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Mediators of Inflammation
Volume 2017, Article ID 9845175, 9 pages
https://doi.org/10.1155/2017/9845175
Research Article

Increased Levels of sRAGE in Diabetic CKD-G5D Patients: A Potential Protective Mechanism against AGE-Related Upregulation of Fibroblast Growth Factor 23 and Inflammation

1Department of Biomedical Sciences for Health, Università degli Studi di Milano, Via L. Mangiagalli 31, 20133 Milan, Italy
2Laboratory of Molecular Pathology, I.R.C.C.S. Policlinico San Donato, Via R. Morandi 30, San Donato Milanese, 20097 Milan, Italy
3Department of Nephrology, Dialysis and Transplantation, San Bortolo Hospital, Viale Rodolfi 37, 36100 Vicenza, Italy
4International Renal Research Institute Vicenza (IRRIV), San Bortolo Hospital, Viale Rodolfi 37, 36100 Vicenza, Italy
5Service of Laboratory Medicine 1-Clinical Pathology, I.R.C.C.S. Policlinico San Donato, Via R. Morandi 30, San Donato Milanese, 20097 Milan, Italy

Correspondence should be addressed to Elena Dozio; ti.iminu@oizod.anele

Received 22 June 2017; Revised 21 August 2017; Accepted 7 September 2017; Published 25 September 2017

Academic Editor: Carmela R. Balistreri

Copyright © 2017 Elena Dozio et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Advanced glycation end products (AGEs) may induce cardiac remodeling in kidney disease by promoting fibroblast growth factor 23 (FGF-23) expression. Since AGEs are increased in diabetes mellitus (DM), our first aim was to evaluate the existence of any potential association between AGEs, FGF-23, inflammation, and increased cardiovascular risk in DM patients on dialysis (CKD-G5D). Secondarily, we explored the potential role of the soluble receptor for AGEs (sRAGE) as a marker of heart failure. Levels of glycated albumin (GA), sRAGE, c-terminal FGF-23 (cFGF-23), brain natriuretic peptide (BNP), and inflammatory mediators were compared between DM and non-DM CKD-G5D patients. The levels of sRAGE, cFGF-23, BNP, and proinflammatory markers were over the ranges of normality in both DM and non-DM groups. Only GA and sRAGE levels were increased in DM compared to non-DM patients. Plasma levels of sRAGE and CRP were the only independent predictors of BNP concentration. In conclusion, in DM CKD-G5D patients, sRAGE appeared to be a marker of cardiac remodeling. Indeed, its increase could be a potential protective mechanism against the increased risk of cardiovascular complications related to AGEs and inflammation. The causal relationship between sRAGE and cardiovascular risk in these patients needs to be further confirmed by mechanistic studies.