Acute Kidney Injury (AKI)

Clinical Options for Minimizing Contrast Exposure and Reducing Contrast-Induced Kidney Injury Risk

Key Takeaways

  • Contrast-induced acute kidney injury (AKI) caused by iodinated contrast medium is associated with high morbidity and mortality in at-risk patients.

  • Previous studies note that automated contrast injectors, removal of contrast from the coronary sinus, and pressure-sensitive diversion devices may help reduce contrast exposure and lower the risk for AKI.


Contrast-induced nephropathy (CIN), one of the prime causes of contrast-induced acute kidney injury (CI-AKI),1 is now the third most frequent cause of hospital-acquired renal failure.2

Characteristics of the patient and/or procedure can increase risk of CI-AKI. Patients with diabetes or preexisting chronic kidney disease must be approached with care as these conditions increase the likelihood of CIN.3 Hemodynamic instability is also another contributing risk factor for the development of CI-AKI. The type of iodinated contrast used as well as the amount administered also influences risk.

CI-AKI prophylaxis is imperative since there is no definitive treatment strategy for the condition once it has occurred. Risk stratification represents an important preventative approach to CI-AKI and one that has been previously studied. Volume expansion via intravenous 0.9% sodium chloride solution at 1 mL/kg/hr for 12 hours prior to and following the procedure is recommended for high-risk acutely ill patients in minimizing CI-AKI.4

Options for Decreasing Contrast Exposure

Automated contrast injectors may help reduce contrast use during therapeutic and/or diagnostic procedures when compared with manual injection. According to one meta-analysis, a 15% relative reduction of CI-AKI was observed with the use of automated contrast injectors and an average 45 mL decrease in contrast use.5

An invasive method for minimizing renal exposure to contrast involves removing contrast from the coronary sinus. A study by Danenberg et al. was able to successfully recover 44% of contrast after the removal and discarding of 60 mL of blood.6

Pressure-sensitive diversion devices may reduce as much as 40% of contrast, according to one study.7

In another study, approximately one third of administered contrast was recovered in patients undergoing coronary angiography.8 Serum hemoglobin levels saw a 0.5 g/dL decrease due to the removal of 169 mL of blood during aspiration. The small sample sizes in these studies were unable to demonstrate a clear reduction in CI-AKI; however, one study by Diab et al. found a significant reduction of CI-AKI with coronary sinus aspiration (5.5% vs 36%).9

There is speculation that lower serum sodium, which correlates with higher inflammatory cytokines, can increase the risk for kidney damage and CIN occurrence. A study by Yin et al. demonstrated a clear association between decreased serum sodium and increased risk of CIN in patients receiving contrast.10 Lower sodium may also be a marker for heart failure, a condition that also increases the risk for CIN following contrast administration.

A retrospective, single-center study by Flaherty et al. also provides insight into how microaxial percutaneous left ventricular assist devices, namely the Impella® heart pump, may offer protection against AKI in high-risk PCI patients.11 According to the retrospective, single-center study, the Impella 2.5® heart pump was associated with a decreased risk for AKI despite depressed ejection fraction and underlying chronic kidney disease. This option, as well as the many others mentioned above, may assist in improving patient care and outcomes, particularly among high-risk patients.

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  1. Goldfarb, S., et al., (2009). Mayo Clin Proc, 84(2), 170-179.
  2. Thomson V.S., et al., (2009). Indian J Urol, 25(4), 437-445.
  3. Heyman, S.N., et al., (2013). Biomed Res Int, 2013, 123589.
  4. Prevention of Contrast Induced Acute Kidney Injury (CI-AKI) In Adult Patients. The Renal Association. Accessed March 17, 2017.
  5. Minsinger, K.D., et al., (2014). Am J Cardiol, 113, 49–53. 
  6. Danenberg, H.D., et al., (2008). Cardiovasc Revasc Med, 9, 9–13. 
  7. Prasad, A., et al., (2015). Catheter Cardiovasc Interv, 86, 1228–1233. 
  8. Duffy, S.J., et al.,  (2010). J Am Coll Cardiol, 56(6), 525-526.
  9. Diab, O.A., et al., (2017). Circ Cardiovasc Interv, 10(1): e004348.
  10. Yin, W.J., et al., (2017). J Am Heart Assoc, 6(2).
  11. Flaherty, M.P., et al., (2017). Circ Res, 120(4), 692-700.