Early diabetic nephropathy in type 1 diabetes: new insights

Curr Opin Endocrinol Diabetes Obes. 2014 Aug;21(4):279-86. doi: 10.1097/MED.0000000000000074.

Abstract

Purpose of review: Despite improvements in glycemic and blood pressure control in patients with type 1 diabetes, diabetic nephropathy remains the most common cause of chronic kidney disease worldwide. A major challenge in preventing diabetic nephropathy is the inability to identify high-risk patients at an early stage, emphasizing the importance of discovering new therapeutic targets and implementation of clinical trials to reduce diabetic nephropathy risk.

Recent findings: Limitations of managing patients with diabetic nephropathy with renin-angiotensin-aldosterone system blockade have been identified in recent clinical trials, including the failure of primary prevention studies in T1D and the demonstration of harm with dual renin-angiotensin-aldosterone system blockade. Fortunately, several new targets, including serum uric acid, insulin sensitivity, vasopressin, and sodium-glucose cotransporter-2 inhibition, are promising in the prevention and treatment of diabetic nephropathy.

Summary: Diabetic nephropathy is characterized by a long clinically silent period without signs or symptoms of disease. There is an urgent need for improved methods of detecting early mediators of renal injury, to ultimately prevent the initiation and progression of diabetic nephropathy. In this review, we will focus on early diabetic nephropathy and summarize potential new therapeutic targets.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Angiotensin II Type 2 Receptor Blockers / therapeutic use*
  • Diabetes Mellitus, Type 1 / diagnosis
  • Diabetes Mellitus, Type 1 / metabolism*
  • Diabetes Mellitus, Type 1 / physiopathology
  • Diabetic Nephropathies / diagnosis
  • Diabetic Nephropathies / metabolism*
  • Diabetic Nephropathies / physiopathology
  • Disease Progression
  • Early Diagnosis
  • Glycopeptides / metabolism
  • Humans
  • Inflammation / physiopathology
  • Kidney Failure, Chronic / metabolism
  • Kidney Failure, Chronic / physiopathology
  • Kidney Failure, Chronic / prevention & control*
  • Renin-Angiotensin System / drug effects*
  • Sodium-Glucose Transporter 2 / metabolism
  • Uric Acid / metabolism

Substances

  • Angiotensin II Type 2 Receptor Blockers
  • Glycopeptides
  • Sodium-Glucose Transporter 2
  • copeptins
  • Uric Acid