Revision 2 for 'Acute tubular necrosis'All Revisions
Acute tubular necrosis
Acute tubular necrosis refers to intrinsic renal failure secondary to reduced tubular flow rate. It is the most common intrinsic cause of acute kidney injury and often reversible. 2,3,4
Acute tubular necrosis is characterized by renal tubular cell damage and death and is usually caused by ischemic or nephrotoxic insults. Deposition of cellular debris within the tubules results in oliguria.
- blood loss
- septic shock
- renal transplant
- amphotericin B
- radiocontrast media
- sulfa drugs
- antiviral (acyclovir, cidofovir, foscarnet)
- immunosuppressant (tacrolimus, cyclosporine, everolimus)
- chemotherapy (cisplatin, ifosfamide, temsirolimus)
As cellular debris deposits within and obstructs the tubules, the renal parenchyma perfusions are preserved with minimal or absent excretion into the pelvicalyceal system.
Fluoroscopy / CT IVP
Contrast imaging typically demonstrates gradual or immediate dense nephrogram. Delayed 24 hours imaging would also demonstrate persistent nephrogram or striated nephrogram due to stasis of contrast within the renal tubules. 3,4
Routine ultrasounds are usually performed to assess the renal parenchyma and exclude other causes of obstruction. In acute tubular necrosis, kidneys are enlarged and increased echogenicity. 5
Renal scintigraphy assists to differentiate acute tubular necrosis from other conditions with other irreversible causes of renal failure such as renal cortical necrosis. It may also be performed for post renal transplant assessment.
Renal perfusion is preserved during angiographic phase with a gradual increase of radiotracer due to minimal or absent excretion. 1