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. 2021 May 11;17(9):605–618. doi: 10.1038/s41581-021-00418-2

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Similar to most other forms of acute kidney injury (AKI), postoperative AKI (PO-AKI) commonly has a multifactorial aetiology, which is mediated by common injury pathways that affect the kidney microcirculation, oxygen demand and inflammation. In most cases, a combination of preoperative risk factors, intraoperative events and postoperative events leads to the development of AKI. Baseline risk factors and the persistence and severity of injurious factors in the postoperative setting also determine the outcomes of AKI, acute kidney disease and eventually chronic kidney disease. Adapted from Acute Disease Quality Initiative 24, www.ADQI.org, CC BY 2.0 (https://creativecommons.org/licenses/by/2.0/).