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Renal N ε-Carboxymethyllysine Deposition After Kidney Transplantation
Author(s) -
Marcus Baumann,
M.M. Caron,
Christoph Schmaderer,
Christian Schulte,
O Viklický,
Claus W. Hann von Weyhern,
Jens Lutz,
Uwe Heemann
Publication year - 2008
Publication title -
transplantation
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 1.45
H-Index - 204
eISSN - 1534-6080
pISSN - 0041-1337
DOI - 10.1097/tp.0b013e31817ef7a5
Subject(s) - medicine , transplantation , glycation , lacidipine , endocrinology , urology , kidney , fibrosis , kidney disease , creatinine , diabetes mellitus , pathology , receptor , antagonist
Accumulation of advanced glycation end products, that is, N(epsilon)-carboxymethyllysine (CML), induces oxidative stress and inflammation, and is present in chronic renal failure. Proximal tubular cells (PTCs) take up advanced glycation end products-bound proteins by apical megalin-receptors and degrade them. We hypothesized that renal transplant dysfunction affects renal CML homeostasis. Therefore, tubular and glomerular deposition of CML was investigated in a rat transplantation model, and in human allograft biopsies.

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