Tubular Necrosis

Acute tubular necrosis

• Ischaemia or toxic insult can lead to extensive necrosis of the renal tubular epithelial cells.
• The proximal convoluted tubules are most susceptible to damage due to their high metabolic rate.
• Oliguria or anuria often occur as a consequence of intratubular obstruction, leakage of urine into the interstitium, or activation of the renin-angiotensin-aldosterone system.
• Protein casts are sometimes seen in the urine.
• The tubular basement membrane usually remains intact therefore allowing for renal function to be restored.
• Consequences depend on the severity of insult and how intact the basement membrane is.
• 2 subtypes exist: ischaemic and nephrotoxic.
  • Ischaemic - this form often causes basement membrane damage and disruption. Severe hypotension can be the cause.
  • Nephrotoxic - antimicrobials, heavy metals, phytotoxins, oxalates, and antineoplastic agents can cause.

Antimicrobials such as aminoglycosides and tetracyclines have been implicated. Their use is contraindicated in animals with preexisting renal disease or dehydration.

Heavy metals such as mercury, lead or arsenic can lead to tubular necrosis.

Oxalates, present in plants such as rape, kale, rhubarb as well as ethylene glycol are excreted through the kidneys and precipitate as crystals. These crystals cause damage, obstruction and eventually lead to uraemia.