eMedicine Specialties > Endocrinology > Adrenal Gland

Hyperaldosteronism, Primary

Author: Gabriel I Uwaifo, MBBS, Clinical and Research Attending, Assistant Professor of Medicine and Endocrinology, MedStar Clinical Research Center, MedStar Research Institute and Washington Hospital Center
Coauthor(s): Nicholas J Sarlis, MBBS, MD, PhD, FACP, Medical Director, Department of Medical Affairs, Oncology Business Unit, US Pharmaceutical Operations, Sanofi-Aventis US
Contributor Information and Disclosures

Updated: Sep 25, 2009

Introduction

Background

Although initially considered a rarity, primary hyperaldosteronism (PH) now is considered one of the more common causes of secondary hypertension (HTN). Litynski reported the first cases, but Conn was the first to well characterize the disorder in 1956. Conn syndrome, as originally described, refers specifically to PH secondary to an adrenal aldosteronoma.

While older data suggested that PH is rare, with an estimated prevalence of less than 1% of all patients with HTN, subsequent data indicated that it may actually occur in as many as 5-15% of patients with HTN. It may occur in an even greater percentage of patients with treatment-resistant HTN. Although still a considerable diagnostic challenge, recognizing this condition is critical because PH-associated HTN can often be cured with the proper surgical intervention. The diagnosis is generally 3-tiered, involving an initial screening, a confirmation of the diagnosis, and a determination of the specific subtype of PH.

Although prior studies suggested that aldosteronomas are the most common causes of PH (70-80% of cases), later epidemiologic work indicated that the prevalence of PH due to bilateral idiopathic adrenal hyperplasia (IAH) is higher than was previously believed. These reports suggested that IAH may be responsible for as many as 75% of PH cases. Moreover, reports have described a rare syndrome of PH characterized by histologic features intermediate between adrenal adenoma and adrenal hyperplasia. Clinically, the distinction between the 2 major causes of PH is vital because the treatment of choice for each is different. While the treatment of choice for aldosteronomas is surgical extirpation, the treatment of choice for IAH is medical therapy with aldosterone antagonists.

The complete list of entities known to cause PH includes aldosterone-producing adenomas (APAs), aldosterone-producing renin-responsive adenomas (AP-RAs), bilateral adrenal (glomerulosa) hyperplasia or IAH, primary adrenal hyperplasia (PAH), and familial forms of PH. (The ovaries and kidneys are the 2 organs described in the literature that, in the setting of neoplastic disease, can be ectopic sources of aldosterone, but this is a rare occurrence.)

Two distinct genetic-familial varieties of PH exist. Sutherland and colleagues first described the type 1 variety of familial PH, glucocorticoid-remediable aldosteronism (GRA), in 1966. In GRA, HTN responds clinically to small doses of glucocorticoids in addition to other antihypertensive agents (see image below).1 The type 1 form of familial PH is due to a chimeric gene product that combines the promoter of the 11beta-hydroxylase gene with the coding region of the aldosterone synthetase gene. The type 2 variant of familial PH (which is not glucocorticoid sensitive) was first described in 1991. Although the exact genetic abnormality for type 2 PH has not been identified, data suggest that this type may be associated or closely linked with the MEN1 gene locus on band 11q13.2

Effects of main antihypertensives on the renin-an...

Effects of main antihypertensives on the renin-angiotensin system.

[ CLOSE WINDOW ]
Effects of main antihypertensives on the renin-an...

Effects of main antihypertensives on the renin-angiotensin system.


Pathophysiology

The cardinal pathophysiologic anomaly causing primary hyperaldosteronism (PH) syndrome is autonomous aldosterone production. In addition to nonsuppressible aldosterone production, suppressed and poorly stimulative levels of plasma renin are in the presence of only mildly expanded intravascular and extravascular fluid volume. Normal regulation of aldosterone secretion is mediated to varying degrees by renin, serum potassium and sodium levels, intravascular volume status, and adrenocorticotropic hormone (ACTH). Regulation of aldosterone production by these factors may be altered in a variable fashion, depending on the subtype of PH. Generally, APAs and PAH (see image below) remain ACTH responsive, while IAH and AP-RAs maintain responsiveness to the renin-angiotensin system (RAS).

