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. 2019 Mar 4;19:30. doi: 10.1186/s12871-019-0698-6

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 3 — Lung oedema due to functional loss of kidney. Factors associated with the initiation of remote lung injury include the accumulation of toxic by-products, enhanced cytokine release and impaired metabolism due to an imbalance of mediators secreted in kidney injury. These insults cause an increase in pulmonary vascular permeability and, therefore, oedema. Key cytokines in the pathogenesis of remote lung injury following AKI are IL-6 and IL-8, which lead to endothelial dysfunction and pulmonary oedema (Modified and reproduced with permission) (Springer Nature; Nature Reviews Nephrology) [13]