Elevated Tissue Polypeptide Antigen as a Risk Factor for Carpal Tunnel Syndrome in Haemodialyzed Patients

Walz, Gerd; Kunzendorf, Ulrich; Schwarz, Anke; Bauer, Renate; Keller, Frieder; Offermann, G.

doi:10.1159/000185133

Cited by 4 publications

(2 citation statements)

References 1 publication

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“…Patients with P 2-microglobulin amyloidosis, nearly exclusively dialysis patients, invariably have high serum levels of P 2-microglobulin. However, many studies have demonstrated that there is no relationship between serum levels of P 2-microglobulin and the incidence of P 2microglobulin amyloidosis (44)(45)(46). Therefore, although it might be "politically correct" to aim to decrease P 2microglobulin serum levels (47), such a strategy has not been proven to prevent or reverse P 2-microglobulin amyloidosis.…”

Section: A) Low Molecular Weight Proteins In General (We)mentioning

confidence: 99%

Uremic Toxicity: Present State of the Art

Vanholder

Argilés

Baurmeister³

et al. 2001

Int J Artif Organs

246

198

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The uremic syndrome is a complex mixture of organ dysfunctions, which is attributed to the retention of a myriad of compounds that under normal condition are excreted by the healthy kidneys (uremic toxins). In the area of identification and characterization of uremic toxins and in the knowledge of their pathophysiologic importance, major steps forward have been made during recent years. The present article is a review of several of these steps, especially in the area of information about the compounds that could play a role in the development of cardiovascular complications. It is written by those members of the Uremic Toxins Group, which has been created by the European Society for Artificial Organs (ESAO). Each of the 16 authors has written a state of the art in his/her major area of interest.

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Section: A) Low Molecular Weight Proteins In General (We)mentioning

confidence: 99%

Uremic Toxicity: Present State of the Art

Vanholder

Argilés

Baurmeister³

et al. 2001

Int J Artif Organs

246

198

View full text Add to dashboard Cite

show abstract

“…However, although a rise in β 2 -microglobulin serum levels seems to be a prerequisite for developing β 2 -microglobulin amyloidosis, from the early reports it appeared likely that it is not sufficient to cause amyloid fibril precipitation in vivo. Actually, many studies have demonstrated that there is no relationship between serum levels of β 2 -microglobulin and the incidence of β 2 -microglobulin amyloidosis [17, 29, 30, 31]. …”

Section: β2-microglobulin Serum Levels In Renal Failure and Dialysis mentioning

confidence: 99%

Antiproteases and Cells in the Pathogenesis of β<sub>2</sub>-Microglobulin Amyloidosis: Role of α<sub>2</sub>-Macroglobulin and Macrophages

Argilés¹,

Mourad²,

Gouin-Charnet³

et al. 2000

Nephron

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Beta 2 microglobulin isoforms in healthy individuals and in amyloid deposits

Argilés

Garcia-Garcia

Derancourt

et al. 1995

Kidney International

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beta 2 microglobulin (beta 2m) is classically known to have isoforms with isoelectric points (pI) 5.7 and 5.3. New isoforms of beta 2m with lower pI, probably due to modifications with advanced glycation end products, were found in the amyloid deposits of dialysis related amyloidosis (DRA), and they were proposed as the amyloidogenic forms of beta 2m. The other modifications in beta 2m from amyloid deposits are partial proteolysis and single amino acid replacement (Asn by ASp at position 17). However, there are no data on the sequence of the different isoforms of beta 2 m from amyloid deposits. Amyloid deposits surgically obtained from the carpal tunnel from 13 dialysis treated patients and urine from 10 healthy volunteers and 5 living-related kidney donors were analyzed for beta 2m content. Two-dimensional gel electrophoresis (2D-PAGE) of beta 2m from amyloid deposits showed the presence of four or more isoforms with pIs < 5.7. All the spots migrating at 12 kDa Mr region and between 4 and 6 pH reacted with rabbit anti-human beta 2m antibody by Western blotting, confirming that they were beta 2m isoforms. beta 2m isoforms from the amyloid deposits were then separately purified with an IEF column (PB94, Pharmacia) for analysis. Enough quantities of three pure beta 2m isoforms could be obtained in two cases. The sequence analysis showed an intact N-terminus in all the isoforms. There was Asn in the 17th residue in all the isoforms sequenced. 2D-PAGE of urine from 8 out of the 10 healthy volunteers showed the presence of beta 2m. In two of them beta 2m also displayed four different isoforms. At least four isoforms were observed in urine of all the kidney donors. The present study shows that the elution peaks of three different beta 2m isoforms in gel isoelectrofocusing contain beta 2m with intact N-terminus. None of them have deamidated their 17th residue. More importantly, the beta 2m isoforms with lower pI are not specific for amyloidosis as they were found in urine from kidney donors and in normal volunteers. These results bring into question the hypothesis that dialysis related amyloidosis is due to the known modifications on beta 2m. They suggest that the precipitation of beta 2m into amyloid fibrils should result from the interaction of beta 2m with other factors with amyloid enhancing activity.

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Elevated Tissue Polypeptide Antigen as a Risk Factor for Carpal Tunnel Syndrome in Haemodialyzed Patients

Cited by 4 publications

References 1 publication

Uremic Toxicity: Present State of the Art

Uremic Toxicity: Present State of the Art

Antiproteases and Cells in the Pathogenesis of β<sub>2</sub>-Microglobulin Amyloidosis: Role of α<sub>2</sub>-Macroglobulin and Macrophages

Beta 2 microglobulin isoforms in healthy individuals and in amyloid deposits

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