Diabetic nephropathy is driven by multiple factors, including hyperglycemia, AGE–RAGE signaling, reactive oxygen species (ROS), and disrupted calcium homeostasis, but their combined effects remain unclear. In this study, we develop a mathematical model linking postprandial glucose fluctuations to AGE–RAGE activation, ROS production, calcium dysregulation, and progressive kidney damage through a system of differential equations with feedback dynamics. Sensitivity analysis shows that calcium extrusion and AGE degradation rates are key determinants of disease progression, highlighting calcium regulation as a potential therapeutic target.