Overview
Acute tubular necrosis (ATN) is the most common cause of acute kidney injury (AKI). It describes the death of tubular epithelial cells in the kidney and occurs due to ischaemia or nephrotoxic drugs. The presence of ‘muddy brown casts’ is pathognomonic for ATN.
Causes
- Any scenario causing hypoperfusion, such as haemorrhage, sepsis, or excessive fluid loss – can lead to ischaemia
- Exposure to nephrotoxic agents such as NSAIDs, ACE inhibitors, aminoglycosides (e.g. gentamicin), radiocontrast media, and ethylene glycol
- Rhabdomyolysis – the release of myoglobin can lead to ATN
- Causes of increased uric acid (e.g. gout or tumour lysis syndrome)
- Causes of increased light chain proteins (e.g. multiple myeloma)
Presentation
Patients may not have any symptoms except for an AKI on blood tests.
- Oliguria and/or anuria may be present
- ATN responds poorly to fluids
Differential Diagnoses
Acute interstitial nephritis (AIN)
- Eosinophilia, rash, and elevated IgE make AIN more likely
- Urinalysis may show sterile pyuria and does not show muddy brown casts in AIN
Investigations
- Urea and electrolytes (U&Es):
- Urea and creatinine may be elevated
- Hyperkalaemia may be present
- Urea:creatinine ratio – calculated by dividing urea by creatinine, ensuring units are the same:
- A ratio of <40:1 suggests a renal cause
- Urinary sodium:
- Elevated – tubular dysfunction leads to increased sodium excretion
- Urinalysis:
- Shows muddy brown casts
Management
Management is supportive (correcting electrolyte and acid-base abnormalities, and maintaining volume status). See Acute Kidney Injury for more information.
