|
Sign In to gain access to subscriptions and/or personal tools.
|
Primary hyperaldosteronism due to adrenal microadenoma: a curable cause of refractory hypertension
Khin Swe Myint
Department of Clinical Pharmacology, Addenbrooke's Hospital, Cambridge, ksm31{at}medschl.cam.ac.uk
Michaela Watts
Department of Clinical Pharmacology, Addenbrooke's Hospital, Cambridge
Derris S Appleton
Radiology, Addenbrooke's Hospital, Cambridge
David J Lomas
Radiology, Addenbrooke's Hospital, Cambridge
Neville Jamieson
Surgery, Addenbrooke's Hospital, Cambridge
Kevin P Taylor
Biochemistry, Addenbrooke's Hospital, Cambridge
Stuart Coghill
Histopathology, Addenbrooke's Hospital, Cambridge
Morris J Brown
Department of Clinical Pharmacology, Addenbrooke's Hospital, Cambridge
The diagnosis of primary hyperaldosteronism due to microadenoma or unilateral adrenal hyperplasia can be challenging, since hypokalaemic alkalosis, high plasma aldosterone and a definite adenoma on imaging may all be absent.
Method and result. We describe three cases of resistant hypertension (on > 5 antihypertensives) where hyperaldosteronism was suspected because of a suppressed plasma renin level despite treatment with multiple drugs which normally elevate renin. Renin mass was measured by a double-site chemi-immunoluminometric assay. All patients had normal plasma aldosterone levels. Hypokalaemia was present in the first two cases but computed tomography did not show clear cut adenomas.Adrenal vein sampling (AVS) revealed lateralisation (> 4 times higher aldosterone to cortisol ratio (ACR) on the affected than contra-lateral side).The third patient was normokalaemic and AVS showed only minimal lateralisation (ACR 1.3:1).The severe hypertension in all cases was reversed by adrenalectomy, with blood pressure falling to target despite withdrawal of all but one to two drugs.
Conclusions. The robotic assay of renin mass permits rapid detection of patients in whom plasma renin is suppressed below the normal range. A suppressed plasma renin indicates abnormal Na+-retention, and — when not overcome by drugs such as angiotensin-converting enzyme-inhibitors or angiotensin receptor blockers — may be the only clue to a curable adrenal adenoma.AVS is required to demonstrate lateralisation of aldosterone secretion, justifying adrenalectomy.
Key Words: adrenal microadenoma adrenal vein sampling hyperaldosteronism renin angiotensin
References
- Fogari R., Preti P., Zoppi A., Rinaldi A., Fogari E., Mugellini A. Prevalence of primary aldosteronism among unselected hypertensive patients: a prospective study based on the use of an aldosterone/renin ratio above 25 as a screening test. Hypertens Res 2007;30:111-17.[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
- Gordon RD, Stowasser M., Tunny TJ, Klemm SA, Rutherford JC High incidence of primary aldosteronism in 199 patients referred with hypertension. Clin Exp Pharmacol Physiol 1994;21:315-18.[Web of Science][Medline]
[Order article via Infotrieve]
- Hood S., Cannon J., Foo R., Brown M. Prevalence of primary hyperaldosteronism assessed by aldosterone/renin ratio and spironolactone testing. Clin Med 2005;5(1):55-60.[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
- de Bruin RA, Bouhuizen A., Diederich S., Perschel FH, BoomsmaF, Deinum J. Validation of a new automated renin assay. Clin Chem 2004;50:2111-16.[Abstract/Free Full Text]
- Hartman D., Sagnella GA, Chesters CA, Macgregor GA Direct renin assay and plasma renin activity assay compared. Clin Chem 2004;50:2159-61.[Free Full Text]
- Derkx FH, de Bruin RJ, van Gool JM et al. Clinical validation of renin monoclonal antibody-based sandwich assays of renin and prorenin, and use of renin inhibitor to enhance prorenin immunoreactivity. Clin Chem 1996;42:1051-63.[Abstract/Free Full Text]
- Hartman D., Sagnella GA, Chesters CA, Macgregor GA Direct renin assay and plasma renin activity assay compared. Clin Chem 2004;50:2159-61.[Free Full Text]
- Mulatero P., Dluhy RG, Giacchetti G., Boscaro M., Veglio F., Stewart PM Diagnosis of primary aldosteronism: from screening to subtype differentiation. Trends Endocrinol Metab 2005;16:114-19.[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
- Stowasser M., Gordon RD, Gunasekera TG et al. High rate of detection of primary aldosteronism, including surgically treatable forms, after 'non-selective' screening of hypertensive patients. J Hypertens 2003;21:2149-57.[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
- Doppman JL, Gill JR Jr., Miller DL et al. Distinction between hyperaldosteronism due to bilateral hyperplasia and unilateral aldosteronoma: reliability of CT. Radiology 1992;184:677-82.[Abstract/Free Full Text]
- Radin DR, Manoogian C., Nadler JL Diagnosis of primary hyperaldosteronism: importance of correlating CT findings with endocrinologic studies. Am J Roentgenol 1992;158:553-7.[Abstract/Free Full Text]
- Ganguly A., Zager PG, Luetscher JA Primary aldosteronism due to unilateral adrenal hyperplasia. J Clin Endocrinol Metab 1980;51:1190-4.[Abstract/Free Full Text]
- Mansoor GA, Malchoff CD, Arici MH, Karimeddini MK, Whalen GF Unilateral adrenal hyperplasia causing primary aldosteronism: limitations of I-131 norcholesterol scanning. Am J Hypertens 2002;15:459-64.[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
Journal of Renin-Angiotensin-Aldosterone System, Vol. 9, No. 2,
103-106 (2008)
DOI: 10.3317/jraas.2008.015

CiteULike Complore Connotea Del.icio.us Digg Reddit Technorati Twitter What's this?
|
|