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. 2020 Oct 6;11(12):2791–2827. doi: 10.1007/s13300-020-00921-y

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, which permits any non-commercial 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-nc/4.0/.

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Fig. 2 — a Structural changes in kidney morphology with diabetic kidney disease. (Reproduced with permission from Alicicet al. [25]). b Hemodynamic changes in diabetic kidney disease. Na⁺ Sodium, SGLT2 sodium-glucose co-transporter 2, TGF tubuloglomerular feedback. (Reproduced with permission from Cherney et al. [30]). c Restoration of tubuloglomerular feedback by SGLT2 inhibitors. (Reproduced with permission from Cherney et al. [30])