resource utilisation1 6

Incomplete recovery of kidney function – many patients will be left with Chronic Kidney Disease (CKD) and/or are at increased risk of progressive loss of GFR over time1 7


Increased risk of poor long term outcomes: reduced life expectancy, increased cardiovascular risk, and poorer quality of life1

In part, these poor outcomes reflect the fact that AKI acts as a ‘force multiplier’ and increases severity of co-existing acute illness. In essence, AKI is a marker of the ‘sick patient’ who requires prompt recognition and management.

Why does Primary Care have an important role?Think Prevention: Up to two-thirds of patients with AKI have already developed it by the time they are admitted to hospital, so preventative strategies need to include a focus on pre-hospital care.5

Think Early Detection and Management: From April 2016, AKI Warning Stage Test Results generated from electronic detection systems situated in biochemistry labs will be sent to primary care, aiming to make changes in serum creatinine concentration are easier to spot (see Appendix D). There is a need to ensure that these test results are considered in a clinical context, with an imperative of treating the patient, not the test result.

Think Post-AKI Care: Improvements are required at discharge from hospital for patients who have had an episode of care complicated by AKI. Patients who have recovered from AKI need clear plans for follow up including review of long term medications that may have been stopped during admission.8 9


2. Testing for AKI in Primary Care

NICE Clinical Guidelines for AKI recommend ‘identifying acute kidney injury in patients with acute illness’ who are deemed at risk of AKI. In primary care, a decision as to whether or not to check kidney function needs to be tailored to the individual circumstance.2 Consideration needs to be given as to whether this will support clinical management. For example, blood tests are not necessary when immediate admission is required (e.g. there is evidence of ‘red flag sepsis’).10 At the other end of the spectrum, checking kidney function tests may not be necessary for patients presenting with a minor self-limiting acute illness, such as a single episode of diarrhoea or vomiting.

Appendix A (Double click to open in full) outlines steps to consider when assessing and managing episodes of illness in primary care (Double click to open in full). Recognising the overlap between sepsis and AKI, the algorithm incorporates guidance developed by The UK Sepsis Trust with NICE guidance regarding the detection and management of AKI. Key factors to consider include2 10 11:

Might this be more that a self-limiting infection/illness?Consider a lower threshold for further clinical evaluation if ONE or MORE of the following are present:

Symptoms of systemic infection (e.g. recent history of fever)History of acute deterioration (despite antibiotic therapy)Unexplained illness

Think Susceptibility & Exposure: As highlighted by the Kidney Disease Improving Global Outcomes (KDIGO) guidelines, ‘it is the interaction between susceptibility and the type and extent of exposure to insults that determines the risk of occurrence of AKI’.1 AKI normally occurs within the context of other illness (e.g. sepsis) on a background of risk. Box 1 outlines risk factors that lower the threshold for clinical evaluation.1 2


Box 1. Risk Factors associated with Acute Kidney Injury1 2

Patient specific - Susceptibility Situation specific - Exposure

Increasing age

Immunosupressed or deficient immunity e.g. malnutrition, patients with cancer

CKD (eGFR <60)

Diabetes mellitus

Heart failure

Liver disease

Past history of AKI

Neurological or cognitive impairment or disability, which may mean limited access to fluids because of reliance on a carer

Symptoms or history of urinary tract obstruction, or conditions that may lead to obstruction

Hypovolaemia, dehydration, reduced oral intake

Hypotension

Sepsis

Post-operative

Use of iodinated contrast agents within the past week

Use of drugs such as non-steroidal anti-inflammatory drugs [NSAIDs], angiotensin-converting enzyme [ACE] inhibitors, angiotensin II receptor antagonists [ARBs] and diuretics) within the past week, especially if hypovolaemic

Primary care assessment of acute illness

Think Sepsis: Clinical evaluation of acute illness requires an assessment for System Inflammatory Response Syndrome (SIRS) and Sepsis.10-12 If present, the patient needs to be assessed for evidence of Red Flag Sepsis, which requires immediate admission (see Appendix A (Double click to open in full)).

