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. 2021 Apr 22;11:8769. doi: 10.1038/s41598-021-88000-5

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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 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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Oxidative stress and vasoactive mediators over the course of AKI to CKD transition. (A) Urinary hydrogen peroxide, (B) mRNA levels of Nfe2l2 (C) mRNA levels of Nos3, (D) mRNA levels of NOX4, (E) mRNA levels of Edn1 and (F) mRNA levels of endothelin receptor A (Endra). Data are represented as the mean ± SE. n = 4, n = 4, and n = 5 for the S, UNx, and IR + UNx groups, in each studied period: 30, 60, 90, and 120 days post-ischemia. The one-way analysis of variance (ANOVA) was used to determine statistical differences, using the Bonferroni correction for multiple comparisons. *p < 0.05 versus S group and + p < 0.05 versus UNx group in their respective period.