Figure 2.

Schematic for pathogenesis of diabetic kidney disease (DKD). Hyperglycemia and hyperinsulinemia induced by diabetes leads to the activation and expression of the different channels and transporters located along the various nephron segments. These changes are exercised either directly or indirectly upon the channel. The multitude of these channel alterations result in interstitial fibrosis, glomerulosclerosis, hypertrophy, breakdown of the glomerular filtration barrier (GFB) and albuminuria. The culmination of the damage to various portions of the nephron is the development of DKD. Abbreviations: calcium activated potassium channel 3.1 (K_Ca3.1); glucose transporters (GLUT1 and 2); sodium glucose cotransporter (SGLT1 and 2); large conductance Ca²⁺-activated K⁺ channel (BK_Ca); epithelial Na⁺ channel (ENaC); transient receptor potential canonical (TRPC) channel.