The interplay between chemical species transport and reactions mechanisms is fundamentally linked to the pathogenesis of common renal diseases. In conditions such as DN, hyperglycemia induces oxidative stress and alterations in glomerular hemodynamics, tubular transport mechanisms, and reaction kinetics of key metabolites . Hyperglycemia leads to increased glucose transport and subsequent alterations in osmotic gradients, ultimately resulting in glomerular hyperfiltration and renal injury. These changes disrupt the normal balance of solute and fluid transport, contributing to the disease's progression . These disruptions impair the biophysical and biomechanical stability of the system by damaging renal cells and extracellular matrix components , leading to glomerulosclerosis, tubulointerstitial fibrosis, and ultimately renal failure, highlighting the implications on the stability of the renal system and functional decline.