A 10‐year‐old girl presenting with short stature had hypertension, severe hyperkalaemia (8.5 mEq/litre), mild acidaemia (arterial pH, 7.30) and periodic paralysis. It was postulated that the basic defect was a renal tubular avidity for sodium at a site proximal to the action of aldosterone, resulting in expansion of blood volume which in turn caused suppression of renin and of aldosterone and “escape” from relentless sodium retention. Plasma volume was increased, plasma renin activity undetectable, the urinary excretion of aldosterone very low and the renal tubule responsive to endogenous and exogenous aldosterone. The hypothesis was tested by appropriate balance studies including demonstration of renal tubular avidity for sodium despite low levels of aldosterone. Correction of all abnormalities followed prolonged dietary sodium restriction which brought about elevation of renin and aldosterone to normal levels. Correction of the hyperkalaemia or of the acidaemia while maintaining strict sodium balance did not correct the other abnormalities. Arterial pressor hypersensitivity to the stimulus of cold and to infused angiotensin and norepinephrine was reduced to normal when dietary sodium was restricted, associated with a return of blood pressure to normal levels. Following institution of dietary sodium restriction, attacks of muscle paralysis ceased and growth rate increased. The components of this syndrome are opposite to those found accompanying another rare congenital renal lesion associated with severely disturbed renin‐aldosterone physiology, and usually referred to as “Bartter's Syndrome”.