SYNOPSIS
The case histories of 4 children with Bartter's syndrome are presented. All were born prematurely and pregnancy was associated with hydramnios. All failed to thrive and had a vasopressin‐insensitive urinary concentrating defect, but were of normal intelligence. Hypo‐kalaemia was not necessarily present when first seen, but serum sodium was low compared with other patients with diabetes insipidus. Salt loading caused a sharp fall in serum potassium, often associated with a paradoxical rise in plasma renin levels. Urine calcium was high in all patients and rose to very high levels with salt loading. Nephrocalcinosis was a constant finding. The basic defect is thought to be one of ion absorption in the proximal tubule, though membrane transport may also be affected in other areas.