Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (6)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Faure, S.
Right arrow Articles by Achard, J.-M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Faure, S.
Right arrow Articles by Achard, J.-M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nephrol Dial Transplant (2003) 18: 2463-2467
© 2003 European Renal Association-European Dialysis and Transplant Association

Editorial Comment

WNK kinases, distal tubular ion handling and hypertension

Sebastien Faure1, Céline Delaloy2, Valérie Leprivey1, Juliette Hadchouel2, David G. Warnock3, Xavier Jeunemaitre2 and Jean-Michel Achard1

1Division of Nephrology and Department of Physiology, Limoges University Hospital, 2Department of Genetics Hôpital Européen G. Pompidou and INSERM U36, Collège de France, Paris, France and 3Division of Nephrology, University of Alabama at Birmingham, AL, USA

Correspondence and offprint requests to: Jean-Michel Achard, Service de Néphrologie. CHU Dupuytren, Limoges, 87042, France. Email: jean-michel.achard@unilim.fr

Keywords: familial hyperkalaemic hypertension; WNK kinases

The first 150 words of the full text of this article appear below.



   Introduction
 
Familial hyperkalaemic hypertension (FHH) was originally described by Paver and Pauline in 1964 [1]. Also referred to as Gordon syndrome [2] or pseudohypoaldosteronism type 2 [3], the FHH syndromes are rare autosomal dominant diseases characterized by the unusual association of low renin hypertension with hyperkalaemia and metabolic acidosis despite normal glomerular filtration rate. These clinical and biological features are the mirror image of the Gitelman syndrome. Together with the peculiar sensitivity of FHH patients to thiazide diuretics [4,5], it suggests an increased sodium reabsorption through the thiazide-sensitive Na–Cl co-transporter (NCCT) as the main mechanism of the disease.

Genetic analyses, however, have excluded NCCT as being directly involved in all the families studied so far, but, instead, found evidence for three loci on chromosomes 1, 17 [6] and 12 [7], and for further genetic heterogeneity [8. . . [Full Text of this Article]



   FHH and WNK4
 
WNK4 and NCCT
WNK4 and paracellular permeability


   FHH and WNK1
 


   Perspectives
 

Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Am. J. Physiol. Renal Physiol.Home page
J.-B. Peng and D. G. Warnock
WNK4-mediated regulation of renal ion transport proteins
Am J Physiol Renal Physiol, October 1, 2007; 293(4): F961 - F973.
[Abstract] [Full Text] [PDF]

Home page
 Nephrol Dial TransplantHome page
F. Verrey
WNK4, as thiazides, shuts off NaCl reabsorption to stimulate Na/K exchange
Nephrol. Dial. Transplant., May 1, 2007; 22(5): 1305 - 1308.
[Full Text] [PDF]

Home page
 CJASNHome page
A. J. Felsenfeld and B. S. Levine
Milk Alkali Syndrome and the Dynamics of Calcium Homeostasis
Clin. J. Am. Soc. Nephrol., July 1, 2006; 1(4): 641 - 654.
[Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
A. R. Subramanya, C.-L. Yang, X. Zhu, and D. H. Ellison
Dominant-negative regulation of WNK1 by its kidney-specific kinase-defective isoform
Am J Physiol Renal Physiol, March 1, 2006; 290(3): F619 - F624.
[Abstract] [Full Text] [PDF]