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Acute kidney injury (AKI)


Epidemiology of acute kidney injury  (AKI)

  • Staging (Kidney Disease Improving Global Outcomes grouping)
    • Uses both serum creatinine and urine output


  • 1.5–1.9 times baseline
  • OR
  • ≥0.3 mg/dl (≥26.5 mmol/l) increase
  • <0.5 ml/kg/h for 6–12 hours
  • 2.0–2.9 times baseline
  • <0.5 ml/kg/h for ≥12 hours
  • 3.0 times baseline
  • OR
  • Increase in serum creatinine to ≥4.0 mg/dl (≥353.6 mmol/l)
  • OR
  • Initiation of renal replacement therapy
  • OR, In patients <18 years, decrease in eGFR to <35 ml/min per 1.73 m2
  • <0.3 ml/kg/h for  ≥24 hours
  • OR
  • Anuria for  ≥12 hours


  • Grading of AKI directly is proportional to mortality
    • Chertow, Glenn M., et al. “Acute kidney injury, mortality, length of stay, and costs in hospitalized patients.” Journal of the American Society of Nephrology 16.11 (2005): 3365-3370.
  • Costs approximately 1.2 billion pounds per year in the UK, not including those who go on to CRF


Causes of acute kidney injury (AKI)

  • AKI is NOT a diagnosis – it is a reflection of an unwell patient
  • Nearly always signifies a systemically unwell patient rather than a primary renal injury- the history is very important!
  • Classically broken into pre-renal, renal and post-renal
  • There can often be a mixture of all aetiologies


Pre-renal causes of acute kidney injury (AKI)

  • Renal blood flow is compromised causing a reduced glomerular filtration rate
  • Fluid
    • Hypovolaemia (bleeding, dehydration, burns, pancreatitis)
    • Hypotension (e.g. septic shock)
    • Heart failure – low cardiac output
    • Liver cirrhosis causing low volume
  • Vascular
    • Renal artery stenosis
  • Impairment of renal blood flow autoregulation
    • Liver disease (hepatorenal syndrome – rare)
    • ACE inhibitors and NSAIDs


Renal causes of acute kidney injury (AKI)

  • Acute tubular necrosis
    • Ischaemia
      • Hypovolaemia, CCF, renal artery stenosis, hepatorenal syndrome
        • Basically all the causes of pre-renal failure, hence why intrinsic and pre-renal disease overlap.
    • Nephrotoxic
      • Endogenous
        • Haemoglobinaemia
          • DIC and other causes of haemolysis
        • Myoglobinuria: Rhabdomyolysis (NB have low ca in these and very high cr>ur)
        • Myeloma kidney disease – light chain nephropathy and tubular cast damage
        • Tubular crystal formation
      • Exogenous
        • Imaging contrast
        • Nephrotoxic medication
          • Drugs
            • Aminoglycosides
            • Amphoteracin
            • Contrast agents
            • NSAIDs
            • Platinum drugs
  • Acute tubulointerstitial nephritis
    • Drugs: NSAIDS, penicillins, diuretics, antiretrovirals and many more
    • Infections: TB, legionella, leptospirosis
    • Autoimmune: Sarcoid and Sjorgen’s
  • Acute glomerulonephritis
  • Vascular
    • Thrombotic micorangiopathies
      • Haemolytic Uraemic Syndrome,
      • Thrombotic Trombocytopaenic Purpura
      • Pre-eclampsia
      • Malignant hypertension
    • Vasculitis


Post-renal causes of acute kidney injury (AKI)

  • These are all some form of obstruction either intraluminal, intramural or extrinsic obstruction
    • Intraluminal
      • Nephrolithiasis
      • Tumours
      • Sloughed papilla (post ATN, DM, sickle, analgesic nephropathy, amyloid and acute pyelonephritis)
      • Clot retention
    • Intramural
      • Reflux
      • Adynamic urethral segments
      • Neurological disorder(MS, spinal cord injury, DM, PD, post-stroke
      • Drugs: Anti-cholinergics and levodopa
      • Tumours
      • Strictures (worldwide post Schistomsomosa haematobium)
    • Extrinsic
      • Gravid uterus
      • Benign and malignant masses
      • Iatorgenic ureteric ligation
      • Benign prostatic hypertrophy/prostate cancer
      • Retroperitoneal pathology
        • Retroperitoneal fibrosis – idiopathic, post inflammatory AAA, drugs (beta blockers and ergots)


