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. 2016 Sep 20;17:133. doi: 10.1186/s12882-016-0348-x

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© The Author(s). 2016

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. 6 — An association of CLU deficiency with more renal tubular injury after 30 days of IRI. The sections of CLU null and WT kidneys, harvested after 30 days of IRI, were stained with periodic acid-Schiff (PAS), and the number of injured tubules, including cellular loss (atrophy), intratubular cast formation, tubular cell flattening and vacuolation, in renal cortex was counted in each microscopic view (200x magnification). a Typical microscopic views of kidney sections in each group (KO: CLU KO kidneys; WT: WT kidneys). G: glomerulus; *: damaged tubules. b The number of injured tubules was counted in at least 20 randomly selected views in two separate sections of each kidney and was presented in average per view. Data are presented as mean ± SD of each group. KO group vs. WT control: P < 0.0001 (two-tailed t-test, n = 8)