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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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter 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
ISSN (print) / ISBN 1748-1708
e-ISSN 1748-1716
Zeitschrift Acta Physiologica
Quellenangaben Band: 225, Heft: 4, Seiten: , Artikelnummer: e13249 Supplement: ,
Verlag Wiley
Verlagsort Hoboken
Begutachtungsstatus Peer reviewed