Pharmacological modulation of AGEs: a unique role for redox-active metal ions.

p harmacological modulation of the effects of advanced glycosylation end-products (AGEs) in pa tients with end-stage renal disease (ESRD) can be approached using three major strategies: ( 1) suppression or prevention offormation, (2) reversal of crosslinks already present on proteins, and (3) inhibition or blockade of the biologic effects of AGEs. This paper will provide a brief review of the literature supporting each of these approaches, and will focus on a newly defined mechanism for accelerated AGE formation and toxicity in ESRD. This novel mechanism, involving redox-active metal binding to proteins, may provide the basis for a unique and simple approach to pharmacologic modulation of AGE effects in ESRD.