Possible involvement of cross-linking advanced glycation endproducts in long-term CAPD peritoneal degeneration

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Division of Kidney and  Hypertension The Jikei University  School of Medicine 3-19-18, Nishishimbashi Minato-ku, Tokyo, Japan Baxter Japan International Inc.¹ 4, Rolcobancho Chiyodaku Tokyo Japan Email: [email protected]

Sir,

It has been demonstrated that advanced glycation endproducts (AGEs) are generated in the peritoneal tissue of continuous ambulatory peritoneal dialysis (CAPD) patients [1], and they are closely related to pathological phenomena, such as enhanced solute transport state, ultrafiltration failure (UFF) and mesothelial damage. Sclerotic degeneration of the peritoneum, known as ‘tanned peritoneum’, has been observed in patients undergoing long-term CAPD treatment; however, the exact mechanism of its progression has not been elucidated. In this respect, whether AGE formation and furthermore what kind of AGE is involved in this pathology is a question that has yet to be answered. Among the characteristics for AGEs, cross-linking with proteins is well known. To explain this cross-linking phenomenon, dimer formation by carbonyl compounds has been reported. For these cross-linking substances, glyoxal lysine dimer (GOLD) and methylglyoxal lysine dimer (MOLD) have recently been cited [2]. Therefore, in the present study, representative non-cross-linking AGEs [N^ϵ-(carboxymethyl)lysine (CML) and N^ϵ-(carboxyethyl)lysine (CEL)], as well as cross-linking AGEs (GOLD and MOLD), were evaluated in the peritoneal tissue of four patients undergoing regular dialysis, including one suffering from encapsulating peritoneal sclerosis (EPS).