Scarpioni R, Ricardi M, Albertazzi V. Secondary amyloidosis in autoinflammatory diseases and the role of inflammation in renal damage. World J Nephrol 2016; 5(1): 66-75 [PMID: 26788465 DOI: 10.5527/wjn.v5.i1.66]
Corresponding Author of This Article
Roberto Scarpioni, MD, Department of Nephrology and Dialysis, AUSL Hospital “Guglielmo da Saliceto”, via Taverna 49, 29121 Piacenza, Italy. rscarpioni@hotmail.com
Research Domain of This Article
Urology & Nephrology
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Nephrol. Jan 6, 2016; 5(1): 66-75 Published online Jan 6, 2016. doi: 10.5527/wjn.v5.i1.66
Secondary amyloidosis in autoinflammatory diseases and the role of inflammation in renal damage
Roberto Scarpioni, Marco Ricardi, Vittorio Albertazzi
Roberto Scarpioni, Marco Ricardi, Vittorio Albertazzi, Department of Nephrology and Dialysis, AUSL Hospital “Guglielmo da Saliceto”, 29121 Piacenza, Italy
Author contributions: Scarpioni R designed the research; Ricardi M and Albertazzi V performed research; all the authors contributed to conception and design of the study and analyzed data; Scarpioni R wrote the paper and all the authors revised and approved the final version of the manuscript.
Conflict-of-interest statement: All the authors declare no conflict of interest.
Open-Access: This article is an open-access article which selected by an in-house editor and fully peer-reviewed by external reviewers. It distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Roberto Scarpioni, MD, Department of Nephrology and Dialysis, AUSL Hospital “Guglielmo da Saliceto”, via Taverna 49, 29121 Piacenza, Italy. rscarpioni@hotmail.com
Telephone: +39-0523-302176 Fax: +39-0523-302174
Received: May 10, 2015 Peer-review started: May 12, 2015 First decision: June 9, 2015 Revised: November 24, 2015 Accepted: December 9, 2015 Article in press: December 11, 2015 Published online: January 6, 2016 Processing time: 241 Days and 16.5 Hours
Core Tip
Core tip: Inflammation may also negatively produce elevation of proinflammatory cytokines. Recently, attention was addressed to the formation of the intracellular inflammasome nod-like receptor protein-3 (NLRP-3) activating caspase-1, the enzyme required for the maturation of interleukin-1. IL1, in turn, regulate serum amyloid A, a major acute-phase with also proinflammatory properties. An interesting new scenario on the pathogenesis of renal diseases (namely ANCA-associated glomerulonephritis vasculitis, urate-crystal nephropathy, contrast nephropathy, acute kidney injury, reactive systemic amyloidosis) and reactive systemic amyloidosis was opened, and NLRP3 inflammasome was recently identified as a possible therapeutic target in the treatment of chronic kidney disease.
