Acute Kidney Injury

Background and Epidemiology

  • AKI is a clinical syndrome- not a diagnosis
  • Increasingly common, particularly in hospitalised patients (up to 15%); older patients and critically ill patients
    • Affects 2-4/1000 patients a year
  • Accounts for 1% of hospital admissions and complicates up to 7% of inpatient episodes
  • It carries significant mortality (as high as 20-30%)

Definition/Classification

  • Stage 1
    • A rise in serum creatinine to 1.5-1.9 × baseline within 7 days OR
    • More than a 26μmol/l rise in serum creatinine within 48 hours OR
    • A urine output of <0.5ml/kg/hour for at least 6 hours
  • Stage 2
    • A rise in serum creatinine to 2-2.9 × baseline within 7 days OR
    • A urine output of <0.5ml/kg/hour for at least 12 hours
  • Stage 3
    • A rise in serum creatinine >3 × baseline within 7 days OR
    • Serum creatinine ≥354μmol/l (≥4mg/dl) OR
    • A urine output of <0.3ml/kg/hour for at least 24 hours OR
    • Anuria for at least 12 hours OR
    • Initiation of renal replacement therapy (e.g. dialysis)

Causes

  • Most common causes include
    • Acute tubular injury secondary to ischaemic tubular damage (e.g. in sepsis, hypotension, nephrotoxic drugs) (45%)
    • Acute tubular injury following surgery (pre-renal cause) (25%)
    • Acute contrast nephropathy (12%)
  • All causes can be grouped into
    • Pre-renal i.e. decreased blood flow.  Most common (40-70% of patients)
      • The blood flow to the kidney and thus GFR remains constant despite a wide range of mean arterial pressures (due to changes in pre- and post-glomerular arteriolar resistance).  However, below a mean arterial pressure of 70mmHg, autoregulation cannot accommodate and GFR falls proportionately

aki

    • Intrinsic i.e. direct kidney tissue damage. (10-50%)

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    • Post-renal i.e. obstruction of urine flow (10%)
      • Important to diagnose because rapid diagnosis and management can reverse AKI and result in complete recovery.
      • Once the obstruction is relieved- it is important to monitor for substantial diuresis and manage appropriately (fluids to avoid hypovolaemia)

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Diagnosis/Presentation

  • 5 main questions to answer
    1. Is this AKI or CKD?
      • Check previous creatinine measurements
      • USS- If the kidney is small this is more likely a chronic problem than an acute one (except in patients with diabetes- who have normal sized kidneys even in disease)
      • Symptoms/signs/markers
        • Chronicity of symptoms e.g. fatigue, nausea, nocturia, itch over long history vs acute illness e.g. fever, breathlessness, diarrhoea, sepsis etc
        • Patients with CKD typically have anaemia, hyperphosphataemia, hypocalcaemia, high PTH (less common in AKI)
    2. Have you excluded obstruction?
      • Previous Hx of stones? Presence of Lower urinary tract symptoms (LUTS)
        • Hesitancy, frequency, nocturia
        • Palpable bladder
      • Complete anuria is highly suggestive of obstruction
      • Arrange Kidney USS immediately
    3. What is the intravascular volume status of the patient?
      • Examine the patient for signs of volume status:
        • Pulse, JVP, Postural BP changes, Daily weights, fluid balance
      • Hypovolaemia is almost always associated with high levels of antidiuretic hormone, causing increased reabsorption of water and urea and a disproportionate rise in the plasma urea:creatinine ratio.
        • Note that this can be skewed by increased catabolism (e.g. in sepsis/corticosteroid use) or protein ingestion (e.g. GI bleed) which will raise plasma urea
      • Consider a cautious fluid challenge (with close monitoring)
    4. Is there evidence of intrinsic AKI other than tubular injury?
      • Despite being rare, it is important for management.
      • Are there features of potential causes e.g. systemic signs/symptoms
        • Rashes, arthralgia, myalgia
        • Recent antibiotics/NSAIDs
        • Check urinalysis, urine microscopy for haematuria/proteinuria for signs of glomerulonephritis or interstitial nephritis
    5. Has a major vascular occlusion occurred?
      • Atherosclerotic disease involving the kidney arteries is relatively common in older people
      • May cause loin pain or may be asymptomatic; may have macroscopic haematuria (if severe) or complete anuria
        • Look for kidney asymmetry on USS
      • Risk factors include use of ACE inhibitors or diuretics with underlying artery stenosis; hypotension; surgery to abdominal vessels
  • Finally, consider cholesterol embolism in patients who have had interventions e.g. angiography, vascular surgery, thrombolysis or anticoagulation.

