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NDT Advance Access originally published online on February 16, 2008
Nephrology Dialysis Transplantation 2008 23(4):1098-1101; doi:10.1093/ndt/gfn011
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Periodic paralyses: when channels go wrong

Jean-Philippe Lengelé, Hendrica Belge and Olivier Devuyst

Division of Nephrology, Université catholique de Louvain Medical School, B-1200, Brussels, Belgium

Olivier Devuyst, Division of Nephrology, Université catholique de Louvain, 10 Avenue Hippocrate, B-1200 Brussels, Belgium. Tel: +32-2-764-54-53; Fax: +32-2-764-54-55; E-mail: olivier.devuyst@uclouvain.be

Keywords: channel; hyperkalaemia; hypokalaemia; transcellular shift

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

In 1865, Claude Bernard wrote that ‘the constancy of the internal milieu is the essential condition to a free and independent life’ [1]. It would be hard to find a more illustrative paradigm for that statement than for the case of hyperkalaemic periodic paralysis (HyperPP) reported by Grgic et al. in this issue [2]. A 14-year-old male was admitted for a sudden ascending paralysis involving the four limbs that appeared shortly after exercise. The symptoms were associated with a severe hyperkalaemia (6.3 mmol/L). Remarkably, both the muscle strength and the K+ level normalized spontaneously within 2 h. Since the patient had presented similar episodes since childhood, a clinical diagnosis of HyperPP was made, later confirmed by provocation with exercise and oral K+ intake. Genetic analysis detected a known mutation (T704M) in the SCN4A gene that encodes the {alpha} subunit of the Nav1.4 voltage-gated sodium channel. . . . [Full Text of this Article]



   Potassium homeostasis
 


   Hyperkalaemia and K+ redistribution
 


   The periodic paralyses, paradigm for muscle channelopathies
 


   From mutations to disease
 


   Conclusion
 

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