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. 2022 Sep 22;37(1):1–19. doi: 10.1038/s41371-022-00751-4

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© The Author(s) 2022

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — An interplay of pathophysiological processes associated with the chronic kidney disease milieu contribute to the pathogenesis of CKD-associated cardiomyopathy. These can be broadly divided into factors which increase afterload, preload, and those which result from maladaptive perturbations of intrinsic factors. AGEs advanced glycation end-products, FGF23 fibroblast growth factor 23, PTH parathyroid hormone, RAAS renin-angiotensin-aldosterone system, SNS sympathetic nervous system.