Definition

 • Acute injury to renal tubules leading to AKI.

• The equivalent terminology ‘acute tubular necrosis’ is less accurate, as only the most severe of cases of acute tubular injury have necrosis as a histological feature.

 Epidemiology

 • One of the most common causes of AKI.

Aetiology

• Ischaemia due to prolonged hypoperfusion (e.g. hypotension, sepsis).

• Nephrotoxins such as specific nephrotoxic drugs (e.g. calcineurin inhibitors), radiological contrast, haemoglobin, myoglobin, oxalate crystals (e.g. hereditary hyperoxaluria or ethylene glycol poisoning), etc.

Pathogenesis

 • Tubular epithelial cells are metabolically active and very sensitive to damage from ischaemia or toxins.

Presentation • AKI.

Histopathology

• The injured tubules are dilated, with flattening of tubular epithelial cells and loss of the brush border (Fig. 1).

Fig1. Acute tubular injury. Haematoxylin and eosin stain. The epithelial cells are flattened and the tubular lumen is widened. Arrow indicates a sloughed tubular epithelial cell in the lumen of a tubule (see Plate 17).

• Sloughed epithelial cells may be seen in the lumen of distal tubules, sometimes combining to form ‘granular casts’.

• The interstitial compartment is expanded by oedema, with few or no inflammatory cells.

• Clues to the underlying cause may be present (e.g. birefringent intraluminal oxalate crystals in ethylene glycol poisoning or typical myoglobin casts in rhabdomyolysis).

Prognosis

 • Depends on underlying cause and reversibility of the cause.

• When seen in the context of ischaemic injury, often associated with a severe circulatory disturbance and a significant mortality rate.