Kidney Week

Abstract: TH-PO066

Precipitous AKI in Association with Vancomycin Exposure: A Cohort Study

Session Information

• AKI: Clinical, Outcomes, and Trials - Epidemiology and Pathophysiology
  October 24, 2024 | Location: Exhibit Hall, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

• 102 AKI: Clinical, Outcomes, and Trials

Authors

• Ellis, Montana D., UQ-Ochsner Clinical School, New Orleans, Louisiana, United States

Montana D. Ellis, MS

• Chalmers, Dustin R., Louisiana State University, Baton Rouge, Louisiana, United States

Dustin R. Chalmers, MD, MS

• Hashem, Ghaith, UQ-Ochsner Clinical School, New Orleans, Louisiana, United States

Ghaith Hashem

• Johnson, Kirsten, UQ-Ochsner Clinical School, New Orleans, Louisiana, United States

Kirsten Johnson

• Aliano, Danielle Nicole, Ochsner Health, New Orleans, Louisiana, United States

Danielle Nicole Aliano, MD

• Varghese, Vipin, University of Michigan Division of Nephrology, Ann Arbor, Michigan, United States

Vipin Varghese, MD

• Kanduri, Swetha Rani, Ochsner Health, New Orleans, Louisiana, United States

Swetha Rani Kanduri, MD, MBBS, FASN

• Velez, Juan Carlos Q., Ochsner Health, New Orleans, Louisiana, United States

Juan Carlos Q. Velez, MD, FASN

Group or Team Name

• Ochsner Group.

Background

Precipitous acute kidney injury (p-AKI) is a distinct form of AKI characterized by a steep rise in serum creatinine (sCr). An association between exposure to vancomycin and p-AKI has been previously reported via large electronic database mining, case reports, and case series. Herein, we aimed to expand our understanding of this entity by examining the relationship between exposure to vancomycin and the incidence of p-AKI in a prospectively generated AKI Cohort.

Methods

We prospectively collected data of patients seen in inpatient nephrology consultation who had a urine specimen subjected to microscopic examination of the urinary sediment (uSEDI) as part of the clinical evaluation for AKI over a 6-year period. AKI was defined by KDIGO criteria. p-AKI was defined as a rise in sCr ≥ 1.6 mg/dL within 24 +/- 2 hrs at any point during the course of the AKI episode. Within this uSEDI cohort, we identified patients who had been exposed to intravenous vancomycin during the preceding 5 days prior to the day of AKI consultation and determine its association with p-AKI occurrence.

Results

801 patients entered the study. Median age was 60, 42% women, 59% White, 31% Black. Preexisting CKD was reported in 42%. Main etiologies of AKI were ischemic acute tubular injury (ATI) (44%), hepatorenal syndrome (13%) and toxic ATI (12%). Exposure to vancomycin was registered in 265 (33%) patients. Median sCr at the time of AKI was 3.2 (IQR 2.4-4.6) mg/dL. p-AKI occurred in 95 (12%) patients, the steepest 24-hr sCr rise recorded was 4.2 mg/dL. Exposure to vancomycin was associated with an increased risk of p-AKI [18% vs. 9%, for exposed to vancomycin vs non-exposed, respectively; odds ratio 2.24 (95% CI 1.45-3.46, z statistic=3.643, p=0.0003)].

Conclusion

Exposure to vancomycin doubles the risk of p-AKI. This study adds to a body of evidence that defines a unique AKI phenotype associated with vancomycin that should be recognized in clinical grounds. The mechanism behind the precipitous sCr rise due to vancomycin may relate to a combination of true ATI and reduced tubular sCr secretion due to injury to proximal tubular organic transporters, but more investigation is still required.