Potential causes of primary hyperaldosteronism.

Potential causes of primary hyperaldosteronism.

[ CLOSE WINDOW ]
Potential causes of primary hyperaldosteronism.

Potential causes of primary hyperaldosteronism.


In GRA, the RAS is suppressed, and aldosterone is regulated by ACTH because of the chimeric genetic combination of an ACTH-sensitive promoter with the coding regions of the aldosterone synthetase gene (which normally does not have such a promoter). Thus, ambient ACTH levels pathologically overstimulate aldosterone synthesis inappropriately.3 In patients with GRA, the administration of dexamethasone (or any other glucocorticoid) at doses sufficient to suppress ACTH production results in a reduction in aldosterone synthesis and natriuresis and in the correction of the biochemical anomalies of PH.4 Histologic studies in this disease have shown specific hyperplasia of the zona fasciculata, with concomitant atrophy of the zona glomerulosa.

Frequency

United States

The exact prevalence of primary hyperaldosteronism (PH) is unclear. PH appears to contribute more significantly than was previously thought to the prevalence of essential hypertension (HTN). Estimates suggest that 5-15% of essential HTN cases may be due to PH. The prevalence of PH is probably higher in patients who have a low serum potassium level, in patients who are elderly, and in patients who have HTN that is resistant to single medication use.

International

No evidence demonstrates that primary hyperaldosteronism, in its more common forms, occurs in relative excess in any part of the world.

Race

Primary hyperaldosteronism occurs worldwide. Several reports suggest a higher prevalence in African Americans, persons of African origin, and, potentially, other blacks. This appears particularly true of the IAH variant of the disease.

Sex

APAs are more common in women than in men, with a female-to-male ratio of 2:1. IAH is more common in men than in women, with a male-to-female ratio of 4:1.

Age

The typical patient with APA is a woman aged 30-50 years. Accumulating data for IAH suggest different demographics. IAH is more prevalent in men than in women and peaks in the sixth decade of life.

Clinical

History

The clinical presentation of primary hyperaldosteronism (PH) is not distinctive, and the correct diagnosis requires a high index of suspicion on the part of the physician.

  • The common clinical scenarios in which the possibility of PH should be considered include the following:
    • Patients with spontaneous or unprovoked hypokalemia, especially if the patient is also hypertensive5
    • Patients who develop severe and/or persistent hypokalemia in the setting of low to moderate doses of potassium-wasting diuretics
    • Patients with refractory hypertension (HTN)
  • The 2 major familial varieties of PH are GRA (type 1 familial PH) and a non – glucocorticoid-remediable type (type 2 familial hyperaldosteronism).
    • The recognition of GRA is particularly important because of its implications for patients who are hypertensive and whose family members are apparently unaffected.
    • HTN, strokes, and other significant cardiovascular events are described in young persons with this syndrome.
    • Although the syndrome is uncommon, heightened levels of suspicion are essential for the diagnosis. Fewer than 150 well-validated cases exist in the literature. All patients with GRA should be treated medically with glucocorticoids and without surgery.
    • Although uncommon, GRA may be more prevalent than was previously presumed. A significant subgroup of patients with the milder normokalemic variety of this syndrome is probably incorrectly presumed to have essential HTN.6
    • A family history of HTN (particularly with a young age of onset), HTN in children, low-renin HTN, and presumed IAH are the typical situations in which this diagnosis should be considered.

Physical

Patients with primary hyperaldosteronism do not present with distinctive clinical findings, and a high index of suspicion based on the patient's history is vital in making the diagnosis.

  • The findings could include the following:
    • Hypertension (HTN) - This condition almost invariably occurs, although a few rare cases of primary aldosteronism unassociated with hypertension have been described in the literature.
    • Weakness
    • Abdominal distension
    • Ileus from hypokalemia
    • Findings related to complications of HTN - These include cardiac failure, hemiparesis due to stroke, carotid bruits, abdominal bruits, proteinuria, renal insufficiency, hypertensive encephalopathy, and hypertensive retinal changes.

