Acute Kidney Injury in Adults Guideline ( Secondary Care )

Publication: 27/11/2012  --
Last review: 06/02/2020  
Next review: 06/02/2023  
Clinical Guideline
CURRENT 
ID: 3166 
Approved By: Trust Clinical Guidelines Group 
Copyright© Leeds Teaching Hospitals NHS Trust 2020  

 

This Clinical Guideline is intended for use by healthcare professionals within Leeds unless otherwise stated.
For healthcare professionals in other trusts, please ensure that you consult relevant local and national guidance.

Acute Kidney Injury in Adults Guideline (Secondary Care)

Summary

This guideline utilises the 5R conceptual approach to help all healthcare professionals identify patients at risk of acute kidney injury (AKI) and institute measures to prevent it. It also describes how to recognise AKI and respond in terms of medical management and renal referral for renal support. Patient rehabilitation is the final component.

How to apply the 5R conceptual approach to AKI:

  • Risk of AKI
    • Risk factors
    • Prevention strategies
      • STOP AKI Care Bundle (will cover the majority of causes of AKI)
      • Specific types of AKI
  • Recognition of AKI
    • Clinical presentation of patients with AKI
    • Definition of AKI
    • Cause of AKI
  • Response to AKI
    • STOP AKI Care Bundle
    • Renal referral
  • Renal Support for AKI
    • Initiation of dialysis
  • Rehabilitation of Patients following an episode of AKI
    • Recovery
    • Patient education
    • Medicines review
    • Follow up with GP/Nephrologist

The guideline draws evidence from the NICE CG 169 AKI guideline.

Other relevant LTHT guidelines include

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Background

Acute kidney injury (AKI) is a rapid deterioration of kidney function that occurs over hours to days. It is recognised that even small increases in serum creatinine are associated with worse short and long-term patient outcomes.1,2

The Kidney Disease: Improving Global Outcomes (KDIGO) definition of AKI has been adopted internationally.3,4 and establishes a new paradigm for AKI, promoting earlier recognition and response.

In 2009 the National Confidential Enquiry into Patient Outcome And Death (NCEPOD) Adding Insult to Injury AKI study reported that only 50% of patients who died from a diagnosis of AKI received good care. Poor management of hypovolaemia and sepsis was highlighted and the recognition of AKI was found to be delayed in 43% of patients who developed hospital-acquired AKI (h-AKI) following admission.5 The incidence of hospital acquired AKI (h-AKI) has been reported to be as high as 18%.6 The incidence of community-acquired AKI (c-AKI) remains to be determined.

Acute kidney injury costs the NHS in England £1.02 billion per year.7 Acute kidney injury is associated with an increase in patient morbidity and mortality, prolonged inpatient stay and the development of chronic kidney disease (CKD).8 The overall mortality from AKI ranges from 10-80%, increasing in acutely ill patients with multi-organ failure.9 The National Institute for Health and Care Excellence (NICE) published the AKI clinical practice guideline (CG 169) in 2013 and NICE AKI Quality Standard 76 in 2014.9,10 The Royal College of Physicians has developed an AKI and Intravenous Fluid acute care toolkit which is freely available online11. The NHS England Think Kidneys AKI programme has produced a wealth of resources for all healthcare professionals and patients12.

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Risk of AKI

There are many recognised risk factors for AKI with the most significant being age over 75 years (relates to a natural decline in kidney function and an association with other co-morbidities) and the presence of CKD. With an increasingly elderly population there is therefore an increased associated risk of AKI in many patients who either develop acute illness or undergo major surgery.

The risk factors can be categorised as inherent to an individual or external in terms of an exposure and may therefore be modifiable.

Risk Factors For AKI:

Inherent risk factors 

  • Age >75 years
  • Chronic Kidney Disease (eGFR < 60 ml/min/1.73m2)
  • Previous episode of AKI
  • Heart failure
  • Liver disease
  • Atherosclerotic peripheral vascular disease
  • Diabetes mellitus

Exposure risk factors

  • Sepsis
  • Toxins -
    • Non Steroidal Anti-Inflammatory Drugs (NSAIDs)
    • Aminoglyclosides
      • Gentamicin
    • Iodinated intravenous/intra-arterial contrast
  • Hypotension/Hypovolaemia

On admission patients should be assessed for their risk of AKI and appropriate preventative measures should be instituted. However it is important to recognise that the risk of AKI may change during the admission and regular assessment of risk should be made.

