Gitelman's syndrome, also known as 'hypocalciuric variant' of Bartter's syndrome, is a primary renal tubular disorder characterized by chronic hypokalaemia, hypomagnesaemia, metabolic alkalosis, hypocalciuria with normocalcaemia, hyperreninaemic hyperaldosteronism, and normal renal function [1—3]. The clinical features allowing its differentiation from 'classical' Bartter's syndrome include low urine calcium excretion, absence of overt urine concentration defect and normal growth velocity [3,4]. The primary defect in this disorder may be in the distal convoluted tubules [3,5,6]. To the best of our knowledge profound hypophosphataemia has not previously been reported in patients with Gitelman's syndrome in the English literature. Herein, we describe a patient with the disease who developed hypophosphataemia with inappropriate phosphaturia, and we discuss the possible pathophysiological mechanisms involved.
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Katopodis et al. (1996) studied this question.
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