Contrast-associated acute kidney injury

Background

• Risk based on eGFR1
  • eGFR >45 mL/min: 2%
  • eGFR <60 mL/min: 5%

Clinical Manifestations

• Presents with AKI following administration of CT contrast dye, usually non-oliguric
• Increase in serum creatinine usually seen 24 to 48 hours after infusion
• Urine microscopy may show findings of acute tubular necrosis with muddy brown casts, epithelial casts, and free renal tubular epithelial cells

Prognosis

• Usually only causes mild AKI that generally starts to recover within 3 to 7 days, with eventual return to baseline renal function
• Rarely progresses to dialysis

Differential Diagnosis

• Renal atheroembolism (with intraarterial contrast)
• Ischemic acute tubular necrosis
• Acute interstitial nephritis
• Prerenal changes related to medication adjustments
• Other causes of acute kidney injury

Management

• Managed similarly for all AKI
  • Stop nephrotoxic medications such as aminoglycosides, vancomycin, non-steroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers
  • Optimize hemodynamics and volume status
  • Closely monitor kidney function and fluid balance
  • Avoid hyperglycemia
  • Avoid further exposure to contrast agents
  • Avoid gelatins, colloids, and chloride-rich solutions

Prevention

• Prophylaxis with preinfusion of saline is common but the only RCT to date showed no benefit2
• The evidence in favour of N-acetylcysteine is similarly poor

Further Reading

• Contrast-associated acute kidney injury: does it really exist, and if so, what to do about it? F1000Res. 2019;8:F1000 Faculty Rev-753. doi: 10.12688/f1000research.16347.1