GENERAL COMMENTARY article

Front. Med., 14 January 2015

Sec. Nephrology

Volume 1 - 2014 | https://doi.org/10.3389/fmed.2014.00059

Reassessing the Reassessment of suPAR in Glomerular Disease

  • 1. Department of Nephrology, UZ Leuven, Leuven, Belgium

  • 2. Department of Microbiology and Immunology, KU Leuven, Leuven, Belgium

  • 3. Department of Medicine, Rush University Medical Center, Chicago, IL, USA

Soluble urokinase receptor (suPAR) is proposed as circulating factor in focal and segmental glomerulosclerosis (FSGS) (). Spinale et al. attempt to validate the role of suPAR in glomerular disease (). Their mouse overexpression experiments of physiological suPAR forms are distinct from the studies by Wei et al. that expressed either alternate suPAR forms or used different mouse models (). Additional experiments will help to further clarify the distinct roles of suPAR variants.

Spinale et al. extend previous clinical studies indicating that glomerular filtration rate (GFR) is an important determinant of suPAR (). This, however, does not imply that suPAR is only bystander, as illustrated by epidemiological studies linking elevated suPAR – independent of the eGFR – to cardiovascular disease in patients with CKD ().

As for most large protein plasma components, the balance between generation and clearance determines suPAR accumulation, adding complexity when studying the direct renal effects of suPAR, especially when possibly also causing kidney disease. Biopsy proven FSGS patients with GFR >40 ml/min have in 50% elevated suPAR levels (), suggesting also suPAR production. In addition, suPAR fragments (measured and unmeasured) may cause podocyte injury, potentially contributing to a reduced GFR. The strong effect of a low GFR on serum suPAR levels in observational studies could obfuscate the effects of suPAR-induced glomerular pathology.

In conclusion, dependence of serum suPAR levels on GFR precludes using suPAR as a single value biomarker for FSGS in conditions of low GFR, but this correlation does not serve as an explanation for elevated suPAR under preserved GFR (Figure 1).

Figure 1

Statements

Conflict of interest

Jochen Reiser is an inventor on pending and issued patents related to anti-proteinuric therapies. He stands to gain royalties from their present and future commercialization. He is also a co-founder and advisor to TRISAQ, a biotechnology company. The Associate Editor Nada Alachkar declares that, despite having previously published with Jochen Reiser, the review process was handled objectively and no conflict of interest exists. Björn K. I. Meijers declares no conflict of interest.

References

Summary

Keywords

suPAR, FSGS, glomerular disease, mouse models, GFR

Citation

Meijers BKI and Reiser J (2015) Reassessing the Reassessment of suPAR in Glomerular Disease. Front. Med. 1:59. doi: 10.3389/fmed.2014.00059

Received

12 December 2014

Accepted

18 December 2014

Published

14 January 2015

Volume

1 - 2014

Edited by

Nada Alachkar, Johns Hopkins University, USA

Reviewed by

Sumant Singh Chugh, University of Alabama at Birmingham, USA

Copyright

*Correspondence:

This article was submitted to Nephrology, a section of the journal Frontiers in Medicine.

Disclaimer

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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