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Bibliometric analysis of immune-related acute kidney injury induced by cancer immunotherapy (2000-2025).

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Naunyn-Schmiedeberg's archives of pharmacology 📖 저널 OA 13% 2023: 1/2 OA 2024: 1/5 OA 2025: 10/58 OA 2026: 20/182 OA 2023~2026 2026 Vol.399(2) p. 2647-2662
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Zhang B, Lau LY, Chen Y, Xie R

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Immune checkpoint inhibitors (ICIs) have revolutionized cancer therapy but are increasingly linked to immune-related kidney injury (irKI).

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APA Zhang B, Lau LY, et al. (2026). Bibliometric analysis of immune-related acute kidney injury induced by cancer immunotherapy (2000-2025).. Naunyn-Schmiedeberg's archives of pharmacology, 399(2), 2647-2662. https://doi.org/10.1007/s00210-025-04582-1
MLA Zhang B, et al.. "Bibliometric analysis of immune-related acute kidney injury induced by cancer immunotherapy (2000-2025).." Naunyn-Schmiedeberg's archives of pharmacology, vol. 399, no. 2, 2026, pp. 2647-2662.
PMID 40924107 ↗

Abstract

Immune checkpoint inhibitors (ICIs) have revolutionized cancer therapy but are increasingly linked to immune-related kidney injury (irKI). This study presents the first bibliometric analysis of irKI research (2000-2025), aiming to identify key trends, mechanistic insights, and pharmacological risk factors. We analyzed 2,179 publications to understand the evolution of irKI research, focusing on areas like T cell-mediated tubular injury, immune system-driven inflammation, and changes in metabolism. Co-prescription of nonsteroidal anti-inflammatory drugs (NSAIDs) and proton pump inhibitors has been identified as a pharmacological risk factor. Biomarkers such as KIM-1 and CXCL9, as well as novel imaging modalities, have shown diagnostic promise but remain underutilized. We also observed a lack of nephrotoxicity profiling for newer therapies such as chimeric antigen receptor T cell (CAR-T). This study highlights gaps in research and collaboration, particularly the need for better understanding of pharmacological risk factors like NSAID and proton pump inhibitor co-prescription. Future research should focus on improving strategies for predicting, diagnosing, and managing irKI. The study also emphasizes immune-driven inflammation, T cell-mediated tubular injury, and metabolic reprogramming as key contributors to irKI pathogenesis. Additionally, underutilized biomarkers (e.g., KIM-1, CXCL9) and emerging imaging techniques offer opportunities for early detection and monitoring.

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