Urogenital ImagingAcute tubular necrosis
a common form of acute
renal failure, characterized pathologically by destruction of
tubular epithelial cells. Recognition of acute
tubular necrosis is of major prognostic significance, because the condition is reversible and compatible with full recovery of
renal function. Acute
tubular necrosis is seen after exposure of the kidney to certain nephrotoxins or after a period of prolonged ischaemia. Accordingly, acute
tubular necrosis may be subclassified as nephrotoxic or
ischaemic, respectively. Nephrotoxic acute
tubular necrosis may be caused by drugs (contrast media, aminoglycosides), heavy metals and solvents.
Ischaemic acute
tubular necrosis is usually seen in severe shock, such as in sepsis or after major burns. Incompatible blood transfusion or other causes of massive haemolysis may also result in
ischaemic acute
tubular necrosis. Cadaveric
renal transplants frequently develop acute
tubular necrosis.
Acute tubular necrosis results in bilateral symmetric renal enlargement, which may be demonstrated by ultrasound (US), CT or MRI. Urography is no longer recommended in the evaluation of suspected acute tubular necrosis, but historically was used for diagnosis by demonstration of dense persistent nephrograms without opacification of the collecting systems. Some cases demonstrate an increasingly dense nephrogram. US findings include increased cortical echogenicity with preservation of corticomedullary differentiation, increased pyramidal echogenicity with a normal cortex and decreased echogenicity with pyramidal swelling. These widely varying findings probably reflect the wide variety of causes of acute tubular necrosis. Occasionally, calcification develops in the proximal convoluted tubules as a late manifestation of acute tubular necrosis, and may be detectable by US or CT. Selective renal arteriography has been performed in patients with acute tubular necrosis, mainly on an investigative basis. These studies have shown reduction in calibre and accentuated tapering of the interlobar and arcuate arteries. The arterial walls, however, remain smooth. The arcuate arteries have been described as attenuated; the arteries of the renal cortex are not discernible. The normally sharp line between cortex and medulla is absent, and the renal vein poorly visualized. It is claimed that these angiographic findings can be used to distinguish acute tubular necrosis from other causes of acute oliguric renal failure.
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