Assessment of lixisenatide-induced nephropathy in chick embryos: Implications for prevention of diabetic kidney disease

Diabetic kidney disease (DKD) is a major cause of end-stage renal disease and the direct renal effects of GLP-1 receptor agonists remain underexplored. Using a hyperglycemic chick embryo model (n=120), we evaluated dose-dependent nephroprotective effects of lixisenatide. Hyperglycemia induced renal hypertrophy, histological injury, oxidative stress, inflammation and apoptosis. Lixisenatide, particularly at high doses, significantly ameliorated these changes, normalizing kidney-to-body ratios and reducing MDA, TNF-α and caspase-3 activity. Thus, we show that lixisenatide directly preserves renal structure and function independent of systemic metabolic control.