It is important to note that primary aldosteronism in and of itself is typically not associated with edema, despite the volume-expanded state associated with it. This is due to spontaneous natriuresis and diuresis (called the aldosterone escape) that occurs in patients with primary aldosteronism and that appears to be mediated by atrial natriuretic peptide (ANP).7,8 Thus, the finding of significant edema in patients who are presumed to have primary aldosteronism suggests either that a wrong diagnosis has been made or that associated complications, such as renal or cardiac failure, are present.

Causes

The exact cause of sporadic primary hyperaldosteronism (PH) due to an adenoma or hyperplasia is unclear. The existence of trophic factors has been postulated in hyperplasia. Somatic mutations of genes leading to growth advantage in the adrenal adenomatous tissue are a possible, but unproven, cause.

  • In familial forms of PH, the molecular basis of GRA is known. GRA is due to a mutation that results from a hybrid gene product.2 The 11beta-hydroxylase and aldosterone synthetase genes that are normally located closely to each other on chromosome 8 cross over to create a novel hybrid gene product. This hybrid gene consists of the regulatory ACTH-responsive sequence of the 11beta-hydroxylase gene, fused to the structural component of the aldosterone synthetase gene.1
  • Most sporadic aldosteronomas arise from the zona fasciculata, and they often have surrounding glandular hyperplasia close to the adenoma. This suggests that a proliferative response of cells to some presently unidentified paracrine/autocrine factor occurs. Within this zone of hyperplasia, a clonal change in a single cell is believed to take place, thus providing the nidus for the developing adenoma.
  • The genetic basis of type 2 familial hyperaldosteronism is unclear; however, several reports of patients with this condition have shown a loss of heterozygosity close to the MEN1 gene locus (band 11q13).2 Whether menin mutations exist in the adrenal tissue of these patients is currently unknown. This syndrome can histologically manifest as hyperplasia or adenomas.
  • The existence of tertiary hyperaldosteronism as a separate entity remains controversial. The entity is presumed to result from chronic elevations in plasma renin levels and secondary hyperaldosteronism, which eventually establishes a state of autonomous, unregulated hyperaldosteronism with a histologic picture of mixed hyperplasia and adenomas in the affected adrenocortical tissue.
    • Few well-described cases exist, but in most, the adrenal glands are hyperplastic, often with nodular hyperplasia (which can cause diagnostic confusion). Virtually all of the cases described are in the setting of renal artery stenosis.
    • Initially, renin levels are elevated, which is typical of secondary hyperaldosteronism. When the tertiary (autonomous) phase develops, the biochemical profile changes to a low-renin/high-aldosterone state. The paradigm is analogous to the pathogenesis of tertiary hyperparathyroidism.

More on Hyperaldosteronism, Primary

Overview: Hyperaldosteronism, Primary
Differential Diagnoses & Workup: Hyperaldosteronism, Primary
Treatment & Medication: Hyperaldosteronism, Primary
Follow-up: Hyperaldosteronism, Primary
Multimedia: Hyperaldosteronism, Primary
References
Further Reading
[ CLOSE WINDOW ]

References

  1. Dluhy RG, Lifton RP. Glucocorticoid-remediable aldosteronism. Endocrinol Metab Clin North Am. Jun 1994;23(2):285-97. [Medline].

  2. Gordon RD, Klemm SA, Tunny TJ, et al. Genetics of primary aldosteronism. Clin Exp Pharmacol Physiol. Nov 1994;21(11):915-8. [Medline].

  3. Stowasser M, Klemm SA, Tunny TJ, et al. Plasma aldosterone response to ACTH in subtypes of primary aldosteronism. Clin Exp Pharmacol Physiol. Jun-Jul 1995;22(6-7):460-2. [Medline].

  4. Litchfield WR, New MI, Coolidge C, et al. Evaluation of the dexamethasone suppression test for the diagnosis of glucocorticoid-remediable aldosteronism. J Clin Endocrinol Metab. Nov 1997;82(11):3570-3. [Medline]. [Full Text].

  5. Cruz DN, Perazella MA. Hypertension and hypokalemia: unusual syndromes. Conn Med. Feb 1997;61(2):67-75. [Medline].

  6. Born-Frontsberg E, Reincke M, Rump LC, et al. Cardiovascular and cerebrovascular comorbidities of hypokalemic and normokalemic primary aldosteronism: results of the German Conn's Registry. J Clin Endocrinol Metab. Apr 2009;94(4):1125-30. [Medline].

