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. 2017 Jun 2;19:120. doi: 10.1186/s13075-017-1317-x

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© The Author(s). 2017

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. 2 — Immunohistochemistry and immunofluorescence reveals loss of megalin and cubilin expression in pSS patients with Fanconi syndrome. Staining of megalin (A, C) and cubilin (B) on kidney biopsies of patients with glomerular minor lesion (GML) (Aa, Ba, Ca), patients of pSS with tubulointerstitial nephritis (Ab, Bb), and pSS patients with Fanconi syndrome (Ac, Bc, Cb). Semiquantitative analysis shows decreased expression of megalin (D) and cubilin (E) in pSS patients with Fanconi syndrome, compared with GML and SS + TIN groups. GML glomerular minor lesion, SS Sjogren syndrome, TIN tubulointerstitial nephritis