Advanced glycation endproducts (AGEs) as uremic toxins.
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 oxidative 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.
Schwenger
V
V
Ruperto Carola University of Heidelberg, Department of Internal Medicine, Bergheimer Strasse 58, D-69115 Heidelberg, Germany.
Zeier
M
M
Henle
T
T
Ritz
E
E
D003928:Diabetic Nephropathies / Q000209:etiology*; D018450:Disease Progression; D017127:Glycation End Products, Advanced / Q000009:adverse effects / Q000097:blood / Q000378:metabolism*; D006801:Humans; D015416:Maillard Reaction; D010531:Peritoneal Dialysis, Continuous Ambulatory; D051437:Renal Insufficiency / Q000209:etiology; D014118:Toxins, Biological / Q000378:metabolism*; D014511:Uremia / Q000150:complications / Q000209:etiology* / Q000628:therapy
D017127:Glycation End Products, Advanced; D014118:Toxins, Biological