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Published in: Pediatric Nephrology 7/2013

01-07-2013 | Review

Serum suPAR in patients with FSGS: trash or treasure?

Authors: Rutger J. H. Maas, Jeroen K. J. Deegens, Jack F. M. Wetzels

Published in: Pediatric Nephrology | Issue 7/2013

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Abstract

The urokinase-type plasminogen activator receptor (uPAR) has important functions in cell migration. uPAR can be shed from the cell membrane resulting in soluble uPAR (suPAR). Further cleavage gives rise to shorter fragments with largely unknown functions. Recent studies have demonstrated that both overexpression of uPAR on podocytes and the administration of suPAR cause proteinuria in mice. The common pathogenic mechanism involves the activation of podocyte β3-integrin. Increased activation of β3-integrin is also observed in patients with focal and segmental glomerulosclerosis (FSGS). These observations form the basis for the hypothesis that suPAR may be the circulating factor causing FSGS. A recent study fosters this idea by demonstrating increased suPAR levels in the serum of patients with FSGS and reporting an association with recurrence after transplantation and response to plasmapheresis. However, this study was heavily biased, and subsequent studies have given conflicting results. Although the experimental work is very suggestive, at present there is no proof that any known human suPAR fragment causes FSGS in humans. We therefore suggest that the measurement of suPAR using currently available assays has absolutely no value at the present time in decision-making in routine clinical practice.
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Metadata
Title
Serum suPAR in patients with FSGS: trash or treasure?
Authors
Rutger J. H. Maas
Jeroen K. J. Deegens
Jack F. M. Wetzels
Publication date
01-07-2013
Publisher
Springer-Verlag
Published in
Pediatric Nephrology / Issue 7/2013
Print ISSN: 0931-041X
Electronic ISSN: 1432-198X
DOI
https://doi.org/10.1007/s00467-013-2452-5

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