Managing chronic kidney disease in diabetes patients with the latest chemical therapies

ABSTRACT

Introduction: During the years, while treatment strategy for diabetes mellitus has improved, the incidence of diabetes worldwide increases continuously. Chronic kidney disease (CKD) is one of the major diabetic microvascular complications, and a primary cause leading to end-stage renal disease (ESRD). The progression to ESRD, affected by hyperglycemia and hypertension, is characterized by microalbuminuria and macroalbuminuria. With advances in understanding the pathogenesis of CKD in diabetic patients, many novel therapeutic targets have been proposed, and the corresponding agents are being developed continually to prevent the progression of CKD.

Areas covered: This review focuses on those tested in phase III clinical trials for the treatment of CKD in diabetic patients, including renin-angiotensin system blockers, aldosterone antagonists, calcium channel blockers, TGF-β inhibitors, protein kinase C inhibitors, advanced glycation end products inhibitors, GLP-1 analogues, DPP-4 inhibitors, SGLT2 inhibitors, endothelin receptor antagonists, and so on.

Expert commentary: The ideal control of glucose and blood pressure and healthy lifestyle are prerequisite for diabetic patients, despite the progression of CKD is inevitable. Over the last few years, several agents have been developed to delay and even reverse progression of CKD in diabetic patients.

KEYWORDS:

• Diabetes
• microvascular complications
• chronic kidney disease
• pharmacological interventions
• phase III clinical trial

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.