Microsoft Word - NEF164BF

Hein A. Koomans, Department of Nephrology, University Hospital, Catharijnesingel 101, NL-3511 GV Utrecht (The Netherlands) Dear Sir, In their article Puschett et al. [1] described a patient with all clinical features of Bartter’s syndrome, but with a normal capacity to form solute-free water during water loading. The latter was concluded from the finding of a normal diluting segment reabsorption, expressed as Ch2o/(Ch2o + Cc1), when related to delivery to this segment, expressed as (C3⁄8o + Ccι)/Ciπuiin. Since originally described patients with Bartter’s syndrome had a substantial dilution defect [2], the authors suggested that their patient had a variant from of Bartter’s syndrome. However, they also found an impaired increase in NaCl excretion after chlorothiazide, from which they concluded that there was a NaCl reabsorption defect in the distal convoluted tubule [1]. Since during water loading the distal convoluted tubule is a part of the diluting segment, it seems paradoxical to assume a reabsorption defect in the distal tubule without a general dilution defect. Diverging reports on some NaCl reabsorption defect in patients with Bartter’s syndrome have been discussed recently [3]. This made us collect in a recent report [4] all maximal free water clearance data from patients with this syndrome we could trace in the literature or studied by ourselves. Since percent diluting segment reabsorption falls with increasing delivery, and since this delivery varied greatly due to different study conditions, the data were compared to findings in normal subjects in whom a large range in distal deliveries had been induced by diet. Figure 1 summarizes these data. The dotted line denotes the ratio of 0.60 between diluting segment reabsorption and diluting segment delivery. This was the maximal percent reabsorption in the 5 patients described by Gill and Bartter [2]. Clearly, according to the normal standards, most patients demonstrate a dilution defect, but this defect is seldomly as pronounced as in the patients of Gill and Bartter [2].