Current status of diabetic kidney disease and latest trends in management

Abstract

Diabetic kidney disease (DKD) is one of the major microvascular complications of diabetes and is leading cause of end-stage renal disease (ESRD) and one of major risk factors of cardiovascular disease (CVD).

Figure 1

Pathogenesis of diabetic kidney disease (DKD). The pathogenesis of diabetic kidney disease (DKD) is most likely the result of the interaction of multiple pathways, including metabolic and hemodynamic abnormalities. In hyperglycemia, increased glucose filtration in the glomerulus and reabsorption in the proximal tubules leads to an inadequate decrease in afferent arteriole resistance and a subsequent increase in intraglomerular pressure, followed by glomerular hypertension and hyperfiltration. In addition, hyperglycemia activates several metabolic pathways, such as polyol pathway, hexosamine pathway, protein kinase C activation, and advanced glycation end‐product (AGE) formation. This all results in the accumulation of reactive oxygen species (ROS). The interaction between metabolic abnormalities, hemodynamic factors and ROS generation affects gene regulation and the activation of transcription factors and stimulates the expression of proinflammatory cytokines. This leads to kidney inflammation and fibrosis, finally resulting in DKD. AGE, advanced glycation end‐product; DKD, diabetic kidney disease; ROS, reactive oxygen species.