  7. Hall JE, Granger JP, Smith MJ Jr. Role of renal hemodynamics and arterial pressure in aldosterone "escape". Hypertension. 1984;6:1183.

  8. Yokota N, Bruneau BG, Kuroski de Bold ML, et al. Atrial natriuretic factor significantly contributes to the mineralocorticoid escape phenomenon. Evidence for a guanylate cyclase-mediated pathway. J Clin Invest. Nov 1994;94(5):1938-46. [Medline]. [Full Text].

  9. Young DB. Quantitative analysis of aldosterone's role in potassium regulation. Am J Physiol. Nov 1988;255(5 Pt 2):F811-22. [Medline].

  10. Quamme GA. Control of magnesium transport in the thick ascending limb. Am J Physiol. Feb 1989;256(2 Pt 2):F197-210. [Medline].

  11. Tzanela M, Effremidis G, Vassiliadi D, et al. The aldosterone to renin ratio in the evaluation of patients with incidentally detected adrenal masses. Endocrine. Oct 2007;32(2):136-42. [Medline].

  12. Diederich S, Mai K, Bahr V, et al. The simultaneous measurement of plasma-aldosterone- and -renin-concentration allows rapid classification of all disorders of the renin-aldosterone system. Exp Clin Endocrinol Diabetes. Jul 2007;115(7):433-8. [Medline].

  13. Wu VC, Chang HW, Liu KL, et al. Primary aldosteronism: diagnostic accuracy of the losartan and captopril tests. Am J Hypertens. Aug 2009;22(8):821-7. [Medline].

  14. Stowasser M, Bachmann AW, Tunny TJ. Production of 18-oxo-cortisol in subtypes of primary aldosteronism. Clin Exp Pharmacol Physiol. Jun-Jul 1996;23(6-7):591-3. [Medline].

  15. Hamlet SM, Gordon RD, Gomez-Sanchez CE, et al. Adrenal transitional zone steroids, 18-oxo and 18-hydroxycortisol, useful in the diagnosis of primary aldosteronism, are ACTH-dependent. Clin Exp Pharmacol Physiol. Apr 1988;15(4):317-22. [Medline].

  16. McAlister FA, Lewanczuk RZ. Primary hyperaldosteronism and adrenal incidentaloma: an argument for physiologic testing before adrenalectomy. Can J Surg. Aug 1998;41(4):299-305. [Medline].

  17. Georgiades CS, Hong K, Geschwind JF, et al. Adjunctive use of C-arm CT may eliminate technical failure in adrenal vein sampling. J Vasc Interv Radiol. Sep 2007;18(9):1102-5. [Medline].

  18. Young WF, Stanson AW, Grant CS, et al. Primary aldosteronism: adrenal venous sampling. Surgery. Dec 1996;120(6):913-9; discussion 919-20. [Medline].

  19. Young WF, Stanson AW, Thompson GB, et al. Role for adrenal venous sampling in primary aldosteronism. Surgery. Dec 2004;136(6):1227-35. [Medline].

  20. Naruse M, Naruse K, Yoshimoto T, et al. Dopaminergic regulation of aldosterone secretion: its pathophysiologic significance in subsets of primary aldosteronism. Hypertens Res. Jun 1995;18 Suppl 1:S59-64. [Medline].

  21. Hood SJ, Taylor KP, Ashby MJ, et al. The spironolactone, amiloride, losartan, and thiazide (SALT) double-blind crossover trial in patients with low-renin hypertension and elevated aldosterone-renin ratio. Circulation. Jul 17 2007;116(3):268-75. [Medline]. [Full Text].

  22. Celen O, O'Brien MJ, Melby JC, et al. Factors influencing outcome of surgery for primary aldosteronism. Arch Surg. Jun 1996;131(6):646-50. [Medline].

  23. Sukor N, Gordon RD, Ku YK, et al. Role of unilateral adrenalectomy in bilateral primary aldosteronism: a 22-year single center experience. J Clin Endocrinol Metab. Jul 2009;94(7):2437-45. [Medline].

  24. Letavernier E, Peyrard S, Amar L, et al. Blood pressure outcome of adrenalectomy in patients with primary hyperaldosteronism with or without unilateral adenoma. J Hypertens. Sep 2008;26(9):1816-23. [Medline].

