Review
Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Nephrol. Jul 6, 2016; 5(4): 308-320
Published online Jul 6, 2016. doi: 10.5527/wjn.v5.i4.308
Reclassification of membranoproliferative glomerulonephritis: Identification of a new GN: C3GN
Maurizio Salvadori, Giuseppina Rosso
Maurizio Salvadori, Department of Renal Transplantation, Careggi University Hospital, 50139 Florence, Italy
Giuseppina Rosso, Division of Nephrology, San Luca Hospital, 55100 Lucca, Italy
Author contributions: Salvadori M coordinated the study; Rosso G reviewed the literature; Salvadori M and Rosso G edited the manuscript.
Conflict-of-interest statement: The authors declare to have no conflict of interest in relation to the present manuscript.
Open-Access: 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/
Correspondence to: Maurizio Salvadori, MD, Department of Renal Transplantation, Careggi University Hospital, viale Pieraccini 18, 50139 Florence, Italy. maurizio.salvadori1@gmail.com
Telephone: +39-055-597151 Fax: +39-055-597151
Received: March 7, 2016
Peer-review started: March 9, 2016
First decision: March 25, 2016
Revised: March 31, 2016
Accepted: May 17, 2016
Article in press: May 27, 2016
Published online: July 6, 2016
Processing time: 114 Days and 8.6 Hours
Core Tip

Core tip: The complement pathway dysregulation has been recognized as the main cause of some membranoproliferative glomerulonephritis (MPGNs). This fact is at the basis of the new classification of the disease and of the findings of new entities as the complement factor H related protein nephropathy. Genetic studies as well as improvement in proteomics allowed recognizing the complement dysregulation as the cause of some renal diseases as the MPGN and the atypical hemolytic uremic syndrome that may be considered as strictly related diseases. The anti-complement drugs represent a new approach in the treatment of these diseases and their use in larger evidence based randomized trials is required.