There are currently no validated AKI risk calculators.

Prevention of AKI

If patients are identified to have a risk of AKI initiate the STOP AKI Care Bundle

STOP AKI Care Bundle (general measures)

  • Sepsis
    • Standard measures should be followed to decrease the risk of infection
    • Close surveillance to identify early signs of infection with appropriate treatment (LTHT antibiotic guidelines)
  • Toxins
    • Avoidance of drugs harmful to the kidneys
      • e.g. NSAIDs, gentamicin
    • Care with intravenous iodinated contrast – see section below
  • Optimise blood pressure/volume status
    • Avoid dehydration e.g. confused patient
    • Treat hypovolaemia promptly
    • Consider with-holding patient anti-hypertensives/diuretics until assessed after major surgery or if patient develops sepsis/hypovolaemia
  • Prevent Harm
    • Identify the cause promptly and manage appropriately to prevent progression
    • Prevent complications by instituting prompt therapy
    • Identify drugs excreted through the kidneys and adjust drug doses promptly if AKI develops (BNF - www.evidence.nhs.uk)
    • Review fluid management plans to prevent inadequate or excessive intravenous fluid administration

Specific Conditions

Prevention of Contrast-Induced AKI (CI-AKI)

The risk of contrast-induced AKI is small in the general population. However there is a risk that must be recognised, and preventative measures must be instituted to reduce this risk.

Always consider whether a patient needs an iodinated intravenous contrast study as there are alternative forms of imaging:

  • Non contrast CT
  • Use of carbon dioxide to minimise contrast volume
  • Magnetic Resonance Imaging
  • Ultrasound/contrast enhanced ultrasound (CEUS)

If there is uncertainty regarding the best imaging for a specific indication discuss with radiology.

Risk Factors for CI-AKI:

Inherent risk factors

  • age > 75 years
  • chronic kidney disease (adults with an eGFR less than 40 ml/min/1.73 m2 are at particular risk)
  • diabetes mellitus but only if eGFR less than 40 ml/ min/1.73 m2
  • heart failure
  • kidney transplant

Exposure risk factors

  • AKI
  • sepsis
  • hypovolaemia
  • toxins – e.g. NSAIDs, gentamicin
  • volume of contrast agent
  • type of intravenous iodinated contrast
  • iodinated intra-venous or intra-arterial contrast received within the previous 48 hours

Ensure that risk assessment does not delay emergency imaging.

Advice on Metformin (as per Royal College of Radiology13)

  • It is recommended that metformin should be withheld in any acutely ill hospitalised patient with AKI – blood sugar should be monitored and alternative treatment for diabetes prescribed if necessary
  • In more stable patients if serum creatinine is above the normal reference range or eGFR is below 60 ml/min/1.73 m2, any decision to stop metformin for 48 hours following iodinated contrast medium administration should be made in consultation with the referring clinician

Angiography with Iodinated Contrast (includes CT angiography)

All angiographic studies in LTHT use iso-osmolar contrast media (IOCM) which has the lowest risk of CI-AKI

In-Patients

  • eGFR >60 mls/min/1.73 m2
    • encourage oral fluids
  • eGFR 40-59 mls/min/1.73 m2
    • oral hydration pre and post (drink 1L prior to scan to volume expand)
  • eGFR <40 mls/min/1.73 m2 and moderate to high risk and one risk factor from the list above
    • clinical assessment of volume status by the referring team
    • 0.9% saline at 1ml/kg for 8-12 hours pre- and post-procedure
    • with-hold
      • Metformin
      • NSAIDs
    • U&E check 48-72 hours post-procedure

Out-Patient (day case)

  • eGFR >60 mls/min/1.73 m2
    • encourage oral fluids
  • eGFR 40-59 mls/min/1.73 m2
    • oral hydration pre and post (drink 1L prior to scan to volume expand)
  • eGFR <40 mls/min/1.73 m2 and moderate to high risk and one risk factor from the list above
    • encourage oral hydration pre-procedure
    • volume status assessment
    • 0.9% saline at 3ml/kg for 1 hours pre- and 1ml/kg for 6 hours post-procedure
    • with-hold
      • Metformin
      • NSAIDs
    • U&E check 48-72 hours post-procedure
    • If contrast volume is >4ml/kg (or 350mls) used further contrast should be avoided for 2 weeks if possible

