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Research Article Free access | 10.1172/JCI118471

Early and advanced glycosylation end products. Kinetics of formation and clearance in peritoneal dialysis.

M A Friedlander, Y C Wu, A Elgawish, and V M Monnier

Department of Medicine, Case-Western Reserve University, Cleveland, Ohio 44106, USA.

Find articles by Friedlander, M. in: PubMed | Google Scholar

Department of Medicine, Case-Western Reserve University, Cleveland, Ohio 44106, USA.

Find articles by Wu, Y. in: PubMed | Google Scholar

Department of Medicine, Case-Western Reserve University, Cleveland, Ohio 44106, USA.

Find articles by Elgawish, A. in: PubMed | Google Scholar

Department of Medicine, Case-Western Reserve University, Cleveland, Ohio 44106, USA.

Find articles by Monnier, V. in: PubMed | Google Scholar

Published February 1, 1996 - More info

Published in Volume 97, Issue 3 on February 1, 1996
J Clin Invest. 1996;97(3):728–735. https://doi.org/10.1172/JCI118471.
© 1996 The American Society for Clinical Investigation
Published February 1, 1996 - Version history
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Abstract

The chronic contact of glucose-containing dialysate and proteins results in the deposition of advanced glycation end products (AGEs) on peritoneal tissues in patients treated by peritoneal dialysis (PD), yet plasma levels of the AGE pentosidine are significantly lower in PD than in hemodialysis (HD). We measured glycation of peritoneal proteins in patients on PD over the time course of intraperitoneal equilibration of fresh peritoneal dialysate. The glycated content of peritoneal proteins (furosine method) was initially identical to plasma but increased 200% within 4 h due to in situ glycation as also demonstrated in vitro. In contrast, peritoneal proteins contained a 2-4 x greater content of the AGE pentosidine at all equilibrium time points. Plasma protein furosine content was identical in patients on PD and on HD. Fractionation by gel filtration of serum from patients on PD and HD revealed that > 95% of the pentosidine was linked to proteins > 10,000 mol wt; < 1% to proteins < 10,000 mol wt; and < 1%, free. Neither HD nor PD affected protein-bound pentosidine. The HD treatment decreased free and < 10,000 mol wt bound pentosidine. However clearance of protein-associated pentosidine by the peritoneal membrane may explain lower steady state levels in patients treated by PD.

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