Renal ischaemia is now well recognised as a cause of hypertension and is frequently secondary to renal artery stenosis. During the last six years a small number of such patients have been recognised who present many features of primary hyperaldosteronism without having a primary suprarenal disorder (Gowenlock and Wrong, 1962; Goldberg and McCurdy, 1963; Itskovitz, Hildreth, Sellers and Blakemore, 1963). We here present a further case with bilateral renal artery stenosis in whom the electrolyte abnormalities did not recur following medical treatment of the hypertension.A female welfare worker aged 49 first attended hospital in July, 1962, complaining of tiredness, anorexia, weakness of the legs, dyspnoea on exertion and the loss of 1½ stones in weight. These symptoms had been present for only a few months. There was no dysuria or polyuria.On examination she was found to have a B.P. of 190/140 in both arms. All peripheral pulses were present. Clinically the heart was enlarged and there were signs of congestive heart failure. No abdominal bruit was heard. Fundi showed grade IV hypertensive retinopathy.Urine contained a moderate amount of albumen, frequent red cells, pus cells and casts. Culture grew a Coliform organism.Serum K was repeatedly between 2·9 and 3·4 mEq/L.Serum Na, Cl and HCO3were within normal limits.Blood urea varied between 50 and 70 mg per cent.Urinary concentrating power was impaired—the maximum concentration after 18 hours dehydration being 1008.Urinary excretion of Na was 5–20 mEq/24 hours.