CT with Iodinated Contrast

In-Patients

  • eGFR >60 mls/min/1.73 m2
    • encourage oral fluids
  • eGFR 40-59 mls/min/1.73 m2
    • oral hydration pre and post (drink 1L prior to scan to volume expand)
  • eGFR <40 mls/min/1.73 m2 and moderate to high risk and one risk factor from the list above
    • clinical assessment of volume status by the referring team
    • 0.9% saline at 1ml/kg for 8-12 hours pre- and post-procedure
    • With-hold
      • Metformin
      • NSAIDs
    • U&E check 48-72 hours post-procedure
    • If contrast volume is >4ml/kg (or 350mls) used further contrast should be avoided for 2 weeks if possible

Out-Patient (day-case)

  • eGFR >60 mls/min/1.73 m2
    • encourage oral fluids
  • eGFR 40-59 mls/min/1.73 m2
    • oral hydration pre and post (drink 1L in dept prior to scan to volume expand)
  • eGFR 30-39 mls/min/1.73 m2
    • oral hydration pre and post (drink 1L in department prior to scan to volume expand)
    • with-hold
      • Metformin
      • NSAIDs
    • U&E check 48-72 hours post-procedure
    • If contrast volume is >4ml/kg (or 350mls) used further contrast should be avoided for 2 weeks if possible
  • eGFR 20-29 mls/min/1.73 m2
    • volume status assessment
    • iv fluid at 3ml/kg for 1 hour followed by 1ml/kg for 4-6 hours
    • with-hold
      • Metformin
      • NSAIDS
    • U&E check 48-72 hours post-procedure
    • If contrast volume is >4ml/kg (or 350mls) used further contrast should be avoided for 2 weeks if possible
  • eGFR <20mls/min/1.73 m2
    • discuss risk vs benefit
    • suggest discussion with Renal Team
    • volume status assessment
    • iv fluid at 3ml/kg for 1 hour followed by 1ml/kg for 4-6 hours
    • with-hold
      • Metformin
      • NSAIDS
    • U&E check 48-72 hours post-procedure
    • If contrast volume is >4ml/kg (or 350mls) used further contrast should be avoided for 2 weeks if possible

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Recognition of AKI

Acute kidney injury may be

  • suspected from clinical presentation or
  • detected by a rise (or fall) in serum creatinine or reduction in urine output

Clinical Presentation:

  • Acutely ill
  • Nausea, vomiting, diarrhea
  • Hypovolaemia
  • Hypotension
  • Decreased urine output
  • Recent exposure to a toxic insult
    • e.g. NSAID, Gentamicin, IV iodinated contrast
  • Systemic symptoms (favour a possible diagnosis of vasculitis)
    • Fever
    • Weight loss
    • Rash
    • Joint pains
    • Haemoptysis
    • Nasal stuffiness
  • Loin pain
  • Prostatic symptoms

A thorough clinical examination of the patient is required, including volume status assessment.

Volume status:

  • Capillary refill time (normal < 3sec)
  • Pulse rate
    • Note beta blockers / diltiazem or hyperkalaemia may prevent tachycardic response to hypovolaemia
  • Jugular venous pressure
  • Skin turgor (over clavicle)
  • Blood pressure
    • Lying and standing
  • Oedema
    • Pulmonary
    • Peripheral/sacral
  • Fluid balance chart – urine output
  • Weight (look at trends)

Passive leg raising is a bedside method to assess fluid responsiveness in a patient. It is best undertaken with the patient initially semi-recumbent and then tilting the entire bed through 45°. Alternatively it can be done by lying the patient flat and passively raising their legs to greater than 45°. If, at 30–90 seconds, the patient shows signs of haemodynamic improvement, it indicates that volume replacement may be required. If the condition of the patient deteriorates, in particular breathlessness, it indicates that the patient may be fluid overloaded

Other clinical signs/features to consider:

  • Palpable bladder
  • Large prostate
  • Features of vasculitis
    • Rash
    • Uveitis
    • Joint involvement
    • Blood and protein on urinalysis

If the patient presents with these clinical features check the U&Es

In LTHT the creatinine value will be compared with any previous creatinine values and run through an AKI algorithm. If the creatinine is elevated compared to previous values and meets the KDIGO criteria for AKI an alert will be triggered (see below).

