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NDT Advance Access published online on September 5, 2007
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfm585
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Hyperkalaemia in a tetraplegic adolescent due to de novo sodium channel mutation

Ivica Grgic1, Han Si1, Candan Depboylu2, Günter U. Höglinger2, Christoph Busch1, Willm-Thomas Heyken1, Uwe Kuhlmann1, Ralf Köhler1 and Joachim Hoyer1

1Division of Nephrology, Department of Internal Medicine and 2Department of Neurology, Philipps-University Marburg, Marburg, Germany

Correspondence and offprint requests to: Dr Ivica Grgic, Department of Internal Medicine—Nephrology, Philipps-University, Baldingerstrasse, 35033 Marburg, Germany. Email: grgic@med.uni-marburg.de

Keywords: de novo mutation; hyperkalaemia; HyperPP; periodic paralysis; SCN4A gene; sodium channel

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



   Introduction
 
Maintenance of potassium homeostasis is crucial for the survival of humans and other mammals. In general, potassium levels result from the relationship between potassium intake, urinary potassium excretion and the distribution of potassium between the intracellular and extracellular space. In healthy subjects, potassium excesses are primarily buffered by rapid cell uptake. In a second step, excessive serum potassium is then largely balanced via potassium excretion in the urine, mediated by the renal cortical collecting tubules. These cellular and urinary adaptations normally prevent significant potassium accumulation in the extracellular fluid.

Hyperkalaemia is defined as a condition in which serum potassium levels exceed concentrations of 5.0–5.5 mmol/l. Nephrologists usually have to deal with hyperkalaemia on a daily basis and the causes thereof are indeed numerous. However, they can be assigned to four major categories: (i) excessive K+-intake and tissue necrosis, (ii) reduced renal K+-excretion, (iii) redistribution of internal K+ via . . . [Full Text of this Article]



   Case report
 


   Discussion
 

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