Kidney function in patients with ovarian cancer treated with poly (ADP-ribose) polymerase (PARP) inhibitors

Author:

Gupta Shruti12ORCID,Hanna Paul E3ORCID,Ouyang Tianqi3,Yamada Karla Sofia1,Sawtell Rani3,Wang Qiyu3ORCID,Katz-Agranov Nurit3,Feghali Lea1ORCID,Krasner Carolyn N4,Bouberhan Sara5,Castro Cesar M5,Sise Meghan E3

Affiliation:

1. Division of Renal Medicine, Department of Medicine, Brigham and Women’s Hospital , Boston, MA, USA

2. Medical Oncology, Adult Survivorship Program, Dana-Farber Cancer Institute , Boston, MA, USA

3. Department of Medicine, Division of Nephrology, Massachusetts General Hospital , Boston, MA, USA

4. Division of Medical Oncology, Dana-Farber Cancer Institute , Boston, MA, USA

5. Department of Medicine, Division of Hematology/Oncology, Massachusetts General Hospital , Boston, MA, USA

Abstract

Abstract Background Poly (ADP-ribose) polymerase inhibitors (PARPi) have revolutionized the treatment of ovarian cancer; however, real-world data on kidney function among patients treated with PARPi are lacking. Methods We identified adults treated with olaparib or niraparib between 2015 and 2021 at a major cancer center in Boston, MA, USA. We determined the incidence of any acute kidney injury (AKI), defined as at least a 1.5-fold rise in serum creatinine from baseline in the first 12 months following PARPi initiation. We calculated the percentage of patients with any AKI and sustained AKI and adjudicated the etiologies by manual chart review. We compared trajectories in estimated glomerular filtration rate (eGFR) among PARPi-treated and carboplatin and paclitaxel-treated patients with ovarian cancer, matched by baseline eGFR. Results Of 269 patients, 60 (22.3%) developed AKI, including 43 of 194 (22.1%) olaparib-treated patients and 17 of 75 (22.7%) niraparib-treated patients. Only 9 of 269 (3.3%) had AKI attributable to the PARPi. Of the 60 patients with AKI, 21 (35%) had sustained AKI, of whom 6 had AKI attributable to the PARPi (2.2% of the whole cohort). eGFR declined within 30 days post-PARPi initiation by 9.61 (SD = 11.017)  mL/min per 1.73 m2 but recovered by 8.39 (SD = 14.05)  mL/min per 1.73 m2 within 90 days after therapy cessation. There was no difference in eGFR at 12 months post-therapy initiation in patients receiving PARPi or controls receiving carboplatin and paclitaxel (P = .29). Conclusions AKI is common following PARPi initiation as is a transient decline in eGFR; however, sustained AKI directly attributable to the PARPi and long-term eGFR decline are uncommon.

Funder

NIH

NIDDK

National Institutes of Health

Publisher

Oxford University Press (OUP)

Subject

Cancer Research,Oncology

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