Low aquaporin-2 excretion in the nephrotic syndrome: an escape from the vasopressin regulating effect
Received 17 June 2018
Accepted for publication 31 August 2018
Published 17 October 2018 Volume 2018:11 Pages 271—277
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Professor Pravin Singhal
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
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