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. 2019 Nov 18;9:16963. doi: 10.1038/s41598-019-53349-1

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© The Author(s) 2019

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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Potential pathways involved in the pathogenesis of AKI. Three important pathways in the pathogenesis of AKI are represented by biomarkers in the model: (1) hypoperfusion (H-FABP), (2) proinflammation (sTNFR1 and sTNFR2 as surrogates for the transient TNFα response) and (3) ischaemia reperfusion injury (MK). Together with clinically measured variables, such as (among others) cardiac output and blood pressure (hypoperfusion and ischaemia reperfusion), cross clamp time and bypass time (proinflammation) biomarkers enable AKI patient risk categorisation. AKI, acute kidney injury; H-FABP, heart-type fatty acid-binding protein; sTNFR1, soluble tumour necrosis factor receptor 1; sTNFR2, soluble tumour necrosis factor receptor 2; TNFα, tumour necrosis factor alpha; MK, midkine.