Kidney Function in Patients with Ovarian Cancer Treated with Poly (ADP-ribose) polymerase (PARP) Inhibitors
Menée aux Etats-Unis à partir de données portant sur 269 patientes atteintes d'un cancer de l'ovaire traité entre 2015 et 2021 par inhibiteurs de PARP, cette étude analyse l'incidence d'une insuffisance rénale aiguë en lien avec un traitement par olaparib ou niraparib
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 2015-2021 at a major cancer center in Boston, Massachusetts. We determined the incidence of any acute kidney injury (AKI), defined as 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/paclitaxel-treated patients with ovarian cancer, matched by baseline eGFR. Results: Of 269 patients, 60 (22.3%) developed AKI, including 43/194 (22.1%) olaparib-treated patients and 17/75 (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 ± 11.017 mL/min/1.73 m2 but recovered by 8.39 ± 14.05 mL/min/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/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.