The National Confidential Enquiry into Patient Outcome and Death (NCEPOD) report into sepsis recommends that ‘an early warning score, such as the National Early Warning Score (NEWS) should be used in both primary care and secondary care for patients where sepsis is suspected. This will aid the recognition of the severity of sepsis and can be used to prioritise urgency of care.’12


Think Hypotension: The development of absolute hypotension (systolic blood pressure less than 90 mmHg) or relative hypotension (an unexpected fall of 40 mmHg from a previous baseline even if blood pressure remains within the normal range) is a clinical red flag. In this setting, consider hypovolaemia, red flag sepsis, review all anti-hypertensive drugs and consider the need for hospital admission.10 11

Think Hypovolaemia:Hypovolaemia associated with any type of insult including dehydration or over-diuresis is probably the most modifiable risk factor for acute kidney injury. Patients who are particularly at risk of dehydration in the community include those who have neurological or cognitive impairment or disability, which may mean limited access to fluids because of reliance on a carer.2

Assessment of volume status is essential. In the community, this requires the clinician to be aware of CKD status and all prescribed and over the counter medications such as ACEi, ARB, NSAIDS and diuretics. Assessment should also include questions on fluid intake and output with a physical examination.* Note that patients may develop oliguric as well as non-oliguric acute kidney injury. If there is evidence of hypovolaemia, admission should be considered for appropriate intravenous fluid replacement and monitoring.

*Note that no single clinical sign is sufficiently sensitive or specific for the diagnosis of hypovolaemia. Consider pulse, blood pressure, JVP, capillary refilling, dry axillae, recent change in weight and postural change in pulse and BP.3 13

Key questions to consider:Is there evidence of poor oral intake/urine output? Is the patient on any medication that may increase the risk of hypovolaemia? e.g. diuretics or may limit the homeostatic response of the kidney to changes in blood pressure e.g. NSAIDSDoes the patient need and have support to ensure they maintain adequate fluid intake and volume status? Is there evidence of hypovolaemia?Is the patient hypotensive?Is there evidence of SIRS +/- Sepsis or Red Flag Sepsis?

Factors prompting acute referral and immediate admissionChecking kidney function needs to be considered in the context of the patient’s clinical history. Testing for biochemical evidence of AKI may not be necessary if the history points towards a minor self-limiting illness. Equally, (re)checking blood tests is not necessary if there are factors indicating the need for immediate transfer for acute medical assessment. As indicated in Appendix A (Double click to open in full), these include10:

Evidence of Red Flag SepsisSepsis with no history of improvement, despite antibiotic therapy and supportive measuresEvidence of a deteriorating patient - change in Early Warning Score12

No clear source of infectionInsufficient professional and carer support to manage the patient in the community


AKI and complicating factors including: o Moderate or severe hyperkalaemia (K≥6.0mmol/l)o Pulmonary oedemao Poor oral intake/urine outputo Suspected intrinsic renal diseaseo CKD stage 4 or 5 or history of renal transplant, especially with other co-morbiditieso Suspected urinary tract obstruction

Testing for AKI in the communityTesting renal function needs to support clinical decision making. Consider testing for AKI in:

Patients with an acute illness managed in primary care who do not necessarily need hospital admission but who may warrant clinical review within 24 to 48 hours. Patients with an illness with no clear acute component who have:

o Unexplained illnesso New or significantly worse urological symptomso Symptoms or signs of multi-system diseaseo Suspected Intrinsic Renal Disease (see page 12)

Should a decision be made to check for AKI in primary care, then it’s important to ensure timely review of the results and that systems are in place to ensure the test result is considered in a clinical context. Appendices A and B provide guidance to support a timely and appropriate initial response to AKI Warning Stage Test Results in Primary Care. Appendix F outlines factors to support appropriate testing and response. These include providing sufficient detail of the clinical history with the test request as well as ensuring information is available (e.g. hand over form) for both in and out of hours care.


3. Responding to AKI Warning Stage Test Results in Primary Care

AKI is a clinical syndrome, not merely a biochemical diagnosis. As such, there is a need to ensure that test results are considered with an understanding of the clinical context in which a blood test was taken. Communicating and providing access to salient clinical information when taking blood tests through use of laboratory forms, in medical records, and through hand over documents can help support a timely and appropriate response to a test result (see Appendix F). This is particularly important when the alert is communicated out of hours to GPs with no knowledge of the patient. This section is not exclusive but highlights key factors to consider when initially responding to an AKI Warning Stage Test Result in primary care:

What is an AKI Warning Stage Test Result? Is it AKI?What is the stage of AKI?Is there a history of acute illness? Are there any complicating factors?o Hyperkalaemiao Is there evidence of poor oral intake/urine output Does the patient have existing significant co-morbidities and risk factors? o AKI Warning Stage Test Results in the context of Chronic Health Failureo AKI Warning Stage Test Results in the context of Chronic Kidney Disease Has there been a recent increase in dose of diuretics, ACE Inhibitors, Angiotensin Receptor Blockers or Aldosterone Antagonists?Is Intrinsic Renal Disease suspected?Is urinary tract obstruction suspected?

What is an AKI Warning Stage Test Result? Generation of an alert for AKI is best regarded as a two-step process. The first stage is the detection of creatinine changes consistent with AKI. This will be delivered by the NHS England detection algorithm running in the laboratory information management system (LIMS) (see Appendix E). This algorithm automatically identifies potential cases of acute kidney injury from laboratory data in real time and produces a test result (i.e. AKI stage 1, 2 or 3). The test result is named an ‘AKI Warning Stage’.

