Low aquaporin-2 excretion in the nephrotic syndrome: an escape from the vasopressin regulating effect

International Journal of Nephrology and Renovascular Disease. 2018;Volume 11:271-277


Journal Homepage

Journal Title: International Journal of Nephrology and Renovascular Disease

ISSN: 1178-7058 (Online)

Publisher: Dove Medical Press

LCC Subject Category: Medicine: Internal medicine: Specialties of internal medicine: Diseases of the genitourinary system. Urology

Country of publisher: United Kingdom

Language of fulltext: English

Full-text formats available: PDF, HTML



Brovko M

Kozlovskaya L

Pulin A

Moiseev S

Sholomova V

Shchekochikhin D

Gognieva D

Milovanova L

Fomin V


Blind peer review

Editorial Board

Instructions for authors

Time From Submission to Publication: 16 weeks


Abstract | Full Text

Mikhail Brovko,1 Lidia Kozlovskaya,1 Andrey Pulin,1,2 Sergey Moiseev,1 Victoria Sholomova,1 Dmitry Shchekochikhin,1 Daria Gognieva,1 Ludmila Milovanova,1 Victor Fomin1 1Sechenov First Moscow State Medical University, Moscow, Russia; 2Laboratory for Cell Technologies and Developmental Pathology, Federal State Budgetary Scientific Institution “Institute of General Pathology and Pathophysiology,” Moscow, Russia Purpose: Experimental studies suggest that the nephrotic syndrome is associated with “vasopressin escape”, characterized by low aquaporin-2 (AQP2) expression in the collecting duct despite high vasopressin secretion. We investigated this phenomenon in patients with the nephrotic syndrome. Patients and methods: We recruited 47 patients with proteinuric kidney disease who were distributed into the following four groups: 1) nephrotic syndrome with kidney dysfunction (n=10); 2) nephrotic syndrome with normal kidney function (n=16); 3) partial remission of nephrotic syndrome (n=10); and 4) minimal proteinuria (n=11). Nine healthy volunteers comprised a control group. Serum copeptin level (as a marker of vasopressin secretion) and urinary AQP2 were measured using ELISA. Results: Nephrotic syndrome was associated with a significant increase in serum copeptin levels compared with those in the other groups (all P<0.05). In patients with nephrotic syndrome and a partial remission of nephrotic syndrome combined, there was more than a ten-fold decrease in the median urinary AQP2 excretion (0.03 ng/mL) compared with healthy volunteers (0.41 ng/mL; P<0.001) and more than a five-fold decrease compared with patients with minimal proteinuria (0.21 ng/mL; P<0.05). Unlike copeptin levels, the median urinary AQP2 excretion in patients with minimal proteinuria also decreased but less significantly than in those with nephrotic syndrome. There was a negative correlation between the urinary AQP2 excretion and daily proteinuria (R=−0.41; P=0.005). Conclusion: Our clinical study was the first to demonstrate low AQP2 excretion in nephrotic syndrome that may indicate an escape from the vasopressin regulating effect. Keywords: nephrotic syndrome, aquaporin-2, copeptin, vasopressin escape