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Artunc, F. ; Wörn, M.* ; Schork, A. ; Bohnert, B.N.

Proteasuria-the impact of active urinary proteases on sodium retention in nephrotic syndrome.

Acta Physiol. 225:e13249 (2019)
Postprint DOI
Open Access Green
Sodium retention and extracellular volume expansion are typical features of patients with nephrotic syndrome. In recent years, from in vitro data, endoluminal activation of the epithelial sodium channel (ENaC) by aberrantly filtered serine proteases has been proposed as an underlying mechanism. Recently, this concept was supported in vivo in nephrotic mice that were protected from proteolytic ENaC activation and sodium retention by the use of aprotinin for the pharmacological inhibition of urinary serine protease activity. These and other findings from studies in both rodents and humans highlight the impact of active proteases in the urine, or proteasuria, on ENaC-mediated sodium retention and edema formation in nephrotic syndrome. Targeting proteasuria could become a therapeutic approach to treat patients with nephrotic syndrome. However, pathophysiologically relevant proteases remain to be identified. In this review, we introduce the concept of proteasuria to explain tubular sodium avidity and conclude that proteasuria can be considered as a key mechanism of sodium retention in patients with nephrotic syndrome.
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Publication type Article: Journal article
Document type Review
Keywords Aprotinin ; Enac ; Nephrotic Syndrome ; Proteasuria ; Proteinuria ; Proteolysis ; Serine Protease; Angiotensin-aldosterone System; Epithelial Na+ Channel; Collecting Duct; Gamma-subunit; Proteolytic Activation; Increased Expression; Edema Formation; Amiloride; Plasmin; Enac
Language
Publication Year 2019
Prepublished in Year 2018
HGF-reported in Year 2018
ISSN (print) / ISBN 1748-1708
e-ISSN 1748-1716
Quellenangaben Volume: 225, Issue: 4, Pages: , Article Number: e13249 Supplement: ,
Publisher Wiley
Publishing Place Hoboken
Reviewing status Peer reviewed
POF-Topic(s) 90000 - German Center for Diabetes Research
Research field(s) Helmholtz Diabetes Center
PSP Element(s) G-502400-001
Scopus ID 85060218561
Erfassungsdatum 2019-01-28