Contrast-induced nephropathy

Background

  • Often defined as creatinine rise of more than 0.5 mg/dL or ≥25% above baseline[1]
  • Vasoconstriction leading to ischemia in the deeper portion of the outer medulla
  • Toxic to kidney tubular cells, inducing vacuolization, change in mitochondrial function, and apoptosis
  • Less likely to occur with low and iso-osmolar contrast agents

Healthy Patients

  • CIN not likely to occur in patients with a Cr<1.5 or a GFR >60ml/min[2][3]

Impaired Renal Function

  • Administration should follow your local hospital protocols
  • Less likely to occur in iso-osmolar contrast agents (iodixanol/Visipaque) and possibly not even an occurrence if the serum creatinine is greater than 2.0 mg/dL. [4]

Clinical Features

  • 0.5mg/dl absolute or >25% relative increase in serum creatinine 48-72hrs after contrast exposure

Differential Diagnosis

  • Poor renal perfusion
  • Nephrotoxic medications

Workup

Management

  • Hydration
  • N-acetylcysteine

See Also

Sources

  • Golshahi, J, Hasri H, Gharipour M. Contrast-induced nephropathy; A literature review. J Nephropathol. 2014;3(2):51-56.
  • Persson PB, Hansell P, Liss P. Pathophysiology of contrast medium induced nephropathy. Kidney Int. 2005;68:14–22

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  1. Goldfarb, S. et al. Contrast-Induced Acute Kidney Injury: Specialty-Specific Protocols for Interventional Radiology, Diagnostic Computed Tomography Radiology, and Interventional Cardiology. Mayo Clin Proc. Feb 2009; 84(2): 170–179 Text
  2. Davenport MS. et al. Contrast material-induced nephrotoxicity and intravenous low-osmolality iodinated contrast material. Radiology. 2013 Apr;267(1):94-105
  3. Sinert R, Brandler E, et al. Acad Emerg Med2012;19(11):1261
  4. McDonald RJ, McDonald JS, et al. Radiology. 2013;267(1):106