Although initially considered a rarity, primary aldosteronism 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 primary aldosteronism due to the presence of an adrenal aldosteronoma (aldosterone-secreting benign adrenal neoplasm). (See Etiology.)
Based on older data, it was originally estimated that primary aldosteronism accounted for less than 1% of all patients with HTN. Subsequent data, however, indicated that it may actually occur in as many as 5-15% of patients with HTN. Primary aldosteronism may occur in an even greater percentage of patients with treatment-resistant HTN and may be considerably underdiagnosed; this is especially true if patients with treatment-refractory HTN are not specifically referred for evaluation to an endocrinologist. (See Epidemiology.)
Although primary aldosteronism is still a considerable diagnostic challenge, recognizing the condition is critical because primary aldosteronism–associated HTN can often be cured (or at least optimally controlled) with the proper surgical or medical intervention. The diagnosis is generally 3-tiered, involving an initial screening, a confirmation of the diagnosis, and a determination of the specific subtype of primary aldosteronism. (See Presentation, Workup, Treatment, and Medication.)
Although prior studies suggested that aldosteronomas were the most common cause of primary aldosteronism (70-80% of cases), later epidemiologic work indicated that the prevalence of aldosteronism due to bilateral idiopathic adrenal hyperplasia (IAH; sometimes also abbreviated as BAH) is higher than had previously been believed. These reports suggested that IAH may be responsible for as many as 75% of primary aldosteronism cases. Moreover, reports have described a rare syndrome of primary aldosteronism characterized by histologic features intermediate between adrenal adenoma and adrenal hyperplasia, which often is unilaterally localized (also referred to earlier literature as “intermediate aldosteronism”) (see Etiology). (See the images below.)
Clinically, the distinction between the 2 major causes of primary aldosteronism is vital because the treatment of choice for each is markedly different. While the treatment of choice for aldosteronomas is surgical extirpation, the treatment of choice for IAH is medical therapy with aldosterone antagonists. (See Treatment and Medication.)
Entities known to cause aldosteronism include the following (see the image below):
Aldosterone-producing adenomas (APAs) 
Aldosterone-producing renin-responsive adenomas (AP-RAs; also abbreviated as RRAs)
Bilateral idiopathic adrenal (glomerulosa) hyperplasia or IAH (also known as primary adrenal hyperplasia or PAH)
Familial forms of primary aldosteronism
Ectopic secretion of aldosterone (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.)
Pure aldosterone-producing adrenocortical carcinomas (very rare; physiologically behave as APAs)
Aldosterone, by inducing renal reabsorption of sodium at the distal convoluted tubule (DCT), enhances secretion of potassium and hydrogen ions, causing hypernatremia, hypokalemia, and alkalosis. (See Prognosis, Workup, and Treatment.)
Three distinct genetic-familial varieties of primary aldosteronism exist. Sutherland and colleagues first described the type 1 variety of familial primary aldosteronism, glucocorticoid-remediable aldosteronism (GRA), in 1966. In GRA, HTN responds clinically to small doses of glucocorticoids in addition to other antihypertensive agents.  The type 1 form of familial primary aldosteronism is due to an aberrantly formed chimeric gene product that combines the glucocorticoid-responsive (inhibitable) promoter of the 11beta-hydroxylase gene (CYP11B1) with the coding region of the aldosterone synthetase gene (CYP11B2). Under ambient glucocorticoid levels, the promoter is not fully transcriptionally silenced, and this leads to overexpression of aldosterone synthetase, with subsequent increased synthesis and secretion of aldosterone. (See Etiology and Workup.)
The type 2 variant of familial primary aldosteronism (which is not glucocorticoid sensitive) was first described in 1991. Although the exact genetic abnormality for type 2 primary aldosteronism has not been identified, data suggest that the locus for this disease is on band 7p22. 
The type 3 variant of familial primary aldosteronism is due to KCNJ5 (potassium inwardly rectifying channel, subfamily J, member 5) potassium channel mutations. This type was described by Lifton’s group in 2011. 
Screening (first-tier) tests for primary aldosteronism include the following:
Confirmatory (second-tier) tests include the following:
Tests for determining the primary aldosteronism subtype (third-tier tests) include the following:
The initial radiologic investigation in the workup of primary aldosteronism is high-resolution, thin-sliced (2-2.5 mm) adrenal computed tomography (CT) scanning with contrast.
