RECOGNITION

  • Acute kidney injury (AKI) is an abrupt reduction in kidney function
    • absolute increase in serum creatinine of either ≥26.4 µmol/L within 48 hr or
    • ≥50% (1.5 x baseline) within 7 days or
    • reduction in urine output documented as oliguria <0.5 mL/kg/hr for >6 hr
  • E-Alert for AKI stages in Patient Management System

AKI stage 1

Clearance

  • Increase in creatinine ≥26.4 µmol/L within 48 hr or
  • 1.5–2 fold increase from baseline within 7 days

Urine output

  • <0.5 mL/kg/hr for >6 hr

AKI stage 2

Clearance

  • Increase in creatinine >2–3 fold from baseline

Urine output

  • <0.5 mL/kg/hr for >12 hr

AKI stage 3

Clearance

  • Increase in creatinine >3 fold or
  • Serum creatinine >350 µmol/L with an acute rise of 1.5 fold within 7 days

Urine output

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

Causes

  • Pre-renal (perfusion)
    • volume depletion
    • hypotension, pump failure
    • sepsis
  • Renal (organ)
    • established acute tubular necrosis – ischaemic or toxic
    • glomerulonephritis/vasculitis
    • tubulointerstitial nephritis
  • Post-renal (obstructive)

ASSESSMENT

Relevant clinical history

  • Obtain previous U&E for evidence of pre-existing renal dysfunction
  • Full medication history
    • prescribed and non-prescribed drugs; iodinated contrast investigations
  • History of urinary tract symptoms OR renal stone disease
  • History suggestive of sepsis
  • History of vascular disease

Fever, arthralgias, rashes

  • Small vessel vasculitis
    • granulomatosis with polyangiitis, microscopic polyangiitis
  • SLE
  • Anti-glomerular basement membrane antibody disease

Haemoptysis

  • Small vessel vasculitis
  • Anti-glomerular basement membrane antibody disease

Haemolysis, thrombocytopenia

  • Haemolytic–uraemic syndrome

Hypercalcaemia, hyperuricaemia, bone pain, lytic lesions

  • Multiple myeloma

Recent vascular intervention

  • Cholesterol emboli syndrome
    • ± livedo reticularis, hypocomplementaemia

Prolonged severe immobility, crush injuries

  • Rhabdomyolysis
    • raised serum creatinine, creatine kinase >10,000 U/L

Physiological observations and examination

  • Haemodynamic (including volume) assessment
    • signs of shock/hypoperfusion
  • Palpation for enlarged bladder
  • Evidence of vascular disease
  • Signs suggestive of a less common cause (e.g. vasculitis)
    • haematuria/proteinuria may indicate acute glomerulonephritis/vasculitis

Sepsis

  • Suspected or confirmed infection
  • qSOFA score >2
    • RR >22 breaths/min
    • Systolic BP <100 mmHg
  • GCS ≤13

Complications of AKI

  • Pulmonary oedema
  • Hyperkalaemia – see Hyperkalaemia guideline
  • Tachypnoea suggests fluid overload and/or acidosis
  • Pericardial/pleural rub
  • Neurological manifestations of uraemia
    • e.g. encephalopathy (exclude other causes of confusion/delirium)

Multiple organ failure

  • Hypotension
    • mean arterial pressure (MAP) <65 mmHg] despite initial fluid resuscitation up to 30 mL/kg, or
    • inotrope or vasopressor dependency
  • Impaired gas transfer: hypoxaemia (PaO2 <10 kPa) despite 40% oxygen
  • Metabolic acidosis – compensated as well as uncompensated
  • Pulmonary shadowing/oedema on chest X-ray
  • Patient looks severely ill/exhausted/obtunded

Ultrasound

  • If cause not identified, renal ultrasound scan within 24 hr of AKI recognition
    • assess renal size/exclude obstruction
  • If pyonephrosis [infected and obstructed kidney(s)] suspected, immediate ultrasound of the urinary tract
    • perform within 6 hr of assessment

IMMEDIATE MANAGEMENT

Referral

Critical care

  • Identify patients with developing or established multiple organ failure early
  • Refer to critical care

Renal

  • Discuss with renal team or AKI specialist nurse any patient with:
    • creatinine >350 µmol/L or >3 fold rise in creatinine from known baseline (AKI Stage 3)
    • CKD stage 5 or renal transplant
    • AKI without obvious cause (e.g. volume depletion, sepsis)
    • AKI with haematuria/proteinuria
    • AKI with complications (see above)
  • Discuss patients with suspected tumour lysis syndrome (massively increased serum uric acid) urgently with renal team or oncology
  • Refer patients whose renal function declines (even if creatinine <300 µmol/L) despite initial resuscitation to renal team within 48 hr of diagnosing AKI

Sepsis

  • See Sepsis guideline

Fluid balance

  • Careful assessment of volume status including calculation of any fluid deficit
  • Accurately chart fluid input and urine output (urinary catheter may be required)
  • Fluid resuscitation with crystalloids to achieve appropriate physiological targets
    • systolic blood pressure >100 mmHg or MAP >65 (higher if normally hypertensive) and/or
    • resolution of tachycardia and/or
    • restoration of adequate urine output as per Fluid resuscitation guideline
  • Insert CVP line if necessary and maintain CVP pressure 10–14 cm H2O
  • In patients who remain oliguric, carry out careful reassessment to avoid fluid overload
  • Once rehydrated, continue IV crystalloid to match urine output + 30 mL/hr plus continuing fluid losses
  • If patient is fluid overloaded (i.e. pulmonary oedema with oliguria), give furosemide 250 mg in 25 mL by IV infusion over 2 hr using infusion pump or syringe driver
    • do not use furosemide unless evidence of fluid overload
  • If no response, contact renal team urgently
  • Recheck U&E daily to assess changes in renal function
  • Do not use dopamine or mannitol

Urinary tract obstruction

  • Undertake nephrostomy or stenting as soon as possible and within 12 hr of diagnosis

Drugs

  • Discontinue/avoid nephrotoxins
    • e.g. NSAIDs/ACE inhibitors/angiotensin-II receptor antagonists
  • Stop metformin/sulphonylurea drugs
    • may accumulate in acute kidney injury
  • Adjust dose of any drugs given in renal failure. consult BNF or renal drug handbook
  • Consider appropriateness of restarting drugs following resolution of AKI

Renal replacement therapy

  • Refer to renal team for possible haemodialysis or continuous renal replacement therapy if evidence of:
    • fluid overload with oliguria
    • potassium >6.5 mmol/L – see Hyperkalaemia guideline
    • uraemia
    • severe acidosis

SUBSEQUENT MANAGEMENT

  • Discuss with renal team

MONITORING TREATMENT

  • Daily weight and fluid balance
  • Daily U&E
  • Monitoring of underlying cause

DISCHARGE AND FOLLOW-UP

  • If renal function remains abnormal despite treatment and eGFR <30 mL/min, arrange outpatient review by renal team
  • U&E check in community within 6 weeks with GP team or, if eGFR <30, within 2 weeks
  • Patient medication advice leaflet available for patients with CKD, hypertension and cardiac failure

© 2022 The Bedside Clinical Guidelines Partnership.

Created by University Hospital North Midlands and Keele University School of Computing and Mathematics.

Research and development team: James Mitchell, Ed de Quincey, Charles Pantin, Naveed Mustfa