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Kidney Week

Abstract: SA-OR019

Contrast-Associated AKI Is Not Reflective of Intrinsic Injury

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical, Outcomes, and Trials

Authors

  • Liu, Caroline, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States
  • Weisbord, Steven D., VA Pittsburgh Healthcare System, Pittsburgh, Pennsylvania, United States
  • Kaufman, James S., VA New York Harbor Healthcare System, New York, New York, United States
  • Thiessen Philbrook, Heather, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States
  • Mor, Maria K., VA Pittsburgh Healthcare System, Pittsburgh, Pennsylvania, United States
  • Palevsky, Paul M., VA Pittsburgh Healthcare System, Pittsburgh, Pennsylvania, United States
  • Parikh, Chirag R., Johns Hopkins University School of Medicine, Baltimore, Maryland, United States

Group or Team Name

  • PRESERVE Trial Study Group
Background

There is controversy regarding the mechanism of contrast-associated acute kidney injury (CA-AKI). Biomarkers may provide insight into whether the etiology of CA-AKI is mediated by nephron injury. The PRESERVE trial followed participants for CA-AKI and 90-day major adverse kidney events and death (MAKE-D) after contrast angiography. In this sub-study, we evaluated the association of the absolute changes (Δ) and relative ratios of urine and plasma biomarkers with CA-AKI and MAKE-D.

Methods

We measured injury (KIM-1, NGAL, IL-18) and repair (MCP-1, UMOD, and YKL-40) proteins in urine and plasma at baseline and 2-4 hours post-angiography in a subset of PRESERVE trial participants. We calculated the absolute Δ and relative ratio between post-operative and baseline levels. We then assessed the association between absolute Δs and relative ratios with CA-AKI and MAKE-D.

Results

Participants (n=922) were predominately male (96%), diabetic (82%) with mean±sd age of 70±8 years. 73 and 60 participants experienced CA-AKI and MAKE-D, respectively. The absolute Δs and relative ratios were not statistically different by CA-AKI status (Figure). The majority of participants experienced an insignificant decrease in biomarkers regardless of CA-AKI or MAKE-D status. Findings remained after indexing urine biomarkers to urine creatinine and after adjusting for baseline eGFR and urine albumin to creatinine ratio.

Conclusion

The lack of significant differences in injury and repair biomarkers in patients by CA-AKI and MAKE-D status suggests that CA-AKI is not mediated by intrinsic nephron injury. While our findings need to be validated, our results can help advance pharmacological developments for the prevention of CA-AKI.

Funding

  • NIDDK Support