Effects of pyridoxamine, a novel post-Amadori AGE inhibitor, on nephropathy induced by glycated albumin.
ASN 30th Annual Meeting, San Antonio
J Am Soc Nephrol (Oct) 8:641A 1997
The role of advanced glycation end products (AGEs) in the pathogenesis of diabetic complications is increasingly accepted as indicated by the explosion in the number of papers on the subject. When Brownlee and Cerami first proposed aminoguanidine as a means of blocking formation of AGEs and thereby preventing nephropathy, retinopathy, and neuropathy in the streptozotocin-induced diabetic rat, a fresh and important approach to the therapy of diabetes was established.
In this report, the authors studied the effects of pyridoxamine, a compound found to inhibit post-Amadori conversion to AGEs, on renal pathology in rats that were injected with ribose-glycated Amdori or AGE containing rat serum albumin to induce hyperfiltration. Pyridoxamine (but not aminoguanidine) appeared to prevent glomerular loss of heparan sulfate and glomerular deposition of glycated albumin in the treated animals.
Comment: There will be many chemicals that block one or another aspect of AGE synthesis. As for all new "drugs" there is a long road from studies in rats to clinical trials in humans. What is noteworthy in this study is the efficacy of a well studied nontoxic compound - pyridoxamine - in pre- empting glomerular lesions linked to AGEs. The next steps in converting this finding to a treatment are well appreciated by the authors and their sponsors. (Eli Friedman, M.D., SUNY Health Science Center, Brooklyn, NY)
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ASN 30th Annual Meeting, San Antonio
Proteinuria/Hematuria : Diabetes