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Clinical studies of advanced glycation end product inhibitors and diabetic kidney disease

Mark E Williams1

  • 1Joslin Diabetes Center, Harvard Medical School, 1 Joslin Place, Boston, MA 02215, USA. mark.williams@joslin.harvard.edu

Current Diabetes Reports
|November 13, 2004
PubMed

Insights

Current treatments for diabetic nephropathy are insufficient to halt disease progression. This review examines advanced glycation end product (AGE) inhibitors like pimagedine, pyridoxamine, and alagebrium in human studies.

Area of Science:

  • Nephrology
  • Endocrinology
  • Pharmacology

Background:

  • Diabetic nephropathy is a serious complication of diabetes mellitus.
  • Sustained hyperglycemia leads to the formation of advanced glycation end products (AGEs), contributing to irreversible kidney damage.
  • The role of AGEs in diabetic nephropathy is well-established through basic research.

Purpose of the Study:

  • To review the clinical development and human study progression of advanced glycation end product (AGE) inhibitors for diabetic nephropathy.
  • To assess the therapeutic potential of AGE inhibitors in managing diabetic kidney disease.

Main Methods:

  • Review of human clinical studies involving AGE inhibitors.
  • Analysis of data on the efficacy and safety of pimagedine, pyridoxamine, and alagebrium.

Main Results:

  • The article discusses the progression of specific AGE inhibitors through clinical trials.
  • Pimagedine, pyridoxamine, and alagebrium are highlighted as key examples of AGE inhibitors investigated in human studies.

Conclusions:

  • Existing treatments for diabetic nephropathy are suboptimal.
  • AGE inhibitors represent a promising therapeutic avenue for halting or slowing the progression of diabetic nephropathy.
  • Further clinical development of AGE inhibitors is warranted.

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