Acute Tubular Necrosis

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  • common in hospital

Causes

Mechanisms

  • entry of calcium into cells
  • induction of nitric oxide
  • increased production of intracellular proteases
  • activation of phospholipase A2, increasing production of free-fatty acids
  • reperfusion injury
  • vasoconstriction
  • liberation of toxic endothelial factors
  • damage from vasodilator endotoxins
  • reduced prostaglandin production
  • tubular obstruction by desquamated cells and casts

Reduced Glomerular Filtration Rate by

  • glomerular contraction
  • reflex afferent arteriolar spasm
  • 'back leak' of filtrate
  • obstruction of tubule

Clinical Course

  • oliguria common
  • recovery of function 7-21 days
    • delayed by continuing sepsis
    • GFR remains low but urine output increases
  • may be up to 6 weeks before full recovery

Clinical Features

Symptoms

  • anorexia
  • nausea
  • vomiting
  • pruritus
  • intellectual clouding
  • drowsiness
  • fits
  • coma
  • haemorrhagic episodes
    • epistaxis
    • GI haemorrhage
  • infection

Signs / Biochemistry

Treatment

  • keep em alive until kidneys recover!!!
  • early transfer to nephrologist / intensivist with access to haemodialysis
  • don't need a catheter (and increases risk of sepsis)
  • Good nursing / physiotherapy
    • fluid balance
    • daily body weight
  • Emergencies
    • hyperkalaemia
    • Pulmonary Oedema
      • will probably need haemodialysis unless diuretics work
    • Sepsis
      • avoid nephrotoxic drugs
      • appropriate alterations of drug dosage
  • Diet
    • sodium and potassium restriction
    • if trying to avoid haemodialysis then protein below 40g / day
      • otherwise 70g+ / day
  • Haemodialysis

Prognosis

  • overall mortality 50%
 

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