Advanced glycation endproducts (AGEs) as uremic toxins

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Abstract
Products of non‐enzymatic glycation accumulate both in diabetic and non‐diabetic patients with renal failure. The increase in concentration is presumably due to increased generation, secondary to oxydative stress and due to decreased (renal) elimination; whether accumulation of AGEs of dietary origin plays a role is currently under investigation. AGE's have been related to progression of diabetic (and possibly also non‐diabetic) renal disease and to a number of complications of the uremic syndrome. These comprise beta‐2‐microglobulin‐derived dialysis‐related amyloidosis, dyslipidemia, vascular dysfunction and accelerated atherogenesis. A specific case is AGE related damage to the peritoneal membrane in CAPD patients. Removal of AGE by dialysis is negligible and even high flux dialysis eliminates only a quantitatively limited amount of AGE. In contrast, a rapid decrease of AGE concentrations in plasma is noted after renal transplantation. Dietary AGEs may contribute significantly to the total AGE load of the body, particularly in uremia.

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