Journal of Clinical Endocrinology & Metabolism, Vol 52, 1027-1032, Copyright © 1981 by Endocrine Society

ARTICLES

The effect of triamterene and sodium intake on renin, aldosterone, and erythrocyte sodium transport in Liddle's syndrome

C Wang, TK Chan, RT Yeung, JP Coghlan, BA Scoggins and JR Stockigt

Liddle's syndrome was diagnosed in a 23-yr-old Chinese girl with hypertension and hypokalemia by the presence of suppressed renin and negligible plasma and urinary aldosterone secretion. Adrenal corticosteroids, including aldosterone, were suppressed by dexamethasone and stimulated by ACTH. While spironolactone was ineffective, triamterene (2,4,7-triamino-6-phenyl-pteridine) treatment corrected the hypertension and hypokalemia and restored PRA to normal provided that sodium intake was not excessive. During long term treatment with triamterene, blood pressure was extremely sensitive to salt intake, increasing promptly with high intake and decreasing with low salt intake. As a result of the chronic hypervolemia and sodium retention consequent upon the patient's persistent high salt intake and increased renal tubular sodium reabsorption, plasma renin and aldosterone remained low. Erythrocyte sodium concentration and membrane permeability were increased. Triamterene with salt restriction was able to lower the intracellular sodium concentration but did not correct the increased sodium permeability. This suggests that there is an abnormality of sodium transport in Liddle's syndrome which affects the erythrocytes as well as the renal tubular cells.

This article has been cited by other articles:

				M. Botero-Velez, J. J. Curtis, and D. G. Warnock Liddle's Syndrome Revisited -- A Disorder of Sodium Reabsorption in the Distal Tubule N. Engl. J. Med., January 20, 1994; 330(3): 178 - 181. [Full Text]

				B. A. Dickson and R. C. Franks Aldosterone-producing Adenoma Presenting with Hypokalemic Myopathy: Case Report and Review Clinical Pediatrics, July 1, 1988; 27(7): 344 - 347. [Abstract] [PDF]