Investigation

  • Imaging
    • Kidney USS crucial (see above)
    • Other imaging may be warranted, particularly in obstruction
  • Urinalysis
    • Blood and protein suggests kidney (in particular glomerular) inflammation
      • Send also for microscopy (e.g. red cell casts for glomerulonephritis)
    • Urine specific gravity may also help determine cause
      • >1.02 suggests pre-renal cause; normal (1.01-1.02) suggests intrarenal;
  • Blood tests
    • FBC
      • Eosinophilia may be present in acute interstitial nephritis, cholesterol embolism or vasculitis
      • Thrombocytopenia suggests thrombotic microangiopathy
    • Coagulation (e.g. DIC)
    • U&Es
      • Hyperkalaemia, hypocalcaemia and hyperphosphataemia can occur after AKI (may also be seen chronically in CKD)
      • Blood urea nitrogen (or urea) : Creatinine ratio
        • May help identify whether the AKI is prerenal, post-renal or intrinsic
        • NB This has been shown to not be an accurate tool for predicting cause and mortality- so is not commonly used
          • >20:1 (BUN:C) or >100:1 (U:C) suggests pre-renal cause (less urea is being filtered)
          • Normal (between 10:1 and 20:1 (or 40-100:1)) suggests post renal cause (not a problem with kidney)  or intrinsic cause
          • Low (<10 or 40:1) has been associated with acute tubular necrosis (intrarenal cause)
    • CRP
    • Creatine kinase (if raised suggestive of rhabdomyolysis)
  • ABGs
    • metabolic acidosis (low bicarbonate and low pH)
  • Immunology
    • You may want to request antibody tests e.g. antinuclear or anti-dsDNA antibodies (for systemic connective tissue/inflammatory diseases e.g. SLE); ANCA (c-ANCA for Wegener’s; p-ANCA for microscopic polyangitis); antiglomerular-basement-membrane antibodies (Goodpasture’s disease)
    • Comlement (SLE, post-infective glomerulonephritis)

Management (for treatment of specific causes see relevant posts)

  • Identify and treat acute complications
    • Hyperkalaemia
      • Check drug chart and stop any potassium (in fluids), any potassium sparing diuretics and ACE inhibitors
      • Urgently obtain 12-lead ECG
      • If K+ >7mmol/l of there are significant ECG changes (loss of P wave, widening QRS, loss of ST segment or tall T waves) give 10ml of 10% calcium gluconate IV stat.  You may need to repeat this (monitor every 10 minutes until ECG normalises)
        • NB Calcium is very irritant so be aware where you are flushing it through
      • If K+ remains >6.5mmol/l and there are no indications for immediate dialysis, give 10 units of actrapid (insulin) in 100ml of 20% dextrose over 15 minutes.
        • Monitor blood glucose for 6 hours
        • Consider nebulised salbutamol also
      • If K+ 6- 6.5mmol/l – you can give calcium resonium 15g QDS with laxatives
      • Check K+ every two hours.  If continues to rise, refer urgently to nephrologist/critical care (dialysis may be required)
    • Acidosis
      • Consider giving 300-600ml of isotonic sodium bicarbonate if venous bicarbonate is <22mmol/l and the patient is not hypernatraemic or in fluid overload.
      • If severe, refer to critical care
    • Pulmonary oedema (often iatrogenic)
      • Give oxygen (high flow)
      • Sit the patient up
      • If haemodynamically stable, give 80mg IV furosemide (note that it may not be effective if kidney is severely injured)
      • Give morphine to aid breathlessness and anxiety (also vasodilates)
        • IV nitrates can also be given (if SBP>100mmHg)- closely monitor BP
      • If severe, refer for possible haemodialysis or haemofiltration 
    • For a patient with severe fluid overload
      • Furosemide bolus (repeat if necessary)
      • If this fails, consider higher dose infusion of furosemide and/or dopamine infusion
      • Next, try nitrate infusion (providing SBP>90mmHg);
      • Finally, transfer to ITU and/or haemofiltration/dialysis
      • Consider venesection of 2-3 units in exceptional circumstances (e.g. no specialist facilities close by)
  • Identify/correct pre-renal and post-renal factors.
    • May require central monitoring if haemodynamic status is difficult to measure or the patient requires critical monitoring
    • Optimise cardiac output and kidney blood flow
      • Fluids to restore circulating volume (if volume deplete) or blood if blood-loss
    • Relieve obstruction if possible with catheter of nephrostomy
  • Review medications
    • Stop nephrotoxic drugs and review renally excreted drug doses
  • Monitor fluid balance and measure daily weights
  • Optimise nutrition (consider K+ restriction)
  • Identify and treat any infection (this may necessitate removal of catheter/indwelling lines etc)
  • Identify and treat any bleeding tendency
    • Avoid aspirin
    • Give H2-receptor blockers or PPIs to prevent GI bleed (AKI reduces gastrin clearance so increases the risk of gastritis/GI bleed)
      • NB only if warranted
  • Absolute indications for dialysis include:
    • Refractory hyperkalaemia; pulmonary oedema; acidosis; uraemia
    • Encephalopathy or pericarditis caused by AKI
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