  25. Milsom SR, Espiner EA, Nicholls MG, et al. The blood pressure response to unilateral adrenalectomy in primary aldosteronism. Q J Med. Dec 1986;61(236):1141-51. [Medline].

  26. Giacchetti G, Turchi F, Boscaro M, Ronconi V. Management of primary aldosteronism: its complications and their outcomes after treatment. Curr Vasc Pharmacol. Apr 2009;7(2):244-49. [Medline].

  27. Minowada S, Fujimura T, Takahashi N, et al. Computed tomography-guided percutaneous acetic acid injection therapy for functioning adrenocortical adenoma. J Clin Endocrinol Metab. Dec 2003;88(12):5814-7. [Medline]. [Full Text].

  28. Abdelhamid S, Muller-Lobeck H, Pahl S, et al. Prevalence of adrenal and extra-adrenal Conn syndrome in hypertensive patients. Arch Intern Med. Jun 10 1996;156(11):1190-5. [Medline].

  29. August JT, Nelson DH, Thorn GW. Response of normal subjects to large amounts of aldosterone. J Clin Invest. Nov 1958;37(11):1549-55. [Medline].

  30. Biglieri EG. Primary aldosteronism. Curr Ther Endocrinol Metab. 1997;6:170-2. [Medline].

  31. Blumenfeld JD, Sealey JE, Schlussel Y, et al. Diagnosis and treatment of primary hyperaldosteronism. Ann Intern Med. Dec 1 1994;121(11):877-85. [Medline].

  32. Bravo EL. Primary aldosteronism. Issues in diagnosis and management. Endocrinol Metab Clin North Am. Jun 1994;23(2):271-83. [Medline].

  33. Bravo EL, Tarazi RC, Dustan HP, et al. The changing clinical spectrum of primary aldosteronism. Am J Med. Apr 1983;74(4):641-51. [Medline].

  34. Brown MA, Cramp HA, Zammit VC, et al. Primary hyperaldosteronism: a missed diagnosis in 'essential hypertensives'?. Aust N Z J Med. Aug 1996;26(4):533-8. [Medline].

  35. Chan NN, Isaacs AJ. Primary aldosteronism in general practice. Lancet. Mar 20 1999;353(9157):1013; author reply 1014. [Medline].

  36. Dluhy RG, Williams GH. Endocrine hypertension. In: Wilson JD, Foster DW, Kronenberg HM, eds. Williams Textbook of Endocrinology. 9th ed. Philadelphia, Pa: WB Saunders; 1998:729-49.

  37. Don BR, Schambelan M. Pathophysiology of adrenal cortical hypertension. In: Izzo JL, Black HR, eds. Hypertension Primer: the Essentials of High Blood Pressure. 2nd ed. Baltimore, Md: Lippincott Williams & Wilkins; 1999:138-40.

  38. Doppman JL, Gill JR Jr. Hyperaldosteronism: sampling the adrenal veins. Radiology. Feb 1996;198(2):309-12. [Medline].

  39. Fraser R, Murray GD, Connell JM. Conn's syndrome: no longer a needle in a haystack?. Clin Endocrinol (Oxf). Dec 1998;49(6):709-10. [Medline].

  40. Gonzalez-Campoy JM, Romero JC, Knox FG. Escape from the sodium-retaining effects of mineralocorticoids: role of ANF and intrarenal hormone systems. Kidney Int. Mar 1989;35(3):767-77. [Medline].

  41. Gordon RD. Primary aldosteronism. J Endocrinol Invest. Jul-Aug 1995;18(7):495-511. [Medline].

  42. Gordon RD, Stowasser M, Tunny TJ, et al. High incidence of primary aldosteronism in 199 patients referred with hypertension. Clin Exp Pharmacol Physiol. Apr 1994;21(4):315-8. [Medline].

  43. Gregoire JR. Adjustment of the osmostat in primary aldosteronism. Mayo Clin Proc. Nov 1994;69(11):1108-10. [Medline].

  44. Irony I, Kater CE, Biglieri EG, et al. Correctable subsets of primary aldosteronism. Primary adrenal hyperplasia and renin responsive adenoma. Am J Hypertens. Jul 1990;3(7):576-82. [Medline].

