Primary aldosteronism (Conn's syndrome).

Gittler, R; Fajans, Stefan S.

doi:10.1210/jcem.80.12.8530580

Cited by 16 publications

(6 citation statements)

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“…The tumor resection reverted the clinical and metabolic alterations and for the first time a relationship between aldosterone excess and the aforementioned features was established. Conn "temporarily" defined the clinical syndrome primary aldosteronism [12,13].…”

Section: Historical Perspectivesmentioning

confidence: 99%

Is Primary Aldosteronism Still Largely Unrecognized?

et al. 2017

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Primary aldosteronism (PA) was first reported by Jerome W. Conn in 1954 when it was considered a rare disorder, only suspected in cases of hypertension and spontaneous hypokalemia. Over the last 30 years, with the wide application of the plasma aldosterone to plasma renin activity ratio as screening test, the clinical spectrum of PA has dramatically changed. Different studies displayed significant differences in term of patients investigated, diagnostic criteria and hormonal assays; however, large prospective studies with robust diagnostic criteria indicated that the prevalence of PA is around 6% of the general hypertensive population and 11% of the patients referred to hypertension centers. In light of these epidemiological studies, the Endocrine Society Guideline recommends the screening for PA of around 50% of patients with hypertension, and identifies the categories of patients at high risk for the disease. However, clinical data obtained from “real-life” show that the screening rate is much lower and PA remains an under-diagnosed and under-treated cause of secondary hypertension with an associated increased risk of cardio- and cerebrovascular mortality and morbidity.

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Section: Historical Perspectivesmentioning

confidence: 99%

Is Primary Aldosteronism Still Largely Unrecognized?

et al. 2017

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“…Conn … established for the first time the relationship among adrenal aldosterone‐producing tumours, hypertension, and hypokalemia. A new era had arrived in the study of hypertension and adrenal mineralocorticoids.’ 2 …”

Section: Introduction: ‘Painting Background’mentioning

confidence: 99%

Primary aldosteronism: renaissance of a syndrome

Young

2007

Clinical Endocrinology

585

486

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Great strides have been made in our understanding of the pathophysiology of primary aldosteronism syndrome since Conn's description of the clinical presentation of a patient with an aldosterone-producing adenoma (APA) more than 50 years ago. It is now recognized that the APA is just one of the seven subtypes of primary aldosteronism. APA and bilateral idiopathic hyperaldosteronism (IHA) are the most common subtypes of primary aldosteronism. Although most clinicians had thought primary aldosteronism to be a rare form of hypertension for more than three decades, it is now recognized to be the most common form of secondary hypertension. Using the plasma aldosterone to plasma renin activity ratio as a case-finding test, followed by aldosterone suppression confirmatory testing, has resulted in much higher prevalence estimates of 5-13% of all patients with hypertension. In addition, there has been a new recognition of the aldosterone-specific cardiovascular morbidity and mortality associated with aldosterone excess. Although thought to be daunting and complex in the past, the diagnostic approach to primary aldosteronism is straightforward and can be considered in three phases: case-finding tests, confirmatory tests and subtype evaluation tests. Patients with hypertension and hypokalaemia (regardless of presumed cause), treatment-resistant hypertension (three antihypertensive drugs and poor control), severe hypertension (>or= 160 mmHg systolic or >or= 100 mmHg diastolic), hypertension and an incidental adrenal mass, onset of hypertension at a young age or patients being evaluated for other forms of secondary hypertension should undergo screening for primary aldosteronism. In patients with suspected primary aldosteronism, screening can be accomplished by measuring a morning (preferably between 0800 and 1000 h) ambulatory paired random plasma aldosterone concentration (PAC) and plasma renin activity (PRA). An increased PAC:PRA ratio is not diagnostic by itself, and primary aldosteronism must be confirmed by demonstrating inappropriate aldosterone secretion. Aldosterone suppression testing can be performed with orally administered sodium chloride and measurement of urinary aldosterone or with intravenous sodium chloride loading and measurement of PAC. Unilateral adrenalectomy in patients with APA or unilateral adrenal hyperplasia results in normalization of hypokalaemia in all these patients; hypertension is improved in all and is cured in approximately 30-60% of them. In bilateral adrenal forms of primary aldosteronism, unilateral or bilateral adrenalectomy seldom corrects the hypertension and they should be treated medically with a mineralocorticoid receptor antagonist.

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“…The case was a 34-year-old woman who had a syndrome of "moderate hypertension," hypokalemia, metabolic alkalosis, mild hypernatremia, and normal renal function. She did not have Cushingoid features, had no evidence of peripheral edema and was found to have an abundant salt-retaining corticoid in the urine (55,115). The salt retaining adrenal steroid was hypothesized to be aldosterone, which had recently been discovered (336).…”

Section: Primary Aldosteronismmentioning

confidence: 99%

Pathophysiology, Diagnosis, and Treatment of Mineralocorticoid Disorders

Magill

2014

Comprehensive Physiology

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The renin-angiotensin-aldosterone system (RAAS) is a major regulator of blood pressure control, fluid, and electrolyte balance in humans. Chronic activation of mineralocorticoid production leads to dysregulation of the cardiovascular system and to hypertension. The key mineralocorticoid is aldosterone. Hyperaldosteronism causes sodium and fluid retention in the kidney. Combined with the actions of angiotensin II, chronic elevation in aldosterone leads to detrimental effects in the vasculature, heart, and brain. The adverse effects of excess aldosterone are heavily dependent on increased dietary salt intake as has been demonstrated in animal models and in humans. Hypertension develops due to complex genetic influences combined with environmental factors. In the last two decades, primary aldosteronism has been found to occur in 5% to 13% of subjects with hypertension. In addition, patients with hyperaldosteronism have more end organ manifestations such as left ventricular hypertrophy and have significant cardiovascular complications including higher rates of heart failure and atrial fibrillation compared to similarly matched patients with essential hypertension. The pathophysiology, diagnosis, and treatment of primary aldosteronism will be extensively reviewed. There are many pitfalls in the diagnosis and confirmation of the disorder that will be discussed. Other rare forms of hyper- and hypo-aldosteronism and unusual disorders of hypertension will also be reviewed in this article.

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Primary aldosteronism (Conn's syndrome).

Cited by 16 publications

References 0 publications

Is Primary Aldosteronism Still Largely Unrecognized?

Is Primary Aldosteronism Still Largely Unrecognized?

Primary aldosteronism: renaissance of a syndrome

Pathophysiology, Diagnosis, and Treatment of Mineralocorticoid Disorders

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