Primary hyperaldosteronism–evaluation of procedures for diagnosis and localization

• Published in: QJM : An International Journal of Medicine Vol. 86; no. 6; pp. 383 - 392
• Main Authors: HAMBLING, C., JUNG, R.T., BROWNING, M.C.K., GUNN, A., ANDERSON, J.M.
• Format: Journal Article
• Language: English
• Published: Oxford University Press 01.06.1993
• ISSN: 1460-2725; 1460-2393; 1460-2393
• DOI: 10.1093/oxfordjournals.qjmed.a068829

We have reviewed the clinical, investigative and pathological findings in 16 patients with primary hyperaldosteronism, 6 with idiopathic adrenal hyperplasia and 10 with an aldosterone-producing adenoma. The ratio of serum aldosterone to plasma renin activity was >1 1400 pmol/μg/l/h in all patients when measured supine on a normal salt diet, negating the need for salt loading to confirm primary hyperaldosteronism. Postural changes in serum aldosterone confirmed the presence of an aldosterone-producing adenoma in all but one patient when results on normal and high salt intakes were reviewed together. Nevertheless, the need for salt loading for discrimination is questioned, as the combination of postural changes in serum aldosterone on normal salt intake combined with CT confirmed and localized all aldosterone-producing adenomas. Urinary aldosterone measurements were of little value. Localizing procedures consisting of CT and isotopic scanning using 75Se-selenomethyl-cholesterol proved most useful; adrenal venous sampling yielded less useful information. The latter may be due to the high predominance of patients (8) showing a background of micronodular hyperplasia with a dominant aldosterone-producing tumour. Only three of these patients have remained normotensive and normokalaemic on no medication. The presence of micronodular background suggests the need for life-long monitoring of such patients.