  45. Jeck T, Weisser B, Mengden T, et al. Primary aldosteronism: difference in clinical presentation and long-term follow-up between adenoma and bilateral hyperplasia of the adrenal glands. Clin Investig. Dec 1994;72(12):979-84. [Medline].

  46. Kaplan NM. Primary aldosteronism. In: Clinical Hypertension. 7th ed. Baltimore, Md:. Williams and Wilkins;1998:365-382.

  47. Litchfield WR, Dluhy RG. Primary aldosteronism. Endocrinol Metab Clin North Am. Sep 1995;24(3):593-612. [Medline].

  48. Matsuda A, Beniko M, Ikota A, et al. Primary aldosteronism with bilateral multiple aldosterone-producing adrenal adenomas. Intern Med. Dec 1996;35(12):970-5. [Medline].

  49. Munver R, Del Pizzo JJ, Sosa RE. Adrenal-preserving minimally invasive surgery: the role of laparoscopic partial adrenalectomy, cryosurgery, and radiofrequency ablation of the adrenal gland. Curr Urol Rep. Feb 2003;4(1):87-92. [Medline].

  50. Naruse M, Demura H, Naruse K, et al. Variant forms of primary aldosteronism: reconsideration of the differential diagnosis and treatment. Intern Med. Dec 1996;35(12):919-21. [Medline].

  51. Orth DN, Kovacs WJ. The adrenal cortex. In: Wilson JD, Foster DW, Kronenberg L, eds. Williams Textbook of Endocrinology. 9th ed. Philadelphia, Pa: WB Saunders; 1998:517-664.

  52. Otsuka F, Otsuka-Misunaga F, Koyama S, et al. Hormonal characteristics of primary aldosteronism due to unilateral adrenal hyperplasia. J Endocrinol Invest. Sep 1998;21(8):531-6. [Medline].

  53. Puccini M, Iacconi P, Bernini G, et al. Conn syndrome: 14 year's experience from two European centres. Eur J Surg. Nov 1998;164(11):811-7. [Medline].

  54. Rossi GP, Rossi E, Pavan E, et al. Screening for primary aldosteronism with a logistic multivariate discriminant analysis. Clin Endocrinol (Oxf). Dec 1998;49(6):713-23. [Medline].

  55. Rossi GP, Sacchetto A, Visentin P, et al. Changes in left ventricular anatomy and function in hypertension and primary aldosteronism. Hypertension. May 1996;27(5):1039-45. [Medline].

  56. Sawka AM, Young WF, Thompson GB, et al. Primary aldosteronism: factors associated with normalization of blood pressure after surgery. Ann Intern Med. Aug 21 2001;135(4):258-61. [Medline].

  57. Shigematsu Y, Hamada M, Okayama H, et al. Left ventricular hypertrophy precedes other target-organ damage in primary aldosteronism. Hypertension. Mar 1997;29(3):723-7. [Medline].

  58. Spence JD. Physiologic tailoring of therapy for resistant hypertension: 20 years' experience with stimulated renin profiling. Am J Hypertens. Nov 1999;12(11 Pt 1):1077-83. [Medline].

  59. Stewart PM. Mineralocorticoid hypertension. Lancet. Apr 17 1999;353(9161):1341-7. [Medline].

  60. Stowasser M, Bachmann AW, Jonsson JR, et al. Clinical, biochemical and genetic approaches to the detection of familial hyperaldosteronism type I. J Hypertens. Dec 1995;13(12 Pt 2):1610-3. [Medline].

  61. Ulick S, Blumenfeld JD, Atlas SA, et al. The unique steroidogenesis of the aldosteronoma in the differential diagnosis of primary aldosteronism. J Clin Endocrinol Metab. Apr 1993;76(4):873-8. [Medline].

  62. Uwaifo GI, Abiose AK, Anwar YA, et al. Primary hyperaldosteronism is an important cause of resistant hypertension. Oral presentation; Spring Scientific Conference of the CT Chapter ACP-ASIM. 1999.

  63. Vallotton MB. Primary aldosteronism. Part I. Diagnosis of primary hyperaldosteronism. Clin Endocrinol (Oxf). Jul 1996;45(1):47-52. [Medline].

