DN exemplifies the roles of disrupted transport and transformation mechanisms in renal disease. Hyperglycemia-induced oxidative stress alters diffusion and reaction pathways, leading to the accumulation of toxic metabolites and inflammatory mediators. These changes compromise the structural and functional integrity of the kidneys, resulting in increased permeability of glomerular capillaries and progressive renal fibrosis. Figure shows a normal kidney and a DN diseased kidney with a detailed flow chart showing the roles of species transport and transformation in its pathogenesis. DN is a consequence of diabetes on the functionality of the nephrons of the kidney. DN begins with transporting oxygenated blood and excess glucose, accessing the nephrons for filtration. The next stage in the DN is an increase in glomerulus filtration rate and pressure due to diabetes-driven hypertension caused by hyperglycemia (high glucose content transported in the bloodstream). The high filtration rate and pressure increase damages the intra-glomerular mesangium and results in the dysfunctionality of the endothelial tissue as an aftermath of the cytokine and free oxygen radical release by the damaged mesangial cells. Mesangial expansion ensues due to hypertrophy and matrix (fibrin and collagen) accumulation within the mesangium. The expansion initiated the fenestration between the podocytes, resulting in glomerulus surface reduction and filtration of large protein molecules. A combination of increased glomerular pressure and mesangial expansion leading to decreased oxygenated blood transport to the nephron and cytokine inflammatory damage to the vasculature will result in nephron ischemia and atrophy . Chronic pathophysiological DN without any medical intervention results in kidney failure. 2) The kidney's nephron filtration unit with glomerular capillary bundle, capillary beds, and tubules. 3) Transport of oxygen and glucose through the arteriores into a glomerulus within a nephron. 4) Increased glomerular pressure, cytokine inflammatory effect on the endothelial dysfunctionality, and podocytes damage due to mesangial expansion structurally deform the kidney. 5) These combined steps lead to DN. Created with BioRender. Despite significant advancements, knowledge gaps remain in fully elucidating the precise molecular mechanisms governing species transport and transformation in renal pathophysiology. Future research should focus on developing comprehensive models that integrate both biochemical and biomechanical aspects of renal function and disease. These models could provide deeper insights into the complex interactions that underlie renal diseases and pave the way for more effective therapeutic strategies . The mechanisms by which specific transport alterations drive the progression of various renal diseases, particularly in terms of timedependent changes and differential responses to treatment, are inadequately understood . Further studies should aim to characterize these relationships with greater precision, integrating interdisciplinary approaches to develop more effective therapeutic strategies. This review highlights the critical roles of chemical species transport, transformation, and fluid dynamics in the pathogenesis of renal diseases, with a particular emphasis on DN. Understanding the interplay between these mechanisms is essential for deciphering the complex biophysical and biochemical disruptions that characterize renal pathophysiology. Bridging the existing knowledge gaps will be key to advancing our understanding and treatment of renal diseases.