Management of Acute Kidney Injury (AKI)

Introduction

Acute kidney injury (AKI) is the loss of kidney function over a short period of time (i.e. hours to days). If creatinine is rising, the eGFR may be close to zero and therefore eGFR is of no value in the assessment of AKI. AKI is common in patients admitted to hospital and is associated with increased mortality.

AKI is defined by ANY of:

  • >1.5 fold rise in creatinine or
  • Oliguria (<0.5ml/kg/hour) for 6 hours or
  • Rise in creatinine of ≥26 µmol/L.

Stages of AKI

AKI stage Serum creatinine criteria Urine output criteria
1

Rise in creatinine of ≥1.5–1.9 times baseline or increase in creatinine >26 µmol/L within 48 hours

<0.5 ml/kg/hour for 6 hours
2 Rise in creatinine of ≥2–2.9 times baseline <0.5 ml/kg/hour for 12 hours
3 Rise in creatinine of ≥3 times baseline or increase in creatinine >354 µmol/L within 48 hours <0.3 ml/kg/hour for 24 hours or anuria for 12 hours

Risk factors for AKI

Common risk factors for AKI include:

  • Advanced age
  • Diabetes
  • Chronic kidney disease (CKD)
  • Chronic liver disease
  • Congestive heart failure

N.B. This list is not exhaustive.

Aetiology of AKI

This can be separated into pre-renal, renal and post-renal causes:

Pre-renal Renal Post-renal
Hypotension

Glomerulonephritis (GN)

Obstruction
Hypovolaemia Vasculitis  
Sepsis Interstitial nephritis  
Medications Contrast  

Assessment / Essential investigations

For an overview of assessment / essential investigations using the ROUNDUP tool:

N.B. For more detailed guidance, see text below.

Ensure an accurate medication history is taken including new or recently started medications/supplements (including recent antibiotic courses) or illicit substances.

Assess fluid state daily:

  • Ask about thirst and volume loss.
  • Monitor input and output using a fluid balance chart.
  • Check blood pressure, heart rate and urine output (minimum of 4 hourly observations in all AKI patients).
  • Signs of dehydration: Dry mucus membranes, reduced skin turgor, increased capillary refill.
  • Signs of fluid overload: Look for peripheral oedema, raised jugular venous pressure (JVP) and pulmonary oedema.

Perform a septic screen:

  • If raised inflammatory markers look for a source of sepsis.
  • Consider chest x-ray (CXR), midstream specimen of urine (MSSU), blood cultures and lactate.

Check bloods (FBCs, U&Es, LFTs, CRP, bone profile, bicarbonate):

  • Daily U&Es and bicarbonate whilst AKI. Consider discussion with senior / renal if K+ >5.7. Minimum twice daily if AKI stage 3 or if severe hyperkalaemia (K+ >6.5).
  • CK if rhabdomyolysis suspected.
  • Blood film, LDH and reticulocytes if haemolytic uremic syndrome (HUS) or Thrombotic Thrombocytopenia Purpura (TTP) suspected.

Check urinalysis (preferably pre-catheterisation) and urinary protein:creatinine ratio.

If the urinalysis is positive for blood or protein then:

  • Request GN screen - ANCA, ANA, anti-GBM antibody, rheumatoid factor and C3/C4 complement, and in those aged >60 years a myeloma screen (serum electrophoresis, immunoglobulins and Bence-Jones protein).
  • Check virology (HCV, HBV, HIV).

In those aged >60 years with negative urinalysis and AKI, a myeloma screen but not a GN screen should be checked.

Consider obstruction:

  • Examine bladder / request bladder scan
  • Request renal tract ultrasound to rule out obstruction if either:
    • Urine output fails to improve
    • Obstruction is suspected

Management

  • Management of pre-renal AKI focuses on the optimisation of fluid balance and cardiovascular support.
  • If volume deplete, give a fluid challenge with IV crystalloid. N.B. 5% glucose is not a suitable replacement fluid on its own. If a patient is well-filled and hypotensive, seek senior advice.
  • Medicines reconciliation – consider withholding medications or dose adjustments:
    • Review ACE inhibitors (ACE-Is), angiotensin receptor blockers (ARBs), non-steroidal anti-inflammatory drugs (NSAIDs), sodium-glucose co-transporter-2 (SGLT2) inhibitors, metformin and diuretics.
    • Caution with morphine as it is renally excreted and therefore can accumulate. Consider switching to low dose oxycodone or alfentanil.*
    • Involve the clinical pharmacist and/or review the Renal Drug Handbook.
    • Avoid trimethoprim/co-trimoxazole as these can cause a spurious rise in potassium and worsen hyperkalaemia.
  • Promptly treat sepsis:
  • Hyperkalaemia is a medical emergency and must be treated promptly.
  • Monitor fluid balance:
    • Ensure fluid balance chart is in place to monitor fluid input and urine output
    • Ensure daily weights if overloaded
  • Catheterise if apparent oliguria (<0.5ml/kg/hour) or possible obstruction.
  • Renal obstruction always needs to be discussed with urology.

