Horm Metab Res 1978; 10(1): 65-71
DOI: 10.1055/s-0028-1093484
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© Georg Thieme Verlag KG Stuttgart · New York

Plasma Renin Activity and Urinary Aldosterone in Cushing's Syndrome

F.  Mantero , D.  Armanini , M.  Boscaro
  • Istituto di Semeiotica Medica dell'Università di Padova (Direttore: Prof. Mario Austoni), Italy
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Publication History

Publication Date:
23 December 2008 (online)

Abstract

The renin-angiotensin-aldosterone system has been evaluated in 19 patients with Cushing's syndrome due to bilateral adrenal hyperplasia and in 2 patients with unilateral adenoma. In the first group urinary aldosterone was within the normal limits with a mean of 8.3 ± 1.86 µg/24 h. Aldosterone excretion did not change significantly after furosemide administration, ACTH infusion or dexamethasone.

Upright PRA was suppressed in 9/16 patients with a mean of 4.9 ± 1.85 ng/ml/3 h and showed only a slight response to furosemide. Dexamethasone alone did not produce any change. Both aldosterone and PRA were to some extent stimulated by an association of dexamethasone and furosemide. In the 2 patients with adenoma, aldosterone excretion was also normal, but PRA was very elevated.

From our data it is concluded that in Cushing's syndrome due to bilateral hyperplasia, PRA and aldosterone excretion are partially suppressed.

From our results on plasma deoxycorticosterone and corticosterone concentration it seems unlikely that these mineralocorticoids are the major cause of this phenomenon. However, it may not be excluded that other yet unidentified hormones could play some role in the pathogenesis of hypertension and renin suppression in Cushing's syndrome.

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