Confirmatory Tests in the Diagnosis of Primary Aldosteronism

Mulatero, Paolo; Monticone, Silvia; Bertello, Chiara; Mengozzi, Giulio; Tizzani, Davide; Iannaccone, Andrea; Veglio, Franco

doi:10.1055/s-0029-1246186

Cited by 44 publications

(35 citation statements)

References 33 publications

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“…In addition, the available diagnostic tools are cumbersome and disease's epidemiology appears to be a continuous spectrum from low-renin hypertension, normotensive forms of normokalaemic PA to hypokalaemic PA, making the establishment of cut-offs used to make the diagnosis rather arbitrary (28,72).…”

Section: Potential Limitations Of Currently Employed Diagnostic Testsmentioning

confidence: 99%

PROGRESS IN ALDOSTERONISM: A review of the prevalence of primary aldosteronism in pre-hypertension and hypertension

Piaditis

Markou

Papanastasiou

et al. 2015

European Journal of Endocrinology

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Primary aldosteronism (PA) secondary to excessive and/or autonomous aldosterone secretion from the renin-angiotensin system accounts for w10% of cases of hypertension and is primarily caused by bilateral adrenal hyperplasia (BAH) or aldosterone-producing adenomas (APAs). Although the diagnosis has traditionally been supported by low serum potassium levels, normokalaemic and even normotensive forms of PA have been identified expanding further the clinical phenotype. Moreover, recent evidence has shown that serum aldosterone correlates with increased blood pressure (BP) in the general population and even moderately raised aldosterone levels are linked to increased cardiovascular morbidity and mortality. In addition, aldosterone antagonists are effective in BP control even in patients without evidence of dysregulated aldosterone secretion. These findings indicate a higher prevalence of