The second stage of the process is the communication of the AKI result to clinicians – the alerting phase of the process. Positive AKI Warning Stage results will be sent from the laboratory system to General Practice Clinical Systems either through interruptive and/or non-interruptive methods of communication. Systems need to be established to ensure timely communication of test results to both in and out of hours primary care services (see Appendix F). 14

Once a test result is communicated, the primary care team need to decide how quickly (if at all) to act on the test results, and what action to take. Appendices A & B provide guidance to support a timely and appropriate initial response to AKI Warning Stage Test Results in Primary Care. With recognition that computerised algorithmic interpretation of serum creatinine tests may generate


both false positives (‘Pseudo-AKI’) and false negatives (‘Atypical AKI’),1 a key question to consider is ‘What was the reason for blood test?’

Is it AKI? The presence of AKI is determined using internationally recognised criteria that are based on individualised changes in serum creatinine concentration with respect to that person’s usual (or baseline) value, and/or reduction in urine volume (see Box 2).1 In practice, the urine output criteria can only be applied to hospitalised patients who are catheterised. However, a reliable history of low or absent urine output should alert the clinician to the possibility of AKI.

Box 2. Staging of Acute Kidney Injury1 (see also Appendix E)

Access to clinical information is important in order to ascertain whether an AKI Warning Stage Test Result represents true AKI. As indicated in Box 2, AKI is defined by any of the following:

Increase in serum creatinine by >26micromol/L within 48 hours; orIncrease in serum creatinine by >1.5 times baseline, which is known or presumed to have occurred*within the prior seven days; or Urine volume <0.5 mL/kg/h for six hours

* This is crucial, because it is common to see patients with an increase in serum creatinine and longer gap between current value and baseline. In this situation, factors to consider include (see also Appendix A (Double click to open in full)):

Is the patient acutely unwell? If so, AKI is more likely.Check if the patient has had a previous creatinine result Is there at least a 50% rise in creatinine?


Adults:

AKI stage 1 is a rise of >1.5x baseline level, or of >26 micromol/L within 48h, or a urine output

<0.5mL/kg/h for 6-12h

AKI stage 2 is a rise of>2x baseline or a urine output <0.5mL/kg/h for ≥12h

AKI stage 3 is a rise of>3x baseline or a rise of >1.5 baseline to >354 micromol/L, a urine output

<0.3mL/kg/h for ≥24h or anuria for ≥12 h

For age <18 years, AKI stage 3 is also defined as a rise in serum creatinine to >3 x the upper limit

of the age-related reference range. The urine output criteria also differ for age <18 years: stage 1

is <0.5mL/kg/h for >8h; stage 2 is <0.5mL/kg/h for more than 16h; stage 3 is <0.3mL/kg/h for 24h

or anuria for 12h.

Is this a false alert? o Is the patient known to have chronic kidney disease (CKD) and is the change in serum

creatinine due to progression of CKD rather than an acute change? o Particularly consider this if the baseline creatinine values are from nearly 12 months ago

or if their real ‘baseline’ creatinine values are different from the one being used by the AKI Algorithm (see Appendix E). Look at all the serum creatinine or eGFR values over a longer period of time to see the pattern.

o Has the patient been treated with Trimethoprim? This drug can cause an increase in serum creatinine without changing Glomerular Filtration Rate, by inhibiting tubular secretion of creatinine – and can thus cause a ‘false positive’ test result.

o Has the patient recently completed a pregnancy? Serum creatinine naturally falls during pregnancy, so a rise in creatinine after delivery may cause a false positive warning stage test result.

o Depending on the clinical history, consider repeating the creatinine within 48-72hrs. A repeat creatinine will help to determine whether the changes are dynamic or are stable (i.e. more consistent with CKD).

What is the stage of AKI?The severity of AKI is described by categorising into three stages, with stage 1 being the least severe and stage 3 being the most severe (see Box 2).1 Appendix B (Double click to open in full) provides guidance on the timeliness of clinical response according to stage, with consideration of a more prompt response required with increasing severity irrespective of other clinical factors.

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

Is there a history of acute illness? If a blood test has been taken in the context of an episode of acute illness, then consider AKI likely until proven otherwise irrespective of stage. What was the reason for the blood test? Have kidney function blood tests been taken in the context of a patient presenting with an episode of acute illness but which was deemed not to require immediate admission at the point of initial assessment? – see Appendices A & B (Double click to open in full) to support timely assessment and management. Examples for consideration include patients who have had blood tests taken in the context of an episode of acute illness such as diarrhoea or vomiting caused by gastroenteritis, urinary tract infection, or respiratory infection. Reviewing the patient to assess for evidence of SIRS, sepsis and Red Flag Sepsis will help determine appropriate management (see previous section and Appendix A(Double click to open in full)).10 11

Are there any complicating factors?

