Primary Aldosteronism: Diagnosis and Differentiation of Subtypes
Authors: MYRON H. WEINBERGER
Journal: Annals of Internal Medicine (1984)

Editorials1 February 1984Primary Aldosteronism: Diagnosis and Differentiation of SubtypesMYRON H. WEINBERGER, M.D.MYRON H. WEINBERGER, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-100-2-300 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptNearly 30 Years have passed since the initial description of primary aldosteronism, a syndrome caused by the excessive production of mineralocorticoid hormones from an adrenal tumor (1, 2). Hypertension, hypokalemic alkalosis, normal glucocorticoid function, and excessive production of aldosterone were the original features of the syndrome. Elucidation of the marked suppression of renin activity, resulting from the mineralocorticoid-induced increase in extracellular fluid, provided a useful marker for detecting this potentially curable form of hypertension (3). However, subsequent studies of plasma renin activity in hypertension have found that a large population of patients have renin suppression, most of whom do not...References1. CONN J. Primary aldosteronism, a new clinical syndrome. J Lab Clin Med. 1955;45:3-17. MedlineGoogle Scholar2. MADERISERI IL. Spontaneous hypopotassemia, hypomagnesemia, alkalosis and tetany due to hypersecretion of corticosterone-like mineralocorticoid. Am J Med. 1955;19:976-88. CrossrefMedlineGoogle Scholar3. CONNCOHENROVNER JED. Suppression of plasma renin activity in primary aldosteronism. JAMA. 1964;190:213-21. CrossrefMedlineGoogle Scholar4. HELMERJUDSON OW. Metabolic studies on hypertensive patients with suppressed plasma renin activity not due to hyperaldosteronism. Circulation. 1968;38:965-76. CrossrefMedlineGoogle Scholar5. WEINBERGERGRIMHOLLIFIELD MCJ. Primary aldosteronism: diagnosis, localization, and treatment. Ann Intern Med. 1979;90:386-95. LinkGoogle Scholar6. SLATONSCHAMBELANBIGLIERI PME. Stimulation and suppression of aldosterone secretion in patients with an aldosterone-producing adenoma. J Clin Endocrinol Metab. 1969;29:239-50. CrossrefMedlineGoogle Scholar7. HORTON R. Stimulation and suppression of aldosterone in plasma of normal men and in primary aldosteronism. J Clin Invest. 1969;48:1230-6. CrossrefMedlineGoogle Scholar8. KEMWEINBERGERMAYESNUGENT DMDC. Saline suppression of plasma aldosterone in hypertension. Arch Intern Med. 1971;128:380-6. CrossrefMedlineGoogle Scholar9. LYONSKEMBROWNHANSONCAROLLO DDRCM. Single dose captopril as a diagnostic test for primary aldosteronism. J Clin Endocrinol Metab. 1983;57:892-6. CrossrefMedlineGoogle Scholar10. GRIMWEINBERGERHIGGINSKRAMER CMJN. Diagnosis of secondary forms of hypertension: a comprehensive protocol. JAMA. 1977;237:1331-5. CrossrefMedlineGoogle Scholar11. KEMWEINBERGERGOMEZ-SANCHEZ DMC. Circadian rhythm of plasma aldosterone concentration in patients with primary aldosteronism. J Clin Invest. 1973;52:2272-7. CrossrefMedlineGoogle Scholar12. GANGULYMELADALUETSCHERDOWDY AGJA. Control of plasma aldosterone in primary aldosteronism: distinction between adenoma and hyperplasia. J Clin Endocrinol Metab. 1973;37:765-75. CrossrefMedlineGoogle Scholar13. ROSS E. Conn's syndrome due to adrenal hyperplasia with hypertrophy of zona glomerulosa, relieved by unilateral adrenalectomy. Am J Med. 1965;39:994-1002. CrossrefMedlineGoogle Scholar14. GANGULYGRIMBERGSTEINBROWNWEINBERGER ACJRM. Genetic and pathophysiologic studies of a new kindred with glucocorticoid-suppressible hyperaldosteronism manifest in three generations. J Clin Endocrinol Metab. 1981;53:1040-6. CrossrefMedlineGoogle Scholar15. GANGULYPRATTWEINBERGERGRIMFINEBERG AJMCN. Differing effects of metoclopramide and adrenocorticotropin on plasma aldosterone levels in glucocorticoid-suppressible hyperaldosteronism and other forms of hyperaldosteronism. J Clin Endocrinol Metab. 1983;57:388-92. CrossrefMedlineGoogle Scholar16. MULROW P. Glucocorticoid-suppressible hyperaldosteronism: a clue to the missing hormone [Editorial]? N Engl J Med. 1981;305:1012-4. Google Scholar17. BIGLIERISCHAMBELAN EM. The significance of elevated levels of plasma 18-hydroxycorticosterone in patients with primary aldosteronism. J Clin Endocrinol Metab. 1979;49:87-91. CrossrefMedlineGoogle Scholar18. KEMBROWNPAINTON DRR. Differentiation of mineralocorticoid-induced hypertension. In: KAUFMANN W, ed. Mineralocorticoids & Hypertension. Berlin: Springer-Verlag; 1983:155-66. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Indiana University School of Medicine Indianapolis, Indiana PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByClinical Syndromes of Metabolic AlkalosisScreening for primary aldosteronism without discontinuing hypertensive medications: Plasma aldosterone-renin ratioPrimary AldosteronismLaboratory diagnosis in hypertensionEvaluation of Elevated Blood PressureSelective Venous Sampling for Adrenal Hormone ExcessCost effectiveness in the detection of renal artery stenosisIs single oral administration of captopril beneficial in screening for primary aldosteronism?Use of the saline infusion test to diagnose the cause of primary aldosteronism7 Disorders of mineralocorticoid activityThe Pituitary and Idiopathic Hyperaldosteronism 1 February 1984Volume 100, Issue 2Page: 300-302KeywordsAdrenal tumorsAldosteroneHormonesHypertensionMineralocorticoidsPlasma renin activity Issue Published: 1 February 1984 PDF DownloadLoading ...