Other tests include the following:
Pharmacologic therapy includes use of the following:
Surgery is the treatment of choice for the lateralizable variants of primary aldosteronism, including typical aldosteronomas, renin-responsive adenomas (RRAs), and primary adrenal hyperplasia (PAH). An adrenalectomy can be performed via a formal laparotomy or by using a laparoscopic technique (with performance of the latter becoming increasingly common).
The most important factors that predict the pathophysiologic association of hypokalemia with primary aldosteronism are (1) aldosterone hypersecretion, which acts on the cortical collecting duct to stimulate potassium secretion into the tubular fluid, thus enhancing renal/urinary potassium wasting  ; (2) adequate intravascular volume, which enables adequate water delivery (tubular flow rate) to the renal distal convoluted tubules (DCTs) and collecting ducts to enable renal potassium loss; and (3) adequate dietary sodium intake, which, in turn, increases total body potassium, renal/ tubular sodium delivery, and, thus, enhances renal potassium loss via the countercurrent transport system.
The absence of 1 or more of the physiologic circumstances described above may explain the absence of frank hypokalemia in many patients with proven primary aldosteronism.
The associated metabolic alkalosis in primary aldosteronism is due to increased renal hydrogen ion loss mediated by hypokalemia and aldosterone.
Almost 20% of patients with primary aldosteronism have impaired glucose tolerance resulting from the inhibitory effect of hypokalemia on insulin action and secretion; however, diabetes mellitus is no more common than in the general population.
The cardinal anomaly causing primary aldosteronism syndrome is autonomous (nonsuppressible) aldosterone production. In addition to nonsuppressible aldosterone production, suppressed and poorly stimulative levels of plasma renin are coexisting with 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 corticotropin.
Regulation of aldosterone production by these factors may be altered in various ways, depending on the subtype of primary aldosteronism. Generally, aldosterone-producing adenomas (APAs) and GRA remain corticotropin responsive, while idiopathic adrenal hyperplasia (IAH) and aldosterone-producing renin-responsive adenomas (RRAs) maintain responsiveness to the renin-angiotensin system (RAS).
In glucocorticoid-remediable aldosteronism (GRA), the RAS is suppressed, and aldosterone is regulated by corticotropin because of the chimeric gene fusion of a corticotropin-sensitive promoter with the coding regions of the aldosterone synthetase gene (which normally does not have such a promoter). Thus, ambient corticotropin levels pathologically overstimulate aldosterone synthesis inappropriately. 
In patients with GRA, the administration of dexamethasone (or any other glucocorticoid) at doses sufficient to suppress excessive corticotropin production results in a reduction in aldosterone synthesis and natriuresis and the eventual correction of the biochemical anomalies of primary aldosteronism.  Histologic studies in this disease have shown specific hyperplasia of the zona fasciculata, with concomitant atrophy of the zona glomerulosa.
The exact cause of sporadic primary aldosteronism due to an adenoma or hyperplasia is unclear. The existence of trophic factors (eg, endothelins, cytokines) has been postulated in cases of hyperplasia. Somatic mutations of genes leading to growth advantage in the adrenal adenomatous tissue are a possible, but unproven, cause.
In familial forms of primary aldosteronism, the molecular basis of GRA is known. GRA is due to a mutation that results from a hybrid gene product.  The 11beta-hydroxylase and aldosterone synthetase genes that are normally located close to each other on chromosome 8 cross over to create a novel hybrid gene product. This hybrid gene consists of the regulatory corticotropin-responsive sequence of the 11beta-hydroxylase gene (CYP11B1) fused to the structural component of the aldosterone synthetase gene (CYP11B2). 
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 aldosteronism is unclear; however, the locus for this disease has been mapped on 7p22 (band 11q13).  This syndrome can histologically manifest as hyperplasia or adenomas.
The genetic basis for type 3 familial aldosteronism has recently been deciphered. Mutations in the KCNJ5 potassium channel-coding gene results in loss of ion selectivity, cell membrane depolarization, increased Ca2+ entry in adrenal glomerulosa cells, and increased aldosterone synthesis. 
The existence of tertiary aldosteronism as a separate entity remains controversial. The entity is presumed to result from chronic elevations in plasma renin levels and secondary aldosteronism, which eventually establishes a state of autonomous, unregulated aldosteronism with a histologic picture of mixed hyperplasia and adenomas in the affected adrenocortical tissue. This clinicopathologic picture is considered to be the irreversible end-result of prolonged neurohumoral effects on vascular resistance and “terminal” hypertrophy of the aldosterone-producing 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, which complicates further the attribution of the hypertensive state to chronic “inappropriate” aldosterone excess.
