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. 2021 Mar 23;43(1):111–120. doi: 10.1038/s41401-021-00628-1

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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. 6 — Correlation of urinary aprotinin concentration with plasma (a) and urinary cystatin C (b) concentration (each n = 11–12). c Immunohistochemical analysis of the tubular deposition and accumulation of aprotinin (each n = 4). d Semiquantitative analysis of aprotinin deposition (each n = 4). e Electron microscopy in different magnifications of proximal tubular cells from mice treated with placebo or aprotinin under a low-salt diet. In mice treated with placebo lysosomes in renal tubular cells appear normal in size and number (white asterisks). Whereas in mice treated with low-salt and aprotinin lysosomes were markedly increased in size and filled with electron-dense material (red asterisks). N nucleus, M mitochondria, RBC red blood cells (each n = 4). Data and statistical analysis: arithmetic means ± SEM. a, b Calculation of Pearson’s correlation coefficient r, P < 0.05; b one outlier removed (Grubb’s test–α = 0.01%). d Kruskal–Wallis test followed by the Dunn’s test. *P < 0.05, aprotinin vs. placebo treatment.