THE PATHOGENESIS AND CONSEQUENCES OF AGE FORMATION IN UREMIA AND ITS TREATMENT

Advanced glycation endproducts (AGEs) accumulate in uraemia as a conse quence of diminished clearance of low molecular weight forms which ret ain their reactivity and may subsequently combine with circulating and tissue macromolecules. Successful renal transplantation is the only f orm of renal replacement therapy which effectively clears these circul ating AGEs; both haemodialysis and peritoneal dialysis are comparative ly ineffective although high-flux haemodialysis confers some benefits. De novo AGE formation may be accelerated in uraemia due to carbonyl a nd oxidative stress leading to further accumulation. The consequences for the patient with chronic renal failure may be acceleration of vasc ular disease, renal failure progression and dialysis-related amyloidos is. Accelerated peritoneal AGE formation as a consequence of treatment with peritoneal dialysis fluids may be detrimental to peritoneal memb rane function but does not appear to contribute to systemic elevation of AGEs.