Initially, renin levels are elevated, which is typical of secondary aldosteronism. 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.
The exact prevalence of primary aldosteronism is unclear, but estimates suggest that 5-15% of essential hypertension (HTN) cases may be due to primary aldosteronism. The prevalence of primary aldosteronism 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.
Primary aldosteronism occurs worldwide. Several reports suggest a higher prevalence in African Americans, persons of African origin, and, potentially, other blacks. This appears to be particularly true of the idiopathic adrenal hyperplasia (IAH) variant of the disease.
Aldosterone-producing adenomas (APAs) are more common in women than in men, with a female-to-male ratio of 2:1. The typical patient with an APA is a woman aged 30-50 years.
Accumulating data for IAH suggest different demographics for this condition, with the idiopathic disease being 4 times more prevalent in men than in women and peaking in the sixth decade of life.
The morbidity and mortality associated with primary aldosteronism, especially Conn syndrome, are primarily related to hypokalemia and hypertension (HTN). [10, 11] Hypokalemia, especially if severe, causes cardiac arrhythmias, which can be fatal.
Complications from chronic HTN include myocardial infarction, cerebrovascular disease, and congestive heart failure. Treatment can also lead to complications, such as drug reactions and complications from surgery.
Evidence exists to show that chronic aldosteronism in and of itself, in the absence of elevated blood pressure (eg, as occurs in secondary aldosteronism), is also associated with increased risk for cardiac injury, including ischemic, hypertrophic, and fibrotic injury. Furthermore, studies have shown that patients with primary aldosteronism are more likely to have or develop left ventricular hypertrophy, stroke, and acute coronary syndromes than are patients with similar degrees of HTN from other causes. [12, 13]
This was supported by a study by Ohno et al, which indicated that the risk of developing cardiovascular disease is higher in individuals with primary aldosteronism than in those with essential HTN. Cardiovascular disease (including stroke, ischemic heart disease, and heart failure) had a prevalence of 9.4% in patients with primary aldosteronism, greater than that in patients with essential HTN. The difference in stroke prevalence between the two groups was particularly large. Risk factors for cardiovascular disease in primary aldosteronism were found to include hypokalemia, unilateral primary aldosteronism, and plasma aldosterone levels at or above 125 pg/mL. 
Of course, patients with HTN due to primary aldosteronism are also at risk of developing the entire spectrum of complications of chronic HTN, including hypertensive nephropathy and retinopathy.
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Gabriel I Uwaifo, MD Associate Professor, Section of Endocrinology, Diabetes and Metabolism, Louisiana State University School of Medicine in New Orleans; Adjunct Professor, Joint Program on Diabetes, Endocrinology and Metabolism, Pennington Biomedical Research Center in Baton Rouge
Gabriel I Uwaifo, MD 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, Endocrine Society
Disclosure: Nothing to disclose.
Nicholas J Sarlis, MD, PhD, FACP Vice President, Head of Medical Affairs, Incyte Corporation
Nicholas J Sarlis, MD, PhD, FACP is a member of the following medical societies: American Association for the Advancement of Science, American Association for Cancer Research, American Association of Clinical Endocrinologists, American College of Physicians, American Federation for Medical Research, American Head and Neck Society, American Medical Association, American Society for Radiation Oncology, American Thyroid Association, Endocrine Society, New York Academy of Sciences, Royal Society of Medicine, Association for Psychological Science, American College of Endocrinology, European Society for Medical Oncology, American Society of Clinical Oncology
Disclosure: Received salary from Incyte Corporation for employment; Received ownership interest from Sanofi-Aventis for previous employment; Received ownership interest/ stock & stock option (incl. rsu) holder from Incyte Corporation for employment.
Romesh Khardori, MD, PhD, FACP Professor of Endocrinology, Director of Training Program, Division of Endocrinology, Diabetes and Metabolism, Strelitz Diabetes and Endocrine Disorders Institute, Department of Internal Medicine, Eastern Virginia Medical School
Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, Endocrine Society
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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 &Ethics, Endocrine Society, and International Society for Clinical Densitometry
Disclosure: Nothing to disclose.
Serge A Jabbour, MD Associate Professor, Department of Medicine, Division of Endocrinology, Jefferson Medical College of Thomas Jefferson University
Serge A Jabbour, MD 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 Thyroid Association, Endocrine Society, and Pennsylvania Medical Society
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Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
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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, andInternational Society for Clinical Densitometry
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