  64. Vallotton MB. Primary aldosteronism. Part II. Differential diagnosis of primary hyperaldosteronism and pseudoaldosteronism. Clin Endocrinol (Oxf). Jul 1996;45(1):53-60. [Medline].

  65. Vantyghem MC, Ronci N, Provost F, et al. Aldosterone-producing adenoma without hypertension: a report of two cases. Eur J Endocrinol. Sep 1999;141(3):279-85. [Medline].

  66. Weinberger MH, Fineberg NS. The diagnosis of primary aldosteronism and separation of two major subtypes. Arch Intern Med. Sep 27 1993;153(18):2125-9. [Medline].

  67. Yoshihara F, Nishikimi T, Yoshitomi Y, et al. Left ventricular structural and functional characteristics in patients with renovascular hypertension, primary aldosteronism and essential hypertension. Am J Hypertens. Jun 1996;9(6):523-8. [Medline].

  68. Young WF. Pheochromocytoma and primary aldosteronism: diagnostic approaches. Endocrinol Metab Clin North Am. Dec 1997;26(4):801-27. [Medline].

[ CLOSE WINDOW ]

Keywords

primary hyperaldosteronism, aldosteronism, hyperaldosteronism, hypertension, adrenal, adrenal hyperplasia, adrenal glands, adrenal adenoma, aldosterone, adrenal tumor, adrenal tumors, secondary hypertension, Conn's syndrome, hyperaldosteronism primary, autonomous hyperaldosteronism, primary adrenal hyperplasia, idiopathic adrenal hyperplasia, Conn syndrome, adrenal aldosteronoma, aldosteronoma, bilateral adrenal hyperplasia, renin responsive adenoma, RRA, aldosterone-producing renin-responsive adenomas, aldosterone-producing adenomas

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Gabriel I Uwaifo, MBBS, Clinical and Research Attending, Assistant Professor of Medicine and Endocrinology, MedStar Clinical Research Center, MedStar Research Institute and Washington Hospital Center
Gabriel I Uwaifo, MBBS is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Medical Association, American Society of Hypertension, and Endocrine Society
Disclosure: Nothing to disclose.

Coauthor(s)

Nicholas J Sarlis, MBBS, MD, PhD, FACP, Medical Director, Department of Medical Affairs, Oncology Business Unit, US Pharmaceutical Operations, Sanofi-Aventis US
Nicholas J Sarlis, MBBS, MD, PhD, FACP is a member of the following medical societies: American Association for Cancer Research, American Association for the Advancement of Science, American Association of Clinical Endocrinologists, American College of Endocrinology, American College of Physicians, American Federation for Medical Research, American Head and Neck Society, American Medical Association, American Society for Therapeutic Radiology and Oncology, American Society of Clinical Oncology, American Thyroid Association, Association for Psychological Science, Endocrine Society, European Society for Medical Oncology, New York Academy of Sciences, and Royal Society of Medicine
Disclosure: Sanofi-Aventis Salary Employment

Medical Editor

Frederick H Ziel, MD, Associate Professor of Medicine, David Geffen School of Medicine at UCLA; Physician-In-Charge, Endocrinology/Diabetes Center, Director of Medical Education, Kaiser Permanente Woodland Hills; Chair of Endocrinology, Co-Chair of Diabetes Complete Care Program, Southern California Permanente Medical Group
Frederick H Ziel, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Federation for Medical Research, American Medical Association, American Society for Bone and Mineral Research, California Medical Association, Endocrine Society, and International Society for Clinical Densitometry
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS, Professor of Medicine (Endocrinology, Adj), Johns Hopkins School of Medicine; Affiliate Research Professor, Bioinformatics and Computational Biology Program, School of Computational Sciences, George Mason University; Principal, C/A Informatics, LLC
Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, American College of Nutrition, American College of Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Informatics Association, American Society for Bone and Mineral Research, American Society of Law Medicine and Ethics, Endocrine Society, and International Society for Clinical Densitometry
Disclosure: Nothing to disclose.

CME Editor

Mark Cooper, MBBS, PhD, FRACP, Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University
Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD, Professor of Medicine, St Louis University School of Medicine
George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.