Renal cortical necrosis

Renal cortical necrosis occurs as a result of severe systemic illness in a variety of settings and can result in permanent renal impairment. The condition is usually bilateral but may occasionally be unilateral. 

Pathology

Etiology

• severe hemodynamic shock

  • hemorrhagic shock

    • postpartum hemorrhage: most common cause, and most often associated with placental abruption in the third trimester ³

    • traumatic blood loss

  • septic shock

  • venom toxin

  • transfusion reaction

  • severe dehydration

  • acute aortic dissection

• microangiopathic hemolysis 

  • hemolytic uremic syndrome (HUS)

• renal transplantation

Radiographic features

CT

Contrast-enhanced CT demonstrates a non-enhancing renal cortex and a normal enhancing renal medulla (reverse rim sign). A very thin rim of contrast enhancement (cortical rim sign) may persist and should not be mistaken for adequate perfusion.

Global atrophy of the kidneys occurs within a few months, leading to small smooth kidneys. 

Eventually dystrophic calcification of the renal cortex may be seen (cortical nephrocalcinosis), sometimes referred to as “tramline” calcification.

MRI

Low signal intensity on both T1 and T2 weighted sequences affecting the inner renal cortex and the columns of Bertin is the major characteristic finding of renal cortical necrosis ¹.

Additional features include:

• swelling of both kidneys

• corticomedullary differentiation seen better on T2-weighted images instead of T1-weighted images

Note that the cortical rim sign can persist in renal cortical necrosis because of its separate capsular blood supply.

Differential diagnosis

• other causes of low signal intensity renal parenchyma on MRI