Hyperkalaemia The presence of hyperkalaemia is a complicating factor and its presence needs to be considered when responding to AKI Warning Stage Test Results. Appendix B(Double click to open in full) provides


guidance on the timeliness in response to AKI Warning Stage Test Results indicating prompt review of AKI in the presence of moderate to severe hyperkalaemia (potassium level ≥ 6.0 mmol/l).15 16

The Renal Association guidelines recommend that all patients with severe hyperkalaemia (≥ 6.5 mmol/l irrespective of kidney function) are referred to secondary care for immediate assessment and treatment.15

http://www.renal.org/guidelines/joint-guidelines/treatment-of-acute-hyperkalaemia-in-adults#sthash.T3aoglXt.f4WXgntA.dpbs

Evidence of poor oral intake/urine output Pre-renal causes of AKI are common. Management in the community includes ensuring maintenance of fluid intake and correction of hypovolaemia. Patients who are particularly at risk of developing acute kidney injury (and worsening clinical state) in the community include those who have neurological or cognitive impairment or disability, which may mean limited access to fluids because of reliance on a carer.2

As indicated in the previous section and Appendix A (Double click to open in full), all acutely ill patients in primary care require assessment of their volume status. Recognising that assessment of fluid balance differs between primary care and secondary care, evaluation of volume status should be based on history, cumulative fluid balance and clinical examination. Consider a history of poor oral intake and urine output based on history and clinical examination (including pulse, blood pressure (BP), jugular venous pressure, capillary refilling, dry axillae; recent change in weight and postural change in pulse and BP; and absence of signs of fluid overload including peripheral oedema).3 13

Key questions to considerIs the patient drinking?Is the patient able to tolerate fluids?Does the patient need and have support to ensure adequate fluid intake and volume status?

Does the patient have existing significant co-morbidities and risk factors? Appendix A(Double click to open in full) and Box 1 highlight factors to consider when responding to an AKI Warning Stage Test Result. Responding to test results in patients with Chronic Heart Failure and/or Chronic Kidney Disease require particular attention.

AKI Warning Stage Test Results in the context of Chronic Heart FailurePatients with chronic heart failure represent a population with increased morbidity and mortality, and account for 5% of all emergency medical admissions to hospital.17 Responding to AKI Warning Stage Test Results generated for patients with known chronic heart failure requires particular attention as:

Patients are at increased risk of acute kidney injury during episodes of acute illness.2 Patients with chronic heart failure require increased monitoring of their renal function: Pharmacological treatment of chronic heart failure can include use of angiotensin-converting enzyme (ACE) inhibitors, angiotensin 2 receptor antagonists (ARB), aldosterone antagonists and diuretics, all of which have a renal effect.17




Better evidence on how to respond to changes in serum creatinine in the context of chronic heart failure is needed. Trade-offs exist, and whilst awaiting an evidence base, an important rule of thumb is to treat the patient and not the blood result. In order to put the blood test in a clinical context, key questions to consider include:

What is the patient’s clinical status and stability? What is the patient’s volume status: is the patient fluid overloaded? About right? Or is it possible that they have become over-diuresed? In which case, hypovolaemia may be causing genuine AKI.Does the patient have an inter-current acute illness?Has there been a recent increase in the dose of pharmacology therapy (diuretics, ACE Inhibitors, ARBs, aldosterone antagonists)?

AKI Warning Stage Test Results in the context of CKDCKD is the most consistently reported condition associated with acute kidney injury and it’s advised that measuring serum creatinine should be carried out in adult patients who have CKD and present with an episode of acute illness.2 7

As indicated above, it is important to determine whether the AKI Warning Stage Test Result represents true AKI (see page 9). Appendix B (Double click to open in full) provides consensus based guidance on the timeliness of response to Warning Stage Test results in context of CKD stages 4, 5 or in a patient who has had a history of a renal transplant.18 They reflect NICE guidance, which recommends discussing the management of these patients with a nephrologist as soon as possible.2

Has there been a recent increase in dose of diuretics, ACE Inhibitors, Angiotensin Receptor Blockers or Aldosterone Antagonists?As indicated within NICE Guidance (cg169), it is important to assess whether the introduction, or change in dose, of a diuretic, ACE Inhibitor, ARB, or aldosterone antagonist may have contributed to a significant rise in serum creatinine.2 7 17

