Empagliflozin: a new strategy for nephroprotection in diabetes

• Main Authors: Anton Ivanovich Korbut, Vadim Valer'evich Klimontov
• Format: Article
• Language: English
• Published: Endocrinology Research Centre 2017-05-01
• Series: Сахарный диабет
• Subjects: diabetes; diabetic nephropathy; chronic kidney disease; sglt2 inhibitors; empagliflozin
• Online Access: https://dia-endojournals.ru/dia/article/viewFile/8005/6362

Empagliflozin, an inhibitor of sodiumglucose symporter type 2 (SGLT2), is a new class of antidiabetic agents with numerous pleiotropic effects. The review summarises data on the influence of empagliflozin on the structural and functional changes in the kidneys of the models of diabetes mellitus (DM) and of patients with DM. A literature search was conducted using the databases of Medline/PubMed, Scopus, Web of Science, ClinicalTrials.gov and eLibrary. The experimental results showed a decrease in the blood glucose level, blood pressure, glomerular hyperfiltration and overexpression of proinflammatory and fibrogenic factors in the kidneys under the influence of empagliflozin. Most clinical studies have demonstrated the albuminuria-lowering effect of empagliflozin in patients with type 2 DM. The EMPA-REG OUTCOME study has demonstrated slowing of the chronic kidney disease progression, decrease in the incidence of end-stage renal failure and death from renal causes in patients with type 2 DM undergoing the empagliflozin treatment compared with those receiving placebo. The mechanisms of the nephroprotective effect of empagliflozin included systemic and renal effects. The decrease in hyperglycaemia, blood pressure and body weight; reduction in glomerular hyperfiltration; enhancement of sodium excretion and suppression of inflammatory and fibrogenic signalling pathways in the kidneys may help slow the development of diabetic kidney damage under the influence of empagliflozin. The possibility of extrapolating the confirmed properties of empagliflozin to other SGLT2 inhibitors needs further investigation.