Treatment of acute kidney injury (AKI)

  • Avoidance of AKI
    • Identify high risk patients: Elderly, CKD, cardia failure, liver disease, diabetes, vascular disease, on nephrotoxic medications
    • Monitor patients appropriately: fluid balance, bloods tests
    • Maintain circulation: Hydration, resuscitation and oxygenation
    • Minimise renal insult: nephrotoxics, contrast hospital acquired infection
    • Manage acute illness
  • Optimise volume status
    • BP, CRT, pulse, oedema, sats, urine output
    • Should have iv fluid protocol
    • If fluid deplete: Crystalloid (500ml) stat bolus THEN REASSESS
    • Maintenance: Hartmanns
      • Need 25-30ml/kg water, 1mmol salt and 50-100g glucose per day
    • Evidence of crystalloid or colloid
      • Volume needed to resuscitate someone is comparable between crystalloid and colloid – SAFE study (2007) showed only 1.3x more crystalloid than colloid needed
      • No evidence from RCTs that colloid is better at all and may cause harm. They are also more expensive.
      • NB. CRISTAL study actually found that colloids (inc HES) improved mortality at 90 days post-ITU admission relative to crystalloid. So a confusing area.
    • Saline or Hartmanns
      • Plasma-lyte better outcomes than saline
  • Stop nephrotoxics
    • ACE-I, diuretics, metformin, allopurinol etc.
    • Also consider stopping antihypertensives
    • Avoid contrast if possible
  • Dialysis or haemofiltration
    • Renal ward
  • Further treatment
    • Treat sepsis – antibiotics should be given within 1 hour of suspicion of sepsis
    • Steroids (in AIN)
    • Cyclophosphamide (vasculitis)
    • Plasma exchange (HUS/TTP)


Complications of acute kidney injury (AKI)

  • Hyperkalaemia
    • Calcium gluconate 10mls of 10% if ECG changes
    • Insulin and dextrose 10units of actarapid in 50ml of 50% dextrose over 15 minutes (if potassium >6.5 mmol/L or ECG changes)
    • Salbutamol 5mg nebulised (caution in tachycardia or heart disease)
    • Insulin and salbutamol work for roughly 4 hours or less
    • Furosemide is useful if the patient is passing good volumes of urine but ONLY IF THE PATIENT IS FLUID OVERLOADED
    • Cation exchange resins are overused – moderate effect with high rates of constipation which might paradoxically make the situation worse – rectal route is preferable if must be used.
    • Renal replacement therapy if refractory
    • Longer term review diet, avoid potassium sparing diuretics/ACE-I, ARBS, NSAIDs.
    • Be wary of the potassium load in blood transfusions
  • Pulmonary oedema
    • Sit patient up
    • High-flow oxygen unless contraindicated – consider CPAP
    • Opiates e.g. IV diamorphine 1.25-2.5 mg or morphine 2.5mg-5mg as both an anxiolytic and a venodilator – don’t give too often due to accumulation in renal failure
    • If haemodynamically stable give 80mg furosemide IV and consider further boluses or infusion of 10mg/hour
    • If haemodynamically stable GTN infusion titrating up from 1mg/hour as tolerated by blood pressure (systolic above 100mmHg)
    • If unstable will need transfer to high dependency setting for urgent filtering
    • If hyperkalaemic with bicarbonate <22mmol/L and not fluid overloaded then can consider 1.26% sodium bicarbonate over 1 hour (can be given via peripheral cannula but avoid in cannula that calcium gluconate was given through)
  • Acidosis
    • Bicarbonate use should be reserved for hyperkalaemia pending specialist help
    • pH<7.15 will need immediate critical care input for filtration
  • Uraemic encephalopathy
    • Acute setting presents as coma
    • Chronically: fatigue, weakness, anorexia, nausea, metallic taste, pruritis, impotence
    • Will need emergency renal replacement therapy in the acute setting
  • Uraemic pericarditis
    • Will need RRT
  • Hypertension (more of a problem in CRF – but acute renal failure can present with hypertensive emergency and needs aggressive treatment, e.g. nitroprusside, beta blockers, ACE-I slowly over 24-48h)
  • Sepsis – avoid or adjust doses of nephrotoxic drugs (e.g. vanc and gent)
  • Electrolyte derangement – fluid, sodium and potassium restriction, and RRT if it is still there.


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