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NDT Advance Access originally published online on December 14, 2007
Nephrology Dialysis Transplantation 2008 23(4):1109-1111; doi:10.1093/ndt/gfm886
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org



Parvalbumin: a key protein in early distal tubule NaCl reabsorption*

Miriam Zacchia and Giovambattista Capasso

Chair of Nephrology, Department of Internal Medicine, Second University of Naples, Italy

Giovambattista Capasso, Chair of Nephrology, Department of Internal Medicine, Second University of Naples, Padiglione 17, Policlinico Nuovo, Via Pansini 5, 80131 Napoli, Italy, E-mail: gb.capasso@unina2.it

Keywords: distal convoluted tubule; Gitelman's syndrome; Na+Cl cotransport; parvalbumin; thiazide diuretics

The first 10% of the full text of this article appears below.



   Summary of key findings
 
The cortical distal nephron is committed to the fine regulation of electrolytes and water balance. Several investigations have addressed the molecular mechanisms implicated in this process. The paper by Belge et al. [1] demonstrates the emerging role of parvalbumin (PV) on distal tubule NaCl reabsorption. PV is a divalent cation buffering protein, exclusively expressed in the early distal convoluted tubule (DCT1). The authors show solid data suggesting a functional relationship between PV and the thiazide-sensitive Na+-Cl cotransporter (NCC), the main entry step for Na+ and Cl through the apical membrane at this nephron site. PV–/– mice exhibit a salt-losing phenotype characterized by increased diuresis, kaliuresis and high aldosterone levels, a phenotype very similar, although not . . . [Full Text of this Article]



   Background
 
What is in it for the practising nephrologist
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