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Newer possibilities of slowing the development of chronic kidney disease and the role of dapagliflozin


Authors: Jan Vachek 1,2;  Kateřina Oulehle 2;  Hana Ciferská 3;  Oskar Zakiyanov 1;  Vladimír Tesař 1
Authors‘ workplace: Klinika nefrologie 1. LF UK a VFN v Praze 1;  Interní oddělení a nefrologická ambulance, Klatovská nemocnice, a. s., Klatovy 2;  Revmatologická klinika 1. LF UK a Revmatologický ústav, Praha 3
Published in: AtheroRev 2022; 7(3): 140-146
Category: Reviews

Overview

According to current estimates, chronic kidney disease will be the 5th leading cause of death worldwide by 2040. The prevalence of chronic kidney disease increases with age and mainly affects patients with obesity, diabetes mellitus and hypertension. The main goal of treating chronic kidney disease is to delay the progression of the disease. Established markers of progression of renal impairment are glomerular filtration rate and albuminuria. Pharmacological blockade of the renin-angiotensin-aldosterone system (RAAS) by angiotensin converting enzyme inhibitors (ACEi) or angiotensin receptor blockers (ARBs) has been the basis of medicamentous slowing of the progression of renal disease for many years. Current recommendations from the Kidney Disease: Improving Global Outcomes (KDIGO) initiative recommend the use of ACEi or ARB in both diabetic and non-diabetic patients with moderate or severe albuminuria. In recent years, a group of drugs known as sodium-glucose transporter 2 (SGLT2i) inhibitors has gained ground in the field of cardioprotection and nephroprotection. Their protective effects are manifested independently of a decrease in blood glucose. SGLT2i will soon be part of the recommendations for the treatment of non-diabetic kidney disease. The first representative of this group of substances, dapagliflozin, is already approved in the Czech Republic for the treatment of chronic kidney disease in adults with and without type 2 diabetes mellitus.

Keywords:

dapagliflozin – diabetes mellitus – chronic kidney disease – renin-angiotensin-aldosterone system – sodiumglucose transporter 2 inhibitors


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