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World J Nephrol. Feb 6, 2015; 4(1): 98-104
Published online Feb 6, 2015. doi: 10.5527/wjn.v4.i1.98
Role of β2-microglobulin in uremic patients may be greater than originally suspected
Aysegul Zumrutdal
Aysegul Zumrutdal, Nephrology Department, Baskent University Adana Teaching and Research Center, Baskent University Hospital, Yuregir, Adana 01230, Turkey
Author contributions: Zumrutdal A solely contributed to this work.
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: Aysegul Zumrutdal, MD, Professor, Nephrology Department, Baskent University Adana Teaching and Research Center, Baskent University Hospital, Yuregir, Dadaloglu Mah, 2591 St, 4/A, Adana 01230, Turkey. azumrutdal@yahoo.com
Telephone: +90-322-3272727 Fax: +90-322-3271274
Received: June 17, 2014
Peer-review started: June 18, 2014
First decision: August 14, 2014
Revised: September 3, 2014
Accepted: October 1, 2014
Article in press: October 10, 2014
Published online: February 6, 2015
Processing time: 234 Days and 17.8 Hours
Abstract

The role of beta2-microglobulin (β2M) in dialysis-related amyloidosis as a specific amyloid precursor was defined in the 1980s. Studies in those years were largely related to β2M amyloidosis. In 2005, for what was probably the first time in the available literature, we provided data about the association between β2M and early-onset atherosclerosis in hemodialysis patients without co-morbidities. In recent years, the role of uremic toxins in uremic atherosclerosis and the interest in β2M as a marker of cardiovascular (CV) and/or mortality risk have grown. In the current literature, clinical studies suggest that β2M is an independent, significant predictor of mortality, not only in dialysis patients, but also in predialysis patients and in the high-risk portion of the general population, and it seems to be a factor strongly linked to the presence and severity of CV disease. It is still unknown whether β2M is only a uremic toxin marker or if it also has an active role in vascular damage, but data support that it may reflect an increased burden of systemic atherosclerosis in a setting of underlying chronic kidney disease. Thus, although there have been some inconsistencies among the various analyses relating to β2M, it promises to be a novel risk marker of kidney function in the awareness and detection of high-risk patients. However, more research is required to establish the pathophysiological relationships between retained uremic toxins and further biochemical modifications in the uremic milieu to get answers to the questions of why and how. In this review, the recent literature about the changing role of β2M in uremic patients will be examined.

Keywords: Beta2-microglobulin; Carotid atherosclerosis; Cardiovascular disease; Cardiovascular risk; Coronary artery disease; Hemodialysis; Mortality; Uremia; Uremic toxins

Core tip: Previously, the clinical significance of beta2-microglobulin (β2M) in uremic patients was limited to β2M-derived amyloidosis; in recent years, its role and power has changed and expanded. Although there have been some inconsistencies among the various analyses relating to β2M, the data generally support β2M as a promising novel marker of kidney function by predicting cardiovascular (CV) risk, CV events and overall mortality.