Except for angiotensin-converting enzyme inhibitors and angiotensin-II receptor antagonists, for many years no drugs capable of improving renal outcomes in DKD patients have been available. The resulting clinical manifestations configure the so-called ‘diabetic kidney disease’ (DKD), characterized by selective and nonselective proteinuria, hypertension and progressive decline in renal function. Renal damage related to T2DM includes both structural (glomerular basement membrane thickening, mesangial expansion, interstitial fibrosis, loss of capillary architecture, hyalinosis of small and medium caliber arteries) and functional (dysfunction of the mitochondrial respiratory chain, over expression of proinflammatory cytokines such as interleukin (IL)-6, IL-8, IL-18, TNF-α, interferon (INF)-γ) alterations induced by hyperglycaemia.

T2DM represents a major cause of chronic kidney disease (CKD) worldwide, and statistics show that the incidence of end-stage renal disease (ESRD) requiring renal replacement therapy varies from 0.04% to 1.8% per year. Type 2 diabetes mellitus (T2DM) is associated with micro- and macrovascular complications, which are often responsible for severe disability in affected patients, with high costs for health and social care. Albuminuria, COVID-19 disease, diabetic kidney disease, GLP-1 receptor agonists, nephroprotection INTRODUCTION

Functional unit of the kidney