Contrast-induced nephropathy

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This page only applies to contrast agents usually used for CT scans. MRIs with contrast use gadolinium, which can cause nephrogenic systemic fibrosis in patients with renal dysfunction.

Background

  • Often defined as creatinine rise of more than 0.5mg/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 contrary to traditional teaching, maybe not even an occurrence in patients with creatinine greater than 2.0mg/dL. [4]

Risk Factors

  • Renal disease
  • Recent contrast study within 72 hrs
  • Hypotension
  • Dehydration
  • DM
  • Multiple myeloma
  • Age > 70
  • hypertension
  • Hyperuricemia
  • Diuretics

Clinical Features

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

Differential Diagnosis

  • Poor renal perfusion
  • Nephrotoxic medications

Contrast induced complications

Evaluation

  • Same as for AKI

Management

Hallmark of management is prevention in at-risk patients.

Hydration

  • Isotonic hydration with Normal Saline 1-1.5L (15ml/kg) prior to the contrast load in patients with impaired renal function may lessen the chances of developing CIN [5][6][7]
  • If suspect the development or confirm the diagnosis continue adequate hydration to maintain urine output of 0.7cc-1cc/kg
  • Early research suggests a potential benefit for forced furosemide diuresis (300ml/h) while continuing intravenous hydration fluids (0.5mg/kg) but should be performed in consult with radiologist and nephrologist[8]

N-acetylcysteine

  • Is not useful for preventing CIN[9][7]

Other Measures

  • Low osmolar contrast agents
  • Bicarbonate infusion
  • Hypertonic saline

See Also

References

  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
  5. Mueller C. et al. Prevention of contrast media-associated nephropathy: randomized comparison of 2 hydration regimens in 1620 patients undergoing coronary angioplasty. Arch Intern Med. 2002;162(3):329
  6. Bertrand Dussol. et al. A randomized trial of saline hydration to prevent contrast nephropathy in chronic renal failure patients. Nephrol. Dial. Transplant. 2006. 21 (8): 2120-2126
  7. 7.0 7.1 Traub SJ, et al. N-acetylcysteine plus intravenous fluids versus intravenous fluids alone to prevent contrast-induced nephropathy in emergency computed tomography. Ann Emerg Med 2013;62(5):511-20 PDF
  8. Marenzi G. et al. Prevention of contrast nephropathy by furosemide with matched hydration: the MYTHOS (Induced Diuresis With Matched Hydration Compared to Standard Hydration for Contrast Induced Nephropathy Prevention) trial. JACC Cardiovasc Interv. 2012 Jan;5(1):90-7
  9. ACT Investigators. Acetylcysteine for prevention of renal outcomes in patients undergoing coronary and peripheral vascular angiography: main results from the randomized Acetylcysteine for Contrast-induced nephropathy Trial (ACT). Circulation. 2011 Sep 13;124(11):1250-9 PDF