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

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

• 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)

 

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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