SGLT2 Inhibitors: Nephroprotective Efficacy and Side Effects

Medicina

Michele Andreucci¹  Michele Provenzano¹  Giuseppe Conte²  MariaElena Liberti²  Silvio Borrelli²  Carlo Garofalo²  Roberto Minutolo²  Luca De Nicola² 

[1] Division of Nephrology, University Magna Grecia, 88100 Catanzaro, Italy;Division of Nephrology, University of Campania “Luigi Vanvitelli”, 80137 Naples, Italy;

关键词: diabetes;    chronic kidney disease;    GFR;    albuminuria;    SGLT-2 inhibitors;    end stage renal disease;    survival;   

DOI  :  10.3390/medicina55060268

来源: DOAJ

【 摘 要 】

The burden of diabetic kidney disease (DKD) has increased worldwide in the last two decades. Besides the growth of diabetic population, the main contributors to this phenomenon are the absence of novel nephroprotective drugs and the limited efficacy of those currently available, that is, the inhibitors of renin-angiotensin system. Nephroprotection in DKD therefore remains a major unmet need. Three recent trials testing effectiveness of sodium-glucose cotransporter 2 inhibitors (SGLT2-i) have produced great expectations on this therapy by consistently evidencing positive effects on hyperglycemia control, and more importantly, on the cardiovascular outcome of type 2 diabetes mellitus. Notably, these trials also disclosed nephroprotective effects when renal outcomes (glomerular filtration rate and albuminuria) were analyzed as secondary endpoints. On the other hand, the use of SGLT2-i can be potentially associated with some adverse effects. However, the balance between positive and negative effects is in favor of the former. The recent results of Canagliflozin and Renal Endpoints in Diabetes with Established Nephropathy Clinical Evaluation Study and of other trials specifically testing these drugs in the population with chronic kidney disease, either diabetic or non-diabetic, do contribute to further improving our knowledge of these antihyperglycemic drugs. Here, we review the current state of the art of SGLT2-i by addressing all aspects of therapy, from the pathophysiological basis to clinical effectiveness.

【 授权许可】

Unknown