*If patient is receiving end of life care, refer to the Scottish Palliative Care Guidelines on prescribing in the last days of life in renal impairment. N.B. There is a last days of life protocol for renal impairment available for prescribing on HEPMA.

If contrast is necessary for any planned imaging and a patient has an AKI or CKD with an eGFR ≤30ml/minute/1.73m2 then the radiologist should be informed and consideration given to the administration of 1 litre of sodium chloride 0.9% in the 12 hours prior to and following the scan. Urgent and essential scans should not be delayed to allow fluid administration. 

Diuretic phase of AKI 

As AKI resolves, patients may develop a diuretic phase which may be extreme. This is particularly common after relieving obstructive uropathy. Ensure the patient has careful monitoring of fluid balance and electrolytes.

Referral to Nephrology

Emergency referral to Nephrology

Single-organ failure should be managed in the renal unit if safe for transfer. If the patient is unfit for transfer or has multi-organ failure, a referral should be made to the intensive care unit. Emergency referral for consideration of renal replacement therapy is indicated for:

  • Pulmonary oedema with oliguria or unresponsive to medical therapy
  • Hyperkalaemia:
    • K+ >7mmol/L at any time
    • K+ >6.5mmol/L with oliguria
    • K+ >6.5mmol/L without oliguria despite initial medical management (calcium and insulin/glucose  administration)
  • Life-threatening uraemia (pericarditis, encephalopathy)
  • Severe acidosis
  • Poisoning if advised by TOXBASE (www.toxbase.org, password required)

Urgent referrals of patients who may require acute dialysis should be made by contacting the on-call renal consultant via switchboard.

Urgent referral to Nephrology

  • Stage 3 AKI
  • Stage 2 AKI that is failing to improve (e.g. after 48 hours) or where the cause is not identified
  • Suspicion of intrinsic renal disease:
    • Systemic vasculitis (+++ blood and protein on urinalysis, inflammatory response without evidence of infection, vasculitic rash, haemoptysis/ atypical pulmonary infiltrates, epistaxis, altered hearing, arthralgia)
    • New nephrotic syndrome (defined as urine protein:creatinine ratio >0.3g/mmol with hypoalbuminaemia and oedema)
    • AKI with suspected interstitial nephritis / HUS-TTP / myeloma
  • Any patients with CKD 5 or on dialysis
  • AKI (any stage) in a renal transplant patient

Referral to the renal service for advice is via email (see Appendix 6 for contact details). All urgent referrals will be dealt with on the same day and routine referrals will be seen or receipt of referral acknowledged within 48 hours.

Follow-up post-AKI

Resolving AKI needs follow-up to ensure full recovery.

  • AKI should always be mentioned in the discharge letter with a follow plan.
  • Some medications cause / exacerbate renal impairment or result in medication toxicity, and will usually be stopped in AKI, e.g. ACE-Is, ARBs, diuretics, NSAIDs, SGLT2 inhibitors, metformin, and proton pump inhibitors (PPIs) and sedating medications. N.B. This list is not exhaustive. Always refer to the BNF and the Renal Drug Handbook. During working hours advice is available from the renal pharmacists (see Appendix 6 for contact details). Out-of-hours advice is available from the medical registrar or oncall pharmacist.
  • It is important that once AKI resolves, medication is re-instated as appropriate and medication doses are re-adjusted as necessary, with particular attention to ensuring antibiotic doses are increased. Caution should be taken when restarting NSAIDs after an incidence of AKI.
  • It is important to discuss “sick day rules” where patients omit their potentially nephrotoxic medications in the presence of intercurrent illness.
  • Patients may be discharged before they have fully returned to their normal baseline renal function, as long as there is clinical and biochemical improvement and senior medical involvement. However, follow-up should be arranged to monitor their renal function and consider medication dose adjustments.
  • Incomplete resolution of AKI might require outpatient renal follow-up.

 

Guideline reviewed June 2024
Page updated August 2024



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