Primary Hyperaldosteronism Clinical Presentation

  • Author: Gabriel I Uwaifo, MBBS; Chief Editor: George T Griffing, MD   more...
 
Updated: Jan 3, 2012
 

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 hypertensive[5]
    • 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.
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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.

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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.
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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,  Vice President, Medical Affairs, Incyte Corporation

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: Incyte Corporation Salary Employment; Sanofi-Aventis Ownership interest Stock option/ restricted stock holder; Incyte Corporation Ownership interest Stock option/ restricted stock holder

Specialty Editor Board

Frederick H Ziel, MD  Associate Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; 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.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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 Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Informatics Association, American Society for Bone and Mineral Research, Endocrine Society, and International Society for Clinical Densitometry

Disclosure: Nothing to disclose.

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.

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Effects of main antihypertensives on the renin-angiotensin system.
Potential causes of primary hyperaldosteronism.
Transitional zone adrenocortical steroids.
Algorithm for screening for potential primary hyperaldosteronism.
Algorithm for confirmation of primary hyperaldosteronism.
Algorithm for distinguishing subtypes of primary hyperaldosteronism.
 
 
 
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