Minireviews
Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
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
Abstract

The release of proinflammatory cytokines during inflammation represents an attempt to respond to injury, but it may produce detrimental effects. The inflammasome is a large, multiprotein complex that drives proinflammatory cytokine production in response to infection and tissue injury; the best-characterized inflammasome is the nod-like receptor protein-3 (NLRP3). Once activated, inflammasome leads to the active form of caspase-1, the enzyme required for the maturation of interleukin-1beta. Additional mechanisms bringing to renal inflammatory, systemic diseases and fibrotic processes were recently reported, via the activation of the inflammasome that consists of NLRP3, apoptosis associated speck-like protein and caspase-1. Several manuscripts seem to identify NLRP3 inflammasome as a possible therapeutic target in the treatment of progressive chronic kidney disease. Serum amyloid A (SAA), as acute-phase protein with also proinflammatory properties, has been shown to induce the secretion of cathepsin B and inflammasome components from human macrophages. SAA is a well recognised potent activator of the NLRP3. Here we will address our description on the involvement of the kidney in autoinflammatory diseases driven mainly by secondary, or reactive, AA amyloidosis with a particular attention on novel therapeutic approach which has to be addressed in suppressing underlying inflammatory disease and reducing the SAA concentration.

Keywords: Inflammation; Autoinflammatory disease; Chronic kidney disease; Interleukin-1; Dialysis; Caspase; Proteinuria; Amyloidosis; Nod-like receptor protein-3

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.