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Nephrol Dial Transplant (2001) 16: 2250-2252
© 2001 European Renal Association-European Dialysis and Transplant Association

Case Reports

Severe hyponatraemia and hypouricaemia in Gitelman's syndrome

Hans Schepkens1,, Joris Stubbe2, Heidi Hoeben1, Raymond Vanholder1 and Norbert Lameire1

1 Department of Internal Medicine, Renal Division and 2 Division of Gastroenterology, University Hospital Gent, Belgium

Keywords: Gitelman's syndrome; hypomagnesaemia; hyponatraemia; hypouricaemia; syndrome of inapropriate ADH release (SIADH); thiazides



   Introduction
 
Gitelman's syndrome (GS) is a variant of classical Bartter's syndrome (BS) in adults characterized by hypokalaemic metabolic alkalosis, hypocalciuria (daily excretion <2.0 mg/kg body weight), hypomagnesaemia (<1.5 mg/dl), together with a normal to low blood pressure [1]. In 1996, Simon et al. [2] reported complete linkage between the syndrome and the thiazide-sensitive sodium chloride coporter (TSC) on chromosome 16q13 (Human Gene Mapping Workshop-approved symbol: SLCA3). Other metabolic features of GS include normonatraemia, hyperuricaemia, normocalcaemia, increased plasma renin and aldosterone/potassium ratio, and inappropriately high renal potassium, magnesium and chloride excretion [3,4]. In this paper, we describe two affected patients who developed severe hyponatraemia and hypouricaemia. To the best of our knowledge, this complication has not been described previously.



   Case 1
 
In 1984, a 27-year-old man diagnosed with a psychoaffective disorder and benzodiazepine addiction complained of muscle weakness, tremor and muscular cramps. Routine biochemical analysis . . . [Full Text of this Article]



   Case 2
 


   Discussion
 


   Notes
 


   References
 

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