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Flashcards in Tubular Necrosis Deck (9)
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What is acute tubular necrosis?

  • Abrupt and sustained decline in GFR within minutes to days after ischaemic / nephrotoxic insult. 
  • It leads to an abrupt rise in urea and creatinine.


What are the risk factors for acute tubular necrosis?

  • Pre-existing CKD
  • CVD
  • ECF volume depletion
  • Multiple renal insults


What are the complications of acute tubular necrosis?

  • Hyperkalaemia
  • Metabolic acidosis
  • Decreased Ca2+
  • Increased PO43-
  • Hypoalbuminaemia


Describe the pathophysiology of acute tubular necrosis.

  • Tubular injury due to ischaemic or toxic insult.
  • Initially, it results in focal loss of tubular epithelial cells.
  • Later, tubules go through a recovery phase where there is regeneration of tubular cells. 
  • This leads to urine which has high fractional excretion of sodium and the excretion of pigmented-granular casts or muddy brown casts. 
    • This is how ATN is distinguished from acute interstitial nephritis or glomerular nephritis. 


What are the 2 causes of acute tubular necrosis?

  • Ischaemia
  • Nephrotoxin


What are the toxic causes of acute tubular necrosis?

  • Exogenous
    • Antibiotics such as aminoglycosides, cephalosporins and amphotericin B.
    • Antivirals
    • Antineoplastics such as cisplastin and methotrexate.
    • Contrast medium 
      • Leads to contrast-induced nephropathy.
      • Can also cause vasoconstriction – so it can cause a nephrotoxic injury and an ischaemic injury.
    • Heavy metals
    • Ethylene Glycol
  • Endogenous
    • Bacterial endotoxins
    • Myoglobin
      • From Rhabdomyolysis – if a patient has severe injury where skeletal muscle is damaged, myoglobin can be liberated into the bloodstream and damage renal tubules
    • Haemoglobin


What are the ischaemic causes of acute tubular necrosis?

  • Hypotension
  • Shock
  • Decreased circulating blood volume (has the same effect as hypotension)
    • Haemorrhage
    • Fluid losses – skin losses or GI losses
  • Decreased effective circulating blood volume
    • Heart failure
    • MI
    • Liver failure – patient has the fluid but it is not being delivered to the kidneys.
    • Anaphylaxis (can lead to decrease in systemic vascular resistance, in effect leading to decreased effective circulating volume to the kidneys).
    • Vessel occlusion – blocks delivery of blood to the kidney (renal artery stenosis can be a cause of this). 


Describe the treatment for acute tubular necrosis.

  • Correct the underlying problem.
    • Identify the nephrotoxic agent and stop it.
    • If injury – correct the rhabdomyolysis.
    • If infection is causing circulation of bacterial endotoxins and this is causing injury the infection should be treated. 
    • If the cause is ischaemic, try to improve BP and if fluid is depleted that should be corrected. 
    • Once these things have been done, treatment is supportive
    • If the ATN is severe or rapidly progressing, early dialysis should be considered. 


How can acute tubular necrosis be prevented?

  • Identify high risk patients and avoid using nephrotoxins if possible. 
  • If imaging is absolutely necessary and the patient needs contrast, patient can be given N-Acetylcystein (600-1200mg PO bid day) – before and after radiographic contrast. Also give IV fluid. 
  • Before contrast procedure, avoid use of diuretics, ACE-inhibitors and cyclosporine.