If there is no previous baseline serum creatinine available and AKI is suspected repeat the creatinine within 24 hours. A rising or falling serum creatinine is supportive of a diagnosis of AKI and further measurements of serum creatinine are recommended.

Acute kidney injury has been defined by the Kidney Diseases: Improving Global Outcomes (KDIGO) international guideline group. The definition is based on rises in serum creatinine or reductions in urine output. There are now many studies in the literature that demonstrate that relatively small rises in serum creatinine are associated with worse patient outcomes.

Definition of Acute Kidney Injury:

  • increase in serum creatinine of 26 µmol/L within 48 hours OR
  • increase in serum creatinine ≥1.5X baseline value within 1 week OR
  • urine output of <0.5 ml/kg/hour for > 6 consecutive hours

Patients that meet the definition for AKI can be staged according to whichever criteria (serum creatinine or urine output) gives them the highest stage (Table 1).

Stage

Serum creatinine

Urine output

1

rise ≥26 μmol/L within 48 hrs
or
rise ≥1.5 to 1.9 X baseline SCr

<0.5 mL/kg/hr for >6
consecutive hr

2

rise ≥2 to 2.9 X baseline SCr

<0.5 mL/kg/hr for >12 hr

3

rise ≥3 X baseline SCr
or
rise ≥ 354 μmol/L
or 
Commenced on renal replacement therapy (RRT) irrespective of stage

<0.3 mL/kg/hr for >24 hr
or
anuria for 12 hr

Table 1: KDIGO definition and staging system for acute kidney injury

Electronic Acute Kidney Injury Alerts:

In LTHT any patient that has a serum creatinine tested in the lab will automatically have an electronic warning triggered if the definition for AKI is met.

An algorithm to calculate the AKI stage has been integrated into the Lab Information Management System (LIMS) based on the KDIGO AKI definition and staging system.

The stage of the AKI will be determined and displayed on

  • Results Server and
  • PPM+

with the comment instructions to refer to the LTHT AKI guidelines

If AKI is not detected then the following message will appear

‘AKI not detected based on current available creatinine values
If AKI is suspected, REPEAT creatinine within 24 hrs’

All wards (except Renal Wards) will have an AKI alert column visible on the electronic white boards for all members of the multidisciplinary team to see (Figure 1). A question mark will appear with the stage of AKI e.g.

Figure 1. Electronic white board with AKI alert, (circled in red) in AKI column. Once the STOP AKI care bundle has been completed the icon will change from red to orange.

The AKI alert will be linked to the STOP AKI care bundle (see Response section) within PPM+, which must be completed for all patients in whom AKI is clinically confirmed. To complete the AKI care bundle go to single patient view and click on the icon in the AKI column (the AKI column can easily be added if not already present), which will open up the care bundle (Figure 2).

After completion of the care bundle the icon will turn orange . The STOP AKI care bundle addresses the most common causes of AKI. The clinical response time from triggering the AKI alert to completion of the care bundle will be audited.

Figure 2. STOP AKI Care Bundle

The STOP AKI care bundle will prompt referral to critical care outreach for patients with confirmed AKI Stage 3

There are important exclusions to completing the STOP AKI care bundle which include

  • patients with end stage kidney disease on dialysis – the alert can be triggered due to the changes in creatinine that follow dialysis
  • patients on an end of life care pathway
  • patients with heart failure who are receiving treatment with diuretics and ACE inhibitors/angiotensin receptor blockers (ARBs)– a rise in creatinine may be acceptable in this group up to 30% of the baseline value

Causes Of Acute Kidney Injury:

Acute kidney injury is a syndrome with many different causes. It is not acceptable to refer to a patient with AKI without offering a cause. It is important to determine the underlying cause of AKI as this allows prompt response which may include urgent renal referral and treatment for the rarer forms of AKI e.g. vasculitis, haemolytic uraemic syndrome (HUS)

The causes of AKI can be considered as

  • Pre-renal
  • Intrinsic
  • Post-renal

 

Figure 3. The causes of AKI

The majority of causes of AKI are secondary to sepsis, toxins, hypotension and/or hypovolaemia. If it is not then consider obstruction or rarer kidney diseases.

