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. 2020 Dec 30;10(1):18. doi: 10.3390/biology10010018

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Pathophysiology and therapeutic strategies of diabetic kidney disease. ACEi, angiotensin-converting-enzyme inhibitors; ARBs, angiotensin receptor blockers; eGFR, estimated glomerular filtration rate; ESRD, end-stage renal disease; H₂O₂, hydrogen peroxide; IL, interleukin; MCP-1, monocyte chemotactic protein-1; NF-κB, nuclear factor-κB; NLRP3, NLR family pyrin domain containing 3; Nox, NADPH oxidase; Nrf2, nuclear factor erythroid 2–related factor 2; O^-₂, superoxide; PDGF, platelet-derived growth factor; RAAS, renin–angiotensin–aldosterone system; ROS, reactive oxygen species; SGLT2, sodium–glucose co-transporter 2; TNF-α, tumor necrosis factor alpha; XO, xanthine oxidase.