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Kidney Week

Abstract: PO2176

Antiemetic Drugs and the Risk of Cisplatin-Induced AKI

Session Information

  • Onco-Nephrology - 1
    October 22, 2020 | Location: On-Demand
    Abstract Time: 10:00 AM - 12:00 PM

Category: Onco-Nephrology

  • 1500 Onco-Nephrology

Authors

  • Shingarev, Roman A., Memorial Sloan Kettering Cancer Center, New York, New York, United States
  • Knezevic, Andrea, Memorial Sloan Kettering Cancer Center, New York, New York, United States
  • Latcha, Sheron, Memorial Sloan Kettering Cancer Center, New York, New York, United States
  • Joy, Melanie S., University of Colorado, Denver, Colorado, United States
  • Aleksunes, Lauren, Rutgers, Rutgers The State University of New Jersey, New Brunswick, New Jersey, United States
  • Jaimes, Edgar A., Memorial Sloan Kettering Cancer Center, New York, New York, United States
Background

Cisplatin (CIS) is an effective first line therapy for a variety of cancers. Acute kidney injury (AKI) is a common side effect of CIS seen in up to 30% of patients (Latcha et al CJASN, 2016). AKI results from the selective uptake and accumulation of CIS in proximal tubules. CIS is a highly emetogenic and fluid loss can also contribute to AKI. This retrospective study evaluated whether anti-emetics modfy the risk of AKI.

Methods

The medical records of adult cancer patients who received CIS between Jan 1, 2010 and Dec 31, 2016 (n=6,889) were reviewed. The association between use of anti-emetics and development of AKI (50% increase in serum creatinine (sCr) ) was evaluated. Inclusion criteria were adults, baseline sCr, CIS dose and administration of anti-emetics. Fisher's exact test was used for univariable associations between categorical values and logistic regression analyzed multivariable associations with AKI at p<0.05.

Results

Out of ~8700 patients, 6889 met search criteria. A total of 3,881 (56.3%) patients received antiemetics. AKI developed after cisplatin in 1,666 (24.2 %) patients. Of those with AKI (n=1666), patients who received any antiemetic represented 52.6% (n=877), while patients with no documented antiemetic use represented 47.4% (n=789). Of patients without AKI (n=5223), patients who received any antiemetic represented 57.5% (n=3004), while patients who did not have documented antiemetic use represented 42.5% (n=2219). (P<0.001 ). Patients who received antiemetics also received a higher cumulative dose of CIS (360 vs 330 mg/m2, P < 0.001). By univariate analysis older age, male gender, black race, and cumulative CIS dose were associated with higher risk for AKI (P<0.001). After adjusting for these variables, use of any antiemetic was protective for AKI (OR 0.84, 95% CI: 0.75, 0.94; P= 0.003).

Conclusion

Our study confirms the high rate of AKI in patients receiving CIS. While anti-emetic use appears to be associated with a lower rate of AKI, additional analyses will be needed to determine risk or benefit profiles of specific agents and/or class of agents given recent data demonstrating inhibition of kidney transporters with certain anti-emetics. Dissecting out other important covariates such as requirements for anti-emetics based on higher cumulative CIS will be necessary in prospective randomized controlled studies.

Funding

  • NIDDK Support