Current guidance is that serum creatinine should be checked one week after initiation of ACEI/ARB and that an increase of up to 30% from baseline is acceptable, as long as this rise is stable. 7 This rise reflects the changes in glomerular haemodynamics as above and is not a sign of nephrotoxicity. AKI would only be diagnosed if this rise was greater than 50% (the increment of >26µmol/l does not apply because the gap between blood tests should be >48hrs).1

Is Intrinsic Renal Disease suspected?Think about acute nephritis based on history or examination including evidence of proteinuria and haematuria on urinalysis without evidence of urinary tract infection, or trauma due to catheterisation. Consider systemic symptoms associated with intrinsic renal disease: arthralgia, arthritis, mononeuritis multiplex, rash, uveitis, epistaxis or haemoptysis. There are some ‘red flag’ signs that help to identify this group of AKI patients so they can be referred to nephrology early . 1 2

19Key questions to consider:


Has urinalysis been carried out and what did it show? o DIP THE URINE: this is an important diagnostic step. o AKI and negative urinalysis: usually pre-renal causes (also consider drug causes).o AKI with blood and protein only (without evidence of UTI, or trauma due to

catheterisation): wider differential diagnosis that includes intrinsic renal disease. In the absence of an obvious cause of AKI, consider if any new drugs have been introduced that have a temporal relationship to the change in renal function: especially antibiotics and PPIs.o AKI in relation to the introduction of a new drug (PPI, NSAID, antibiotic, diuretic,

allopurinol) without any other explanations for AKI (NB, eosinophilia should increase suspicion, but many patients with drug-induced interstitial nephritis do not have eosinophilia).

AKI with systemic symptoms of inflammatory process: vasculitic rash, arthralgia, epistaxis or haemoptysis.AKI in context of high calcium (hypercalcaemia can cause AKI; may also be an indicator of myeloma).

If there are clinical pointers to intrinsic renal disease, these patients will need specialist referral. Appendix B(Double click to open in full) provides consensus based guidance on the timeliness of response to AKI Warning Stage Test Results in cases where intrinsic renal disease is suspected. They reflect NICE guidance, which recommends discussing the management of AKI with a nephrologist as soon as possible when there is possible tubulointerstitial nephritis, glomerulonephritis (indicated by haematuria/proteinuria), systemic vasculitis, or myeloma.19

Is urinary tract obstruction suspected? Consider urinary tract obstruction when history or examination suggests the patient may have renal stones, pyonephrosis, blocked catheter, pelvic mass, enlarged prostate, known prostate or bladder disease, abdominal or pelvic carcinoma, retroperitoneal fibrosis, known previous hydronephrosis, recurrent UTI; or other conditions consistent with possible obstruction, for example anuria, single functioning kidney, or neurogenic bladder.1 2 19

N.B. Think about concomitant pathologies (e.g. pre-renal and post-renal) contributing to the development of AKI.

Think about the cause of AKI and if clinical assessment points to evidence of urinary tract obstruction then the patient needs urgent specialist urology referral. Guidance on timeliness in response is highlighted in Appendix B(Double click to open in full) .


4. Managing patients with AKI in Primary Care

Management of the patients with an episode of care complicated by AKI depends on identification of the underlying causes. As highlighted in the previous sections, placing an AKI Warning Stage Test Result in a clinical context is important in order to determine a timely and appropriate initial response. Depending on the stage of AKI and underlying cause(s), some patients will require early referral to secondary care whilst for some patients management in primary care may be an appropriate next step. Though clinical judgement must always prevail, Appendices A and B aim to support decision making. If any clinical doubt, then consider discussion with the local on-call nephrology/medical team.

Key factors prompting urgent review and acute referral to hospital include:

An AKI Warning Stage 3 Test Result

AKI in the context of moderate or severe hyperkalaemia irrespective of the stage of AKI

Suspected urinary tract obstruction

Suspected intrinsic renal disease

Clinical deterioration and concern irrespective of AKI (e.g. AKI in presence of Sepsis)

Key steps underpinning primary care management of patients with care complicated by AKI:

Avoid/correct dehydration

Conduct a medication reviewo Refer to Think Kidneys Medicines Optimisation Toolkit for AKI (see Appendix D)o Are there any new drugs with temporal relationship to onset of AKIo Consider temporary cessation of ACEi, ARB, diuretics, antihypertensive medication;

metformin2 3 o Stop NSAIDS (prescribed or OTC)

Early clinical review with repeat kidney function testIf getting worse, discuss with the on call medical/nephrology team


https://www.thinkkidneys.nhs.uk/aki/wp-content/uploads/sites/2/2015/11/Medicines-optimisation-toolkit-for-AKI-v13.pdf

5. Post-AKI Management in Primary Care

This section outlines key steps to consider for patients who have had an episode of care complicated by AKI. This applies to patients who have either been managed in primary care and those who have had a recent hospital admission.

Develop an AKI Register Care complicated by AKI represents a significant episode of illness and should be coded and remain active in a patient’s electronic medical records. A history of AKI is a marker of vulnerability and creating an AKI register will help capture a patient population who are at higher risk of future AKI and associated complications. Registers may help audit and feedback and in doing so support quality improvement (see Appendix G). 8

Read codes for AKI include:Acute Kidney Injury (K04.|12Hq7|C|Acute kidney injury)AKI 1 (K04C.|00HqU|C|Acute kidney injury stage 1)AKI2 (K04D.|00HqV|C|Acute kidney injury stage 2)AKI3 (K04E.|00HqW|C|Acute kidney injury stage 3)

Plan ‘post-AKI’ care AKI is a marker of a significant episode of illness. A national CQUIN has been introduced to improve the quality of hospital discharge summaries for patients who have had AKI.9 Within general practice, creating and communicating a plan of care includes documenting:

The diagnosis of AKI (even when not the primary diagnosis)The stage of AKIThe reasons/causes for the AKIOutcome of a medicines reviewWhether blood monitoring is required including frequencyCommunication with patients about AKI and associated risks o Read code 8OAGA review date aligned with a future medication review

Key factors to consider:

Assess degree of renal recoveryUse the creatinine at discharge and consider whether a repeat measure of renal function is required for those patients who have not returned to their normal baseline renal function.2 7 As stated with NICE Guidelines for CKD, monitor for the development or progression of CKD for at least 2 to 3 years after an episode of care complicated by AKI, even if the serum creatinine has returned to baseline. Consider rechecking serum creatinine at 3 months post AKI to assess for development or progression in CKD.7


If you are concerned about a significant reduction in renal function following an episode of AKI, then contact nephrology for advice.

Review and optimise medicines managementRestart appropriate medications that may have been stopped during an AKI episode:

Blood pressure tablets are often stopped but consider restarting when blood pressure rises during recovery.ACEi/ARB can be restarted (unless specific advice to the contrary) once the renal function has stabilised – kidney function and electrolytes should be checked within 1-2 weeks after reintroduction.7 17 Cardiovascular risk: if aspirin (75mg once daily) and statins were stopped, these should be restarted unless specific reason not to. Aspirin 75mg is not nephrotoxic. If a drug has been specifically implicated in causing AKI (e.g. PPI leading to interstitial nephritis or NSAIDs), practice records should be updated to prevent the patient receiving these in future.

Communicate kidney health with patientsProvide patients (and carers) with information about AKI2: Patient leaflet https://www.thinkkidneys.nhs.uk/aki/wp-content/uploads/sites/2/2015/11/BKPA-RCGP-A4-Printout-Plain-Leaflet_v2.pdf


https://www.thinkkidneys.nhs.uk/aki/wp-content/uploads/sites/2/2015/11/BKPA-RCGP-A4-Printout-Plain-Leaflet_v2.pdf



6. Acknowledgements

RAND Panel members

Members of Think Kidneys workstreams

Royal Derby Hospital and Southern Derbyshire CCG

NIHR CLAHRC Greater Manchester

NIHR Greater Manchester Primary Care Patient Safety Translational Research Centre

Royal Berkshire NHS Foundation Trust

Central Manchester Foundation Trust, Salford Royal Foundation Trust & Salford CCG

NIHR CLAHRC West/ University of Bristol

Add others as document evolves and wider engagement


Appendix C: Flow Diagram to support Post-AKI Management in Primary Care


Step 1Monitoring kidney health: Has renal function recovered?

Consider repeat creatinine after 2-4 weeks to assess for further recoveryNew onset CKD: check proteinuria and repeat renal function in three months, manage as per CKD guidelinesSignificant decline in renal function: consider nephrology referral (≥25% decline in eGFR or change in CKD stage)Monitor for the development or progression of CKD for at least 2 to 3 years after an episode of care complicated by AKI, even if the serum creatinine has returned to baseline.

Step 2Review and optimise medicines management: have medications been stopped that now need restarting?

Blood pressure tablets are often stopped but need restarting post dischargeConsider restarting ACEi/ARB once the renal function has stabilised. Renal function and electrolytes should be checked one week after reintroductionIf aspirin (75mg) and statins were stopped, these should be restarted unless specific reason not toIf a drug has been specifically implicated in causing AKI, update practice records to prevent re-prescribing

Step 3Communicate kidney health: Provide advice to help prevent further AKI episodes

Consider:Provide AKI patient information leaflet


Avoiding prescription of long term NSAIDs where possible, particularly in high risk patients and those with CKDAvoiding prescribing triple combination of spironolactone, NSAID and ACEi/ARBMonitor renal function after introducing certain medications: ACE inhibitors, ARB, loop diuretics, aldosterone antagonists



Appendix D: Useful Resources

Acute Kidney Injury Warning Algorithm Best Practice Guideline https://www.thinkkidneys.nhs.uk/wp-content/uploads/2014/12/AKI-Warning-Algorithm-Best-Practice-Guidance-final-publication-0112141.pdf

Communities at risk of developing Acute Kidney Injury https://www.thinkkidneys.nhs.uk/wp-content/uploads/2015/07/Communities-at-risk-of-developing-AKI-Think-Kidneys-010715.pdf

Guidelines for Medicines Optimisation in Patients with Acute Kidney Injury in Secondary Care (need primary care version)https://www.thinkkidneys.nhs.uk/wp-content/uploads/2015/09/Medicines-optimisation-toolkit-for-AKI-v12.pdf

Acute Kidney Injury Patient Information Leaflet https://www.thinkkidneys.nhs.uk/aki/wp-content/uploads/sites/2/2015/11/BKPA-RCGP-A4-Printout-Plain-Leaflet_v2.pdf

https://www.thinkkidneys.nhs.uk/wp-content/uploads/2015/04/Salford-AKI- Leaflet.pdf


Appendix E: National AKI Algorithm


Appendix F: Think Safety: Ensuring safe and reliable systems for managing tests20

Measure Rationale Suggested ActionsOrdering Kidney Function Tests

Are ALL the individual blood test(s) requested by the clinician clearly recorded?

When a clinician makes a decision to test kidney function, the reason should be clearly communicated to the appropriate personnel. This includes communication to a) the laboratory, b) the practice team; and c) out of hours services

Provide information about the clinical context:Acute illnessSignificant co-morbidities especially CKD and stage of CKD, heart failure.Recent increase dose in ACEi, ARB or diureticVolume status, poor oral intake/urine output

Obtaining a sample1 15 16 21 22

Are ALL the individual blood test(s) taken clearly recorded?

Errors relating to test implementation include tests not carried out, specimens improperly collected and specimens lost.

Potential for false positive tests and spurious hyperkalaemia needs to be acknowledged

Ensure patient details are clearly recorded

Document any difficulties collecting the sample: avoid clench fist, or shaking sample

Document time sample taken will help determine length of storage and potential spurious hyperkalaemia

Check and document if patient had heavy protein (meat) meal with 12 hours of sample

Management of AKI Warning Stage Test Results to Primary Care18

Were ALL the test(s) results forwarded to a practice clinician within a timely manner?

RAND Consensus process suggest interruptive communication is required for patients with AKI stage 3 test results.See Appendix BRAND Consensus Process suggest waiting to 72 hours to respond to an AKI warning stage test result is inappropriate

Ensure systems (both in and out of hours) of communication in place to manage AKI Warning Stage Tests results in timely manner:

System for dealing with interruptive communication from labs as well as use of monitored email systems

Clinical Review of AKI Warning Stage Test Results in Primary Care

Was the AKI Warning Stage Test Result reviewed and documented by a clinician within appropriate time frame (see Appendix B)?

Need to ensure place test result in a clinical context. RAND Consensus Process informed guidance on timeliness in response to AKI Warning Stage Test Results in Primary Care – see Appendix B.

Ensure all members of clinical team have copies of Think Kidneys Guide.

Develop systems to enable clinician to review previous results and observe trend in serum creatinine results

Action and documentation of AKI Warning Stage Test Results20

Have the decisions for ALL test results been ‘actioned’ by the practice/clinical team, including the patient being informed if required?

Reconciliation should be done on a regular basis i.e. weekly to ensure all abnormal results are returned to the practice in a timely manner to ensure prompt action.This enables practices to see how reliable the laboratory system is in processing and returning blood test results: information they can feedback to and discuss with the laboratory.

Ensure systems to communicate results between In and Out of Hours services

Primary Care Providers (both In and Out of Hours Services) to undertake Audit & Feedback –all members of the clinical team to be involved.

In addition to audit and feedback, for practice teams to learn from cases studies (see Appendix H: Reflective Template for AKI Case Studies)


Appendix G: Audit Measures

StructuresResponding to AKI Warning Stage Test Results

Establish practice systems to ensure safe and timely response of AKI Warning Stage Test Results sent via Clinical Pathology Services. These systems need to ensure response to critical results sent through interruptive methods (e.g. telephone call from Clinical Pathology Service) and response to test results sent via non-interruptive methods of communication (i.e. Results sent to an NHS email address that is known to be monitored regularly during working hours).

Post-AKI CareEstablish an AKI register to identify patients who have a) had a past history of AKI, and b) had a recent history of AKI.

Processes Preventing AKI

Avoid triple whammy repeat prescribing of NSAIDS, ACE inhibitors and diuretics.

Responding to AKI Warning Stage Test ResultsBased on findings from a RAND Consensus Process, there is agreement that in nearly all cases, waiting AKI Warning Stage Test Results within 72 hours is an inappropriate response.

Post-AKI CareProportion of patients with an episode of care complicated by AKI with a relevant read code for AKI diagnosis in their GP medical records.

Proportion of patients with an episode of care complicated by AKI who have been given information about AKI (Read Code 8OAG).

Proportion of patients who have had a medication review with their GP within specified time following episode of AKI (?within 2-4/52 post discharge)

Proportion of patients who have had repeat kidney function tests 3 months after an episode of care complicated by AKI.


Appendix H: Reflective template for AKI case studies*

What Happened?

What went well/not so well?

How did affect me? The patient? Colleagues?

What were the reasons for things going well/not going well?

Develop an Action plan

Specific?

Measureable?

Achievable?

Relevant?

Time-bounded?

Evaluate the Action plan

*In addition to personal reflective practice, Think Kidneys welcome anonymised case studies to help support on-going wider learning about AKI in primary care. If interested, please contact [email protected]


mailto:[email protected]

References

1. Kidney Disease Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney International Supplement 2012;2(1):1–138.

2. Health NNIf, Excellence C. CG169 Acute kidney injury: full guideline.3. Feehally J, Gilmore I, Barasi S, et al. RCPE UK consensus conference statement: management of

acute kidney injury: the role of fluids, e-alerts and biomarkers. J R Coll Physicians Edinb 2013;43(1):37 - 8.

4. Liano F, Pascual J. Epidemiology of acute renal failure: A prospective, multicenter, community-based study. Kidney Int 1996;50(3):811-18.

5. Selby NM, Kolhe NV, McIntyre CW, et al. Defining the Cause of Death in Hospitalised Patients with Acute Kidney Injury. PLoS ONE 2012;7(11):e48580.

6. Kerr M, Bedford M, Matthews B, et al. The economic impact of acute kidney injury in England. Nephrology Dialysis Transplantation 2014;29(7):1362-68.

7. National Institute for Health and Clinical Excellence (NICE). Chronic kidney disease. Early identification and management of chronic kidney disease in adults in primary and secondary care (CG182). London: NICE, 2014.

8. Blakeman T, Harding S, O’Donoghue D. Acute kidney injury in the community: why primary care has an important role. British Journal of General Practice 2013;63(609):173-74.

9. Team NECaI. Commissioning for Quality and Inovation Guidance for 2015/16. Leeds: NHS England, 2015.

10. Trust TUS. Toolkit: General Practice management of Sepsis: The UK Sepsis Trust developed in partnership with the Royal College of General Practitioners, 2014.

11. Physicians RCo. Acute care toolkit 9: Sepsis. London: Royal College of Physicians, 2014.12. Goodwin APL SV, Shotton H, Protopapa K, Butt A, Mason M. Just Say Sepsis! A review of the

process of care received by patients with sepsis. London: National Confidential Enquiry into Patient Outcome and Death, 2015.

13. Colleges AoMR. Acute kidney injury: a competency framework. Defining the role of the expert clinician. London: Academy of Medical Royal Colleges, 2011.

14. ISO. 15189:2012 Medical Laboratories – requirements for quality and competence: International Organization for Standardization, 2012.

15. Association UR. Clinical Practice Guidelines: Treatment of Acute Hyperkalaemia in Adults: UK Renal Association, 2014.

16. McDonald TJ, Oram RA, Vaidya B. Investigating hyperkalaemia in adults. BMJ 2015;351.17. (NICE) NIfHaCE. Management of chronic heart failure in adults in primary and secondary care.

Manchester: NICE, 2010.18. Fitch K BS, Aguilar MD, Burnand B, LaCalle JR, Lazaro P, van het Loo M, McDonnell J, Vader JP,

Kahan JP. The RAND/UCLA Appropriateness Method User's Manual. Santa Monica: RAND, 2001.

19. (NICE) NIfHaCE. Clinical Knowledge Summaries: Acute Kidney Injury: NICE.20. Care HISSPSP-P. Results Handling Change Package: Health Improvement Scotland, 2015.21. Smellie WSA. Spurious hyperkalaemia. BMJ 2007;334(7595):693-95.22. Nair S, O’Brien SV, Hayden K, et al. Effect of a Cooked Meat Meal on Serum Creatinine and

Estimated Glomerular Filtration Rate in Diabetes-Related Kidney Disease. Diabetes Care 2014;37(2):483-87.


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