Hypertension,Hypokalemia and Hypoaldosteronism with Suppressed Renin:A Clinical Study of a Patient with Liddle′s Syndrome

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  • SAKAMOTO NOBORU
    Division of Hypertension, Department of Medicine, National Cardiovascular Center
  • UDA MASANOBU
    Division of Hypertension, Department of Medicine, National Cardiovascular Center
  • KOJIMA SHUNICHI
    Division of Hypertension, Department of Medicine, National Cardiovascular Center
  • TSUCHIYA MASAYUKI
    Division of Hypertension, Department of Medicine, National Cardiovascular Center
  • ITO KEIICHI
    Division of Hypertension, Department of Medicine, National Cardiovascular Center
  • OGINO KOICHI
    Division of Hypertension, Department of Medicine, National Cardiovascular Center
  • IKEDA MASAO
    Division of Hypertension, Department of Medicine, National Cardiovascular Center
  • WATABE RYOJI
    Division of Hypertension, Department of Medicine, National Cardiovascular Center Department of Medicine, Wakayama Red Cross Hospital

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タイトル別名
  • Hypertension, hypokalemia and hypoaldosteronism with suppressed renin: a clinical study of a patient with Liddle's syndrome.
  • Hypertension Hypokalemia and Hypoaldost

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説明

A 24-yr-old woman with hypertension, hypokalemic alkalosis, low plasma renin and hypoaldosteronism was studied. Plasma aldosterone, renin and potassium returned to normal and blood pressure fell after sodium restriction or the administrationof triamterene. Thiazide therapy also normalized her blood pressure while dexamethasone, spironolactone and furosemide did not improve her symptoms. Plasma aldosterone levels were low and responded poorly to a short term ACTH injection, but responded well to the maximal adrenal stimulation by ACTH-Z. Plasma levels of cortisol, corticosterone and deoxycorticosterone were within the normal range. Adrenalscintigram with 131I-adosterol and abdominal computed axial tomography did not reveal the presence of a sizeable adrenal tumor. In addition, the urinary kallikrein excretion was low after sodium restriction and showed no response to saline infusion. These findings suggest that the excessive secretion of unusual mineralocorticoids may not exist in this case. From these observations and the results of the therapeutic responses to the diuretic agents, we conclude that the primary cause of the disorder of this patient seems to be a renal defect in the distal tuble in handlingsodium and potassium which is similar to that in Liddle's syndrome.

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