Kidney Week

Abstract: SA-PO027

Vancomycin-Associated AKI with a Steep Rise in Serum Creatinine

Session Information

• AKI Clinical: Epidemiology and Outcomes
  November 04, 2017 | Location: Hall H, Morial Convention Center
  Abstract Time: 10:00 AM - 10:00 AM

Category: Acute Kidney Injury

• 003 AKI: Clinical and Translational

Authors

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

Juan Carlos Q. Velez,

• Obadan, Ndidiamaka O., Medical University of South Carolina, Charleston, South Carolina, United States

Ndidiamaka O. Obadan,

• Alzubaidi, Mohammed, Medical University of South Carolina, Charleston, South Carolina, United States

Mohammed Alzubaidi,

• Bhasin, Bhavna, Medical College of Wisconsin, Milwaukee, Wisconsin, United States

Bhavna Bhasin,

• Arthur, John M., University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States

John M. Arthur,

• Phadke, Gautam M., University of North Dakota School of Medicine, Fargo, North Dakota, United States

Gautam M. Phadke,

Background

The incidence of vancomycin-associated (VA) acute kidney injury (AKI) has increased after the Infectious Diseases Society of America updated their recommendations for higher therapeutic trough levels for methicillin-resistant Staphylococcus aureus infections. However, distinct laboratorial features of VA-AKI have not been described.

Methods

We defined precipitous AKI as a case with an increase in serum creatinine (sCr) ≥ 1.5 mg/dL/day. After encountering 2 cases of adults with VA-AKI presenting with an unusually steep rise in sCr, we probed for similar cases by surveying nephrologists at the American Society of Nephrology Communities online forum and by searching for published cases of VA-AKI via PubMed or Google to extract those with criterion for precipitous AKI. We also collected daily sCr values of consecutive AKI cases not associated with vancomycin exposure as a control group (non-VA-AKI).

Results

Seven original cases of VA-AKI characterized by an abrupt and exceedingly large rise in sCr shortly after a cumulative dose of vancomycin of ≥ 5 g given over 1 - 4 days were compiled from 4 different medical centers (mean age 41.6 years, 43% women, 57% black, mean body mass index 32 kg/m²). In 3 cases, simultaneously obtained serum cystatin C (sCy) values did not reveal relative steep increments from the upper limit of normal (mean: 2.6 vs. 0.5 mg/dL, for sCr and sCy, respectively), suggesting that the reductions in glomerular filtration rate were overestimated by the sCr increase. In addition, we extracted 4 published cases of precipitous AKI due to vancomycin. The median initial 24-hour rise in sCr in all 11 VA-AKI cases compiled was 2.5 mg/dL (range 1.4 – 3.5 mg/dL). The slope of the initial 48-hour sCr rise of the VA-AKI (n = 11) cases was greater than that of non-VA-AKI (n = 44) cases [2.01 (CI: 1.6-2.4) vs 0.61 (CI: 0.5-0.7) mg/dL/day; p<0.0001]. A concomitant steep rise in blood urea nitrogen was not observed in these VA-AKI cases.

Conclusion

VA-AKI can occasionally manifest with a precipitous rise in sCr after a high cumulative dose of vancomycin. True toxic tubular injury overrepresented by the sCr rise is possibly present in these cases. Whether interference of vancomycin with tubular secretion of creatinine explains the phenomenon requires further study.