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NDT Advance Access originally published online on September 23, 2006
Nephrology Dialysis Transplantation 2007 22(1):268-271; doi:10.1093/ndt/gfl520
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Elevated plasma asymmetric dimethyl-L-arginine in a patient with Gordon syndrome

Ewa Wieczorek-Surdacka1, Andrzej Surdacki2, Stefanie M. Bode-Böger3, Bibianne Schubert4 and Wtadystaw Sulowicz1

1Chair and Department of Nephrology, 22nd Department of Cardiology, Jagiellonian University, Cracow, Poland, 3Institute of Clinical Pharmacology, Otto-von-Guericke University, Magdeburg and 4Institute of Clinical Pharmacology, Hannover Medical School, Hannover, Germany

Correspondence and offprint requests to: Andrzej Surdacki, MD, 2nd Department of Cardiology, Jagiellonian University, 17 Kopernika Street, 31-501 Cracow, Poland.Email: surdacki.andreas@gmx.net

Keywords: asymmetric dimethyl-L-arginine; Gordon syndrome; hyperkalaemia; hypertension; nitric oxide

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



   Introduction
 
Studies of rare genetic syndromes associated with arterial hypertension provide insight into factors affecting blood pressure and thus into the pathophysiology of essential hypertension (EH) [1]. Pseudohypoaldosteronism type II, also called Gordon syndrome or chloride shunt, is an autosomal dominant defect, combining volume-dependent salt-sensitive hypertension, hyperkalaemia, hyperchloraemia and metabolic acidosis associated with normal glomerular filtration rate and high responsiveness to thiazides and dietary sodium restriction, whereas plasma aldosterone is variable, being a net effect of low reninaemia and hyperkalaemia.

Gordon syndrome attracts a special attention because this set of features (hypertension, hyperkalaemia and acidosis) is usually caused by renal insufficiency, a relatively frequent cause of elevated blood pressure. Recently, the molecular basis of Gordon syndrome has been elucidated resulting from loss-of-function mutations within WNK (with no lysine kinase) type 4 (WNK4) and gain-of-function mutations of WNK type 1 (WNK1), with consequent loss of WNK4-mediated tonic inhibition of thiazide-sensitive . . . [Full Text of this Article]



   Case report
 
Dimethyl-L-arginines assay


   Comments
 
Differential diagnosis
Elevated ADMA in Gordon syndrome

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