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Contrast-Induced Nephropathy


KEY FACTS

Terminology

  • Acute kidney injury (AKI) within 24-48 hours following intravascular administration of contrast material (CM); must exclude other causes of AKI

    • AKI: Absolute increase in serum creatinine of 0.5 mg/dL or relative 25% increase from baseline value

Imaging

  • Delayed nephrogram on subsequent CT or KUB

Top Differential Diagnoses

  • AKI

    • Other causes of AKI, such as nephrotoxic drugs, prerenal azotemia, urinary obstruction, etc.

    • It may be difficult to recognize exact cause of acute tubular necrosis (ATN) in inpatients since they are exposed to multiple risk factors

  • Acute interstitial nephritis

  • Renal atheroembolic phenomena

Pathology

  • Animal models have indicated that ATN is underlying pathogenesis, but mechanism by which ATN occurs is not well understood

    • Renal vasoconstriction

    • Direct tubular injury

  • Risk of CIN is deterministic (dose dependent)

Clinical Issues

  • Prophylaxis

    • Consider alternative imaging methods not requiring CM

    • Use lower dose of CM; avoid closely spaced contrast-enhanced studies

      • –

        Hypoosmolar and isoosmolar nonionic CM have been shown to be superior to hyperosmolar ionic agents

    • Intravenous hydration

    • N-acetylcysteine, orally or IV

    • Discontinuing nephrotoxic drugs

    • No benefit in prophylactic hemodialysis

Radiograph taken 18 hours after a coronary angiogram shows persistent nephrograms
, a finding indicating acute tubular necrosis. The densely opacified bile within the gallbladder
is due to vicarious excretion of contrast through the hepatobiliary system to compensate for the decreased renal excretion.

Axial NECT shows dense bilateral nephrograms
with otherwise normal-appearing kidneys in a patient with acute renal failure following angiography. Ascites is also present
.

Photomicrograph in a patient with osmotic tubulopathy associated with use of iodinated contrast shows tubular profiles that have cytoplasmic swelling, vacuolization, and preservation of the brush borders
. (From DP: Kidney, 2e.)

Photomicrograph, H&E staining, in a patient with acute tubular necrosis shows epithelial attenuation, loss of apical cytoplasm, prominent dilated tubules, and focal, largely distal, tubular epithelial vacuolization
. (From DP: Kidney, 2e.)

TERMINOLOGY

Abbreviations

  • Contrast-induced nephropathy (CIN)

Definitions

  • Acute kidney injury (AKI) within 24-48 hours following intravascular administration of contrast material (CM); must exclude other causes of AKI

    • AKI: Absolute increase in serum creatinine of 0.5 mg/dL or relative 25% increase from baseline value

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