From Pathophysiology to Pathology—an Update on Diabetic Kidney Disease

Dear Colleagues,

Diabetes mellitus is becoming a global epidemic in all parts of the world, with a consequent increase in the complications of diabetes. Kidney disease occurs in 35–40% of all patients with diabetes, and is the most common cause of end-stage kidney failure requiring renal replacement therapy. While several advances have occurred in our understanding of the pathogenesis and even more impressive developments have taken place in the recent past relating to the management of diabetic kidney disease (DKD), there remain significant gaps in the etiopathogenesis of this condition, and hence no optimal therapy to prevent its development or halt its progression. The role of uncontrolled hyperglycemia and systemic hypertension in the causation and progression of DKD is well established. Furthermore, the impact of activation of the renin–angiotensin–aldosterone system (RAAS) on its pathogenesis and progression is clearly evident by the therapeutic success of inhibitors of the RAAS. The recent past has witnessed an explosive growth in investigative reports on the various aspects of pathogenesis, biomarker development, and the exploration of genetic as well as epigenetic factors. Newer research methodologies, such as NextGen sequencing and single-cell RNA studies, confocal microscopy, and other advanced imaging techniques, have helped identify novel disease mechanisms as well as new pathogenic pathways and expanded the clinical spectrum with the characterization of non-proteinuric variants. Specifically, the past decade was notable for several successful therapeutic randomized clinical trials involving SGLT-2 inhibitors, GLP-1 agonists, and mineralocorticoid receptor blockers, which resulted in more therapeutic options with which to slow down DKD. The presentation of the various aforementioned developments in pathogenesis as well as novel therapeutic strategies in several state-of-the-art manuscripts is the primary focus of this Special Issue.

We encourage the submission of manuscripts that provide an update on the complex pathophysiological mechanisms of DKD, covering recent advances in molecular and cellular insights, including, but not limited to, the following general topics:

• Natural history, clinical features, and phenotypes of DKD;
  • Non-proteinuric DKD; non-diabetic renal disease in diabetics;
• Pathogenesis of diabetic kidney disease;
  • Glomerular and systemic hypertension in DKD;
  • Hyperglycemia, AGE, and other metabolic factors;
  • Renin–angiotensin–aldosterone system in DKD;
  • Growth factors and DKD;
  • Mesenchymal transition of glomerular and tubular cells;
  • Vasoactive factors (endothelins, nitric oxide, and prostaglandins) and DKD;
• Pathology of DKD;
• Genetics and epigenetics of DKD.

For readers interested in Epidemiology and Therapeutic Perspectives of DKD, please visit the Special Issue: An Update on Diabetic Kidney Disease: Epidemiology, Diagnosis, Treatment.

Dr. Sharma Prabhakar
Guest Editor

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• diabetic kidney disease
• epithelial–mesenchymal transition
• renin–angiotensin–aldosterone system
• sodium glucose transporter 2
• albuminuria