fig1

Figure 1. Pathogenesis and progression of DKD. The upper panel outlines the primary triggers of DKD in the diabetic milieu, viz. hyperglycemia, dyslipidemia, and microinflammation (a chronic low-grade inflammatory state can predict and predispose an individual to diabetes and DKD). These triggers induce several metabolic, hemodynamic, and inflammatory factors. The interconnected factors cause intracellular changes followed by progressively detrimental alterations to the renal architecture, leading to fibrosis, scarring, and functional decline, ultimately resulting in renal failure. The lower panel recounts pathophysiological changes with the progression of DKD. AGEs: Advanced glycation endproducts; CCL: CC motif chemokine ligand; CTGF: connective tissue growth factor; DKD: diabetic kidney disease; EMT: epithelial-to-mesenchymal transition; EndMT: endothelial-to-mesenchymal transition; GFR: glomerular filtration rate; ICAM: intercellular adhesion molecule; IL: interleukin; NO: nitric oxide; NOX: NADPH oxidase; PDGF: platelet-derived growth factor; PKC: protein kinase C; RAAS: renin-angiotensin-aldosterone system; ROS: reactive oxygen species; TGF: transforming growth factor; TNF: tumor necrosis factor; VCAM: vascular cell adhesion molecule; VEGF: vascular endothelial growth factor.