Renoprotective Mechanism of Sodium-Glucose Cotransporter 2 Inhibitors: Focusing on Renal Hemodynamicsopen access
- Authors
- Kim, Nam Hoon; Kim, Nan Hee
- Issue Date
- Jul-2022
- Publisher
- 대한당뇨병학회
- Keywords
- Diabetes mellitus; Hemodynamics; Renal insufficiency; Sodium -glucose transporter 2 inhibitors
- Citation
- Diabetes and Metabolism Journal, v.46, no.4, pp 543 - 551
- Pages
- 9
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- Diabetes and Metabolism Journal
- Volume
- 46
- Number
- 4
- Start Page
- 543
- End Page
- 551
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/61853
- DOI
- 10.4093/dmj.2022.0209
- ISSN
- 2233-6079
2233-6087
- Abstract
- Diabetic kidney disease (DKD) is a prevalent renal complication of diabetes mellitus that ultimately develops into end-stage kidney disease (ESKD) when not managed appropriately. Substantial risk of ESKD remains even with intensive management of hyperglycemia and risk factors of DKD and timely use of renin-angiotensin-aldosterone inhibitors. Sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce hyperglycemia primarily by inhibiting glucose and sodium reabsorption in the renal proximal tubule. Currently, their effects expand to prevent or delay cardiovascular and renal adverse events, even in those without diabetes. In dedicated renal outcome trials, SGLT2 inhibitors significantly reduced the risk of composite renal adverse events, including the development of ESKD or renal replacement therapy, which led to the positioning of SGLT2 inhibitors as the mainstay of chronic kidney disease management. Multiple mechanisms of action of SGLT2 inhibitors, including hemodynamic, metabolic, and anti-inflammatory effects, have been proposed. Restoration of tubuloglomerular feedback is a plausible explanation for the alteration in renal hemodynamics induced by SGLT2 inhibition and for the associated renal benefit. This review discusses the clinical rationale and mechanism related to the protection SGLT2 inhibitors exert on the kidney, focusing on renal hemodynamic effects.
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Collections - 2. Clinical Science > Department of Endocrinology and Metabolism > 1. Journal Articles
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