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Diabetes is the most common cause of end-stage kidney disease. Therapies such as sodium-glucose co-transporter-2 inhibitors have been identified over the last decade as effective oral hypoglycemic agents that also confer additional cardio and kidney protection. Knowledge of their mechanism of action and impact on patients with diabetes and albuminuria is vital in galvanizing prescriber confidence and increasing clinical uptake. This manuscript discusses the pathophysiology of diabetic kidney disease, patho-physiological mechanisms for sodium-glucose co-transporter-2 inhibitors, and their impact on patients with type 2 diabetes mellitus and albuminuric kidney disease. Sodium-glucose co-transporter-2 inhibitors reduce albuminuria with consequent benefits on cardiovascular and kidney outcomes in patients with diabetes and severe albuminuria. While they have been incorporated into guidelines, the uptake of these agents into clinical practice has been slow. Increasing the uptake of these agents into clinical practice is necessary to improve outcomes for the large number of patients with diabetic kidney disease globally. P LAIN LANGUAGE SUMMARY People with type 2 diabetes and severe urinary protein loss are at high risk of progression to kidney failure requiring dialysis or transplantation. Preventing or slowing down loss of kidney function is crucial to preventing kidney failure. This review will discuss how diabetic kidney disease occurs, how a new family of glucose-lowering agents, the sodium-glucose co-transporter-2 inhibitors, work and how they affect people with type 2 diabetes mellitus who also have protein leaking from their kidneys. It will also detail the current data that underpins the guideline recommendations for use of these agents in the management of patients with and without diabetes.

Impact of SGLT2 inhibitors on the kidney in people with type 2 diabetes and severely increased albuminuria