Inflammatory Mechanisms in Diabetic Kidney Disease

Up to half of all patients with diabetes will develop diabetic kidney disease (DKD), the leading cause of end-stage kidney disease worldwide. The excess morbidity and mortality experienced by individuals with diabetes are primarily driven by the development of this microvascular complication. Recent research findings implicate inflammation as a major mechanism underlying kidney damage, including the pathological changes associated with DKD. Historically, there has been a paucity of therapies that are effective in arresting the development and progression of DKD. Recently, however, glucose-lowering agents in the glucagon-like peptide-1 receptor agonist (GLP-1 RA) class of medications have been shown to preserve declining kidney function and reduce albuminuria in patients with diabetes. In addition to controlling modifiable risk factors such as hyperglycemia, blood pressure, and weight, it appears that GLP-1 signaling imparts direct anti-inflammatory, antifibrotic, and antioxidant effects. Thus, a number of clinical trials are underway to examine the impact of GLP-1 RAs on DKD development and progression.