Acute tubular necrosis is commonly caused by renal ischemia resulting from conditions such as volume depletion, hypotension, septic shock, heart failure, cirrhosis, and DIC. It is also caused by exposure to various nephrotoxic medications including aminoglycosides, amphotericin B, ACE inhibitors, NSAIDs, antiviral drugs, and also caused by exposure to radio contrast substances.

• Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.
• Life-threatening causes of acute tubular necrosis may include marked volume depletion, septic shock, DIC, and hypotension.

Acute tubular necrosis is commonly caused by renal hypoperfusion resulting in ischemia, nephrotoxic medications and nephrotoxic substance exposure.

• Ischemic acute tubular necrosis:
  • Volume loss:^[1]
    • Hemorrhage
    • Severe vomitings and diarrhea
    • Burns^[2]
    • Third space fluid sequestration (eg, fractures, crush injuries)
    • Extensive use of diuretics and osmotic diuresis
  • Profound hypotension^[3][4]
  • Sepsis^[5]
  • DIC^[6][7]
  • Heart failure^[8]
  • Cirrhosis^[9]
  • Drug adverse effects:
    • ACE inhibitors^[10]
    • NSAIDs^[11]

• Toxic acute tubular necrosis: Acute tubular necrosis can occur due to direct or indirect tubular cell toxicity secondary to medications or substance exposures.
  • Exogenous nephrotoxins:
    • Aminoglycosides^[12]
    • Amphotericin B^[13]
    • Contrast media^[14]
    • Cisplatin^[15]
    • Ifosfamide^[16]
    • Foscarnet^[17]
    • Pentamidine^[18]
    • Cidofovir^[19]
    • Tenofovir ^[20]
    • Acyclovir^[21]
    • Bisphosphonates^[22]
    • Cephalosporin^[23]
    • Naproxen^[24]
    • Tacrolimus^[25]
    • Mannitol^[26]
    • Intravenous immunoglobulins:^[27] These contain sucrose which is toxic to tubular cells.
    • Cyclosporine^[28]
    • Certain herbal medications^[29]
  • Endogenous nephrotoxins:
    • Multiple myeloma^[30]: In multiple myeloma, kidney injury and renal failure is mostly caused by accumulation of light chains in renal tubules leading to obstruction as well as direct toxic effect of light chains on tubules.
    • Heme pigment–associated kidney damage: Myoglobinuria and hemoglobinuria
      • Traumatic or non traumatic rhabdomyolysis leads to release of myoglobin, which may cause tublar blockage, direct tubular injury and vasoconstriction.
      • Hemolysis leads to hemoglobinuria.
    • Crystal induced nephropathy: May be seen in association with malignancies and cytotoxic therapy^[31][32], ethylene glycol poisoning^[33] and excessive intake of vitamin C^[34]

List the causes of acute tubular necrosis in alphabetical order.