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The intensive treatment of the multiple risk factors reduces the development/progression of renal disease18 which is why guidelines insist on comprehensive management of the patient with diabetes (glycemic control and control of cardiovascular risk factors, use of renin-angiotensin system inhibitors, as well as lifestyle changes, including smoking cessation or weight loss in overweight/obese individuals, among others).19 However, the residual renal risk remains very high in optimally treated patients.20 More recently, iSGLT2 has been shown to reduce the risk of cardiovascular and renal events, but still, the residual risk of renal disease progression remains high.21,22 Nevertheless, although the rate of diabetes-related complications (such as myocardial infarction, stroke, lower limb amputations or mortality) have decreased significantly in recent decades, this is not the same for CKD patients requiring renal replacement therapy attributed to diabetic kidney disease (DKD).23 Therefore new treatments are needed that improve glycemic control independently of GFR, with a low risk of hypoglycemia and able to reduce cardiovascular and renal risk in this population

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Secondary Mechanisms: FAK-Paxillin and Growth Hormone Receptor Beyond the two primary pathways, published studies have identified additional mechanisms relevant to specific tissue types

Laboratory research record on GLP-1S [PMID: 29748996] PubMed laboratory record discussing GLP-1S in a research context