Redox imbalance and mapk activation mediates pneumoperitoneum-induced kidney injury during minimally invasive surgery

You have accessJournal of UrologyCME1 Apr 2023PD17-03 REDOX IMBALANCE AND MAPK ACTIVATION MEDIATES PNEUMOPERITONEUM-INDUCED KIDNEY INJURY DURING MINIMALLY INVASIVE SURGERY Charbel Chalouhy, Nassim Fares, Youakim Saliba, Pedro Maria, Ahmed Aboumoouhamed, Marwan Kassis, Alexander Small, and Justin Loloi Charbel ChalouhyCharbel Chalouhy More articles by this author , Nassim FaresNassim Fares More articles by this author , Youakim SalibaYouakim Saliba More articles by this author , Pedro MariaPedro Maria More articles by this author , Ahmed AboumoouhamedAhmed Aboumoouhamed More articles by this author , Marwan KassisMarwan Kassis More articles by this author , Alexander SmallAlexander Small More articles by this author , and Justin LoloiJustin Loloi More articles by this author View All Author Informationhttps://doi.org/10.1097/JU.0000000000003272.03AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract INTRODUCTION AND OBJECTIVE: Given the widespread use of laparoscopic and robotic surgeries, the effects of pneumoperitoneum (PNP) during minimally invasive surgery on kidney function become of great interest. PNP during laparoscopy causes transient renal functional impairment via various detrimental factors, such as oxidative stress. We, therefore, investigated the oxidative signaling pathways inherent to PNP-induced kidney injury. METHODS: PNP was established at an intraperitoneal CO 2 pressure of 12 mmHg in Wistar rats randomly allocated into three groups: Sham, PNP1, and PNP24. PNP1 and PNP24 animals were sacrificed at one and 24 hours following PNP deflation, respectively. Renal histology, function, redox status, and signaling pathways were assessed. RESULTS: PNP induced kidney injury and dysfunction with altered KIM-1 profile. Both expression and activity of antioxidant (CAT, SOD1/2) and oxidant (NOS3) enzymes, lipid peroxidation, and renal RNA/DNA damage biomarkers revealed redox imbalance after PNP, with an excess H2O2 production. Moreover, the antioxidant gene regulators FoxO3a and Nrf2 were activated. Nevertheless, PNP had no effect on the cellular apoptotic pathways Bcl2, Bid, Caspase 3 and 8. Finally, PNP stimulated the p38 and JNK mitogen-activated protein kinase (MAPK) pathways in the kidney. CONCLUSIONS: Our results demonstrate for the first time that PNP induces acute kidney injury due to renal redox imbalance linked to MAPK activation. These insights may open the way for further investigation into the renal therapeutic impact of managing PNP-associated oxidative stress during robotic surgery and explore procedure-specific kidney function recovery patterns i.e. after robotic partial nephrectomy or robotic kidney transplant. Source of Funding: none © 2023 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 209Issue Supplement 4April 2023Page: e495 Advertisement Copyright & Permissions© 2023 by American Urological Association Education and Research, Inc.MetricsAuthor Information Charbel Chalouhy More articles by this author Nassim Fares More articles by this author Youakim Saliba More articles by this author Pedro Maria More articles by this author Ahmed Aboumoouhamed More articles by this author Marwan Kassis More articles by this author Alexander Small More articles by this author Justin Loloi More articles by this author Expand All Advertisement PDF downloadLoading ...