Contrast-induced nephropathy

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