Investigations:

Haematology:

  • Full blood count (FBC)
    • High or low WBC consider sepsis
    • If haemolytic anaemia and thrombocytopenia consider
      • haemolytic uraemic syndrome (HUS)
      • thrombotic thrombocytopenic purpura (TTP)

Biochemistry:

  • Urea & Electrolytes (U&Es)
  • Bicarbonate (you must request as not routine part of U&E)
  • Liver function tests
    • if abnormal consider liver disease e.g. Hepato-renal syndrome
  • Calcium profile
    • if hypercalcaemia consider Myeloma

Urine dipstick:

  • Leucocytes & nitrites
    • if present may indicate infection-send MSU/CSU
  • Blood & protein occurs with
    • infection – send MSU/CSU
    • inflammatory process e.g. Vasculitis, glomerulonephritis

Radiology:

  • Chest radiograph – may demonstrate
    • fluid overload
    • infection
    • pulmonary haemorrhage e.g. vasculitis
  • Renal Ultrasound – not all patients need e.g. if recovering from AKI BUT request within
    • 12 hours if obstruction suspected or
    • 6 hours if pyeonephrosis (infected obstructed kidneys) suspected – will need urgent nephrostomy Do Not Delay
    • 24 hours if failure to respond to initial treatment or if cause not clear
      • Assess kidney size - small scarred kidneys < 8-9cm may be consistent with CKD

Further tests to be considered dependent upon clinical presentation:

Biochemistry

  • Creatine Kinase (CK)
    • elevated with Rhabdomyolysis (trauma/ muscle tenderness)
  • C-reactive protein (CRP)
    • elevated with infection or inflammation e.g. Vasculitis
  • Urine for Protein Creatinine Ratio (PCR)

Immunology:

  • ANCA – e.g. vasculitis
  • ANA – e.g. lupus
  • Complement levels – e.g. low in lupus
  • anti-GBM – Goodpastures Disease
  • serum electrophoresis - myeloma
  • Immunoglobulins - myeloma
  • Urine for Bence-Jones protein - myeloma

Microbiology:

  • Blood cultures - if sepsis suspected
  • Urine cultures – if sepsis suspected
  • Hepatitis B&C serology

Radiology:

  • KUB X-ray: if renal stone disease is suspected

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Response to AKI

The mainstay of managing AKI is supportive therapy and attention to detail with close monitoring.

If the AKI alert has been triggered the first question is to confirm whether the patient has AKI, if the answer is yes the STOP AKI care bundle must be initiated (Table 2), which focuses on treating sepsis promptly if present, optimising BP, optimising volume status, avoiding toxins and preventing harm to the patient and identifying the underlying cause. A quick reference card has been developed to support the implementation of the care bundle (Figure 4).

STOP AKI

Response

Sepsis - consult LTH antibiotic guidelines

 

Search for source
Sepsis 6 care bundle:

  • Blood/Urine Cultures
  • Urine Output/U&Es
  • Fluids – consider iv
  • Antibiotics
  • Lactate & Haemoglobin
  • Oxygen – high flow

Toxins

 

Stop/avoid potential toxins

  • Gentamicin
  • NSAIDs
  • iodinated contrast

Optimise BP/Volume Status

 

Volume status assessment

  • consider IV Fluids

Consider withholding

  • antihypertensives
  • diuretics

Consider vasopressors

Prevent Harm

 

Identify the cause and investigate (urinalysis)

  • The majority of causes of AKI are secondary to sepsis, toxins, hypotension and/or hypovolaemia. If it is not then consider obstruction or rarer kidney diseases.  

Treat complications

  • Hyperkalaemia
  • Acidaemia

Review medication doses
Review fluid prescription

Table 2. STOP AKI Care Bundle

Table 2. STOP AKI Care Bundle – The STOP AKI care bundle will also prompt referral to critical care outreach for patients with confirmed AKI Stage 3

Figure 4. STOP AKI Quick reference card

Complications of AKI

Complication of AKI

Management

Hyperkalaemia:
K+ > 6.0mmol/L and no ECG changes

 

8 units soluble insulin to 50mls 50% dextrose intravenously over 15 mins (lasts 4-6hours)
salbutamol 10-20mg (5mg back to back) nebuliser 6 hourly (caution if tachycardia or ischaemic heart disease)

Hyperkalaemia:
K+ > 6.0mmol/L with ECG changes or K+ > 6.5mmol/L with or without ECG changes

30mls of 10% calcium gluconate iv over 2 minutes (can be given again every 10 minutes until the ECG normalises up to 50mls)

Acidosis: pH < 7.15

IV sodium bicarbonate can be considered
immediate critical care/ICU referral
remember to correct hypocalcaemia (with respect to the ionised calcium) prior to correcting acidaemia due to risk of exacerbating the hypocalcaemia and lowering seizure threshold

Pulmonary oedema

 

Sit patient up
O2 15 L/min via reservoir mask
IV GTN (50mg in 50ml 0.9% sodium chloride) commence 2ml/hr & titrate up to 20ml/hr maintaining systolic BP > 95mmHg
Furosemide only if patient haemodynamically stable and well filled intravascularly

Uraemic encephalopathy/pericarditis

Renal replacement therapy

Medication Management
In patients with AKI it is important to identify medications that are normally metabolised and/or excreted by the kidneys, and either avoid or make appropriate dose adjustments. Discuss these medications with the ward pharmacist if uncertain how to adjust dose. Common examples include:

  • Penicillins
  • Cephalosporins
  • Vancomycin
  • Antivirals
    • aciclovir
  • Morphine (metabolites will accumulate)
  • Low Molecular Weight Heparins
  • e.g.tinzaparin

Nephrotoxic medications should be avoided if possible (unless life-saving) and include:

  • Non-steroidal anti-inflammatory drugs (NSAIDs)
  • Aminoglycosides e.g. Gentamicin
  • Amphotericin (liposomal formulations less toxic)

Resuscitation Fluid Therapy

Intravenous fluids will be required to restore and maintain the circulation and the function of vital organs if the patient is hypovolaemic e.g.

  • blood loss from injury or surgery
  • acute pancreatitis
  • gastrointestinal or renal losses of salt and water.

Response:

Infuse 500mls (250mls if cardiac failure) over 15 mins of a

  • balanced crystalloid (e.g. Hartmann’s solution) or
  • 0.9% sodium chloride

(Appendix 1 from LTHT IV Fluids guideline)

Hartmann's Solution is suggested as the first choice resuscitation fluid but the priority is to re-establish haemodynamic stability through restoring the intravascular volume and therefore if not available 0.9% sodium chloride can be used initially.

0.9% sodium chloride is preferred if

  • the patient is not monitored on in an HDU or ICU environment and potassium > 5.5mmol/L in the setting of oliguric AKI or
  • AKI is secondary to rhabdomyolysis due to the risk of hyperkalaemia

Consider human albumin solution 4–5% for fluid resuscitation only in patients with severe sepsis. This must be discussed with a consultant.

Volume Assessment:

The clinical response should be assessed immediately following administration of the fluid bolus by reassessing the volume status:

  • capillary refill time (reduction)
  • pulse (reduction in pulse if tachycardic)
  • jugular venous pressure (rise in JVP)
  • blood pressure (rise in BP)
  • pulmonary oedema
  • urine output (increasing if oliguric)

Response:

If no clinical response and no pulmonary oedema:
Administer further 500ml of crystalloid and reassess clinically and discuss with senior member of team (SpR or consultant).

If a clinical response to the fluid bolus:
Continue with iv fluids and discuss further fluid therapy management plan with senior member of team (SpR or consultant).

Volume unresponsive AKI:
If the patient develops oliguric AKI (urine output < 0.5 mls/kg/hr) despite adequate volume resuscitation consider the patient as having volume unresponsive AKI.

Further excessive fluid resuscitation may result in pulmonary oedema. Continue with iv fluid cautiously, matching urine output and monitoring for signs of respiratory distress (rising respiratory rate, pulmonary oedema or falling oxygen saturations). Request advice a senior member of team (SpR or consultant).

Continued resuscitation fluid therapy:
If 0.9% sodium chloride has been used initially conversion to a balanced crystalloid can be considered once potassium levels are known and good urine output established.

Once resuscitation of the volume status has been achieved as assessed by normalisation of vital signs and urine output or of parameters from more invasive measurements, the prescriber should switch to a Routine Maintenance regimen with accurate replacement of any on-going losses.

Referral to renal team
Not all patients with AKI will need referral to the renal team; this depends upon the stage/severity and clinical presentation.

Prior to referral the following should be performed

  • A thorough clinical history and examination (including fluid balance assessment)
  • Completion of the electronic STOP AKI care bundle if e-Alert triggered on PPM+
  • Initial investigations (as recommended above)
  • Initial supportive management (as recommended above)

Early renal referral is recommended in the following patients

  • AKI stage 3 ( increase in SCr ≥3 × baseline value)
  • Persistent oliguria and/or rising serum creatinine despite supportive therapy
  • Complications refractory to medical treatment
    • Hyperkalaemia (K+ >6.0 mmo/L)
    • Pulmonary oedema
    • Acidosis (pH <7.15)
    • Uraemic encephalopathy
    • Uraemic pericarditis
  • AKI plus
    • Absence of defined cause , e.g. sepsis, hypovolaemia
    • Systemic features e.g. rash, joint pains, blood and protein on urinalysis
    • Paraprotein
    • Haemolysis and low platelets – HUS/TTP
    • Poisoning suspected e.g.
      • ethylene glycol
      • methanol
      • lithium

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Renal Support

Indications for renal replacement therapy (RRT) for AKI must be assessed in the clinical context and should be considered for:

  • Complications refractory to medical treatment
    • Hyperkalaemia (K+ >6.5 mmo/L)
    • Pulmonary oedema
    • Acidosis (pH <7.15)
  • Uraemic encephalopathy
  • Uraemic pericarditis
  • Overdose
    • Ethylene Glycol
    • Methanol
    • Aspirin (severe)
    • Lithium
  • Renal replacement therapy for AKI includes
  • Haemodialysis
    • Intermittent
      • Patient must be haemodynamically stable
      • Continuous (on ICU)
        • Reserved for haemodynamically unstable patients

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Rehabilitation

Recovery

The first signs of recovery from AKI may be

  • an increase in urine output if the patient was oliguric and/or
  • a reduction in the rise in the daily serum creatinine followed by a plateau in its value prior to a fall

Recovery from AKI can result in a polyuric state in some patients with the production of large urine volumes until the capacity of the renal tubule to concentrate urine returns. There must therefore be careful attention to the patient’s volume status and fluid requirements.

Patients can be at risk of developing

  • Hypernatraemia (sodium > 145 mmol/L- secondary to a free water deficit and requires an increased intake of water (intravenous 5% glucose if unable to take water orally). Failure to address the free water deficit promptly will not only slow renal recovery but will also put the patient at risk of neurological complications.
  • Hypokalaemia (potassium < 3.3 mmol/L- which requires appropriate therapy due to the risk of cardiac arrhythmias and ileus.

It is important to consider the rehabilitation that is required for a patient following an episode of AKI.

Discharge and follow up after AKI

  • Patients who have had an episode of AKI are at risk of chronic kidney disease long-term. The risk depends upon the severity and duration of the episode of AKI
    • Patients with recovered or recovering AKI will need repeat U&Es checked in the community to assess the extent of the recovery and whether longer term review is required
  • Medications should be reviewed prior to discharge with a plan to reintroduce medications that may have been held during the acute illness e.g. anti-hypertensives, diuretics at an appropriate time. This may require an early follow up with the GP
    • Failure to provide advice on restarting a medication may lead to an adverse outcome e.g. failing to restart an ACEi in patient with cardiac failure
  • Patients should be informed as to why they developed AKI and their risk factors. LTHT patient AKI leaflets have been developed
  • Electronic discharge letter (EDAN) should include
    • AKI Stage (max stage during admission)
    • Cause of AKI e.g. sepsis secondary to chest infection and hypotension
    • Advice on whether medications need to be reviewed or reintroduced e.g. ACEi should be restarted once patient well and kidney function has recovered and stable
    • Advice on follow up and further monitoring of U&Es (if within 1 week LTHT must take responsibility)
      • If still recovering from AKI recommend U&Es check in 2 weeks initially and then GP to determine further checks if necessary
      • If recovered from AKI recommend U&Es check in 2-4 weeks, then 3 months initially and then GP to determine further checks if necessary
      • If patient fails to recover and has chronic kidney disease (CKD) eGFR < 30ml/min/1.73m2 recommend U&Es check in 2-4 weeks and GP refers to NICE guidance for CKD

Figure 5. Electronic discharge summary quick reference card

Further Resources

 

Provenance

Record: 3166
Objective:

The aims of the guideline are to improve the

  • recognition of patients at risk of AKI and its prevention
  • management and rehabilitation of patients with AKI in line with the recommendations from:
    • National Confidential Enquiry into Patient Outcomes and Death (NCEPOD) Acute Kidney Injury Adding Insult to Injury report (2009)
    • NICE CG 169 Acute Kidney Injury guideline (2013)
    • NICE AKI Quality Standard 76 (2014)

The objectives are for the reader to understand the evidence-based recommendations using the 5R approach to improve the quality of patient care and follow up.

Clinical condition:

Acute Kidney Injury (AKI)

Target patient group: >18year olds, especially those with AKI risk factors.
Target professional group(s): Secondary Care Doctors
Adapted from:

Evidence base

A. Meta-analyses, randomised controlled trials/systematic reviews of RCTs
B. Robust experimental or observational studies
C. Expert consensus.
D. Leeds consensus. (where no national guidance exists or there is wide disagreement with a level C recommendation or where national guidance documents contradict each other)

  1. Lassnigg, A, Schmidlin, D, Mouhieddine, M, et al. Minimal changes of serum creatinine predict prognosis in patients after cardiothoracic surgery: a prospective cohort study. J Am Soc Nephrol 2004; 15:1597. (B)
  2. Mehta, RL, Chertow, GM. Acute renal failure definitions and classification: time for change? J Am Soc Nephrol 2003; 14:2178. (C)
  3. KDIGO clinical practice guidelines on acute kidney injury. Kidney International Vol 2 supplement 1 March 2012 (C)
  4. Acute Kidney Injury 5th Clinical Practice Guidelines. Lewington AJP, Kanagasundaram NS. Nephron Clin Pract. 2011;118 Suppl 1:c27-70
  5. NCEPOD. Adding insult to injury – A review of care of patients who died in hospital with a primary diagnosis of acute kidney injury (acute renal failure). The National Confidential Enquiry into Patient Outcome and Death. 2009 (C)
  6. Uchino S, Bellomo R, Goldsmith D, Bates S, Ronco C. An assessment of the RIFLE criteria for acute renal failure in hospitalised patients. Crit Care Med 2006;34:1913-7. (B)
  7. Kerr M, Bedford M, Matthews B, O'Donoghue D.The economic impact of acute kidney injury in England. Nephrol Dial Transplant. 2014 Jul;29(7): Kerr M, O’Donoghue
  8. Lines S, Lewington A. Acute kidney injury. Clin Med. 2009 Jun;9(3):273-7. (B)
  9. NICE Acute kidney injury: prevention, detection and management CG 169 https://www.nice.org.uk/Guidance/CG169
  10. NICE Acute Kidney Injury Quality Standard QS 76 https://www.nice.org.uk/guidance/qs76
  11. Royal College of Physicians Acute care toolkit 12: Acute kidney injury and intravenous fluid therapy. https://www.rcplondon.ac.uk/guidelines-policy/acute-care-toolkit-12-acute-kidney-injury-and-intravenous-fluid-therapy
  12. NHS England Think Kidneys AKI programme. https://www.thinkkidneys.nhs.uk/aki/
  13. Royal College of Radiology. Standards for intravascular contrast administration to adult patients, Third edition. https://www.rcr.ac.uk/publication/standards-intravascular-contrast-administration-adult-patients-third-edition

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Approved By

Trust Clinical Guidelines Group

Document history

LHP version 1.0

Related information

Glossary

AKI - Acute kidney injury
ANA - Anti nuclear antibody
ANCA - Anti neutrophil cytoplasmic antibody
Anti-GBM - Anti glomerular basement membrane antibody
CKD - Chronic kidney disease
KDIGO - The international guideline group Kidney Diseases: Improving Global Outcomes
NCEPOD - National Confidential Enquiry into Patient Outcomes and Death
NICE - The National Institute for Health and Clinical Excellence
NSAIDs - Non steroidal inflammatory drugs
Rhabdomyolysis - breakdown of muscle secondary to many different aetiologies (e.g. viral infection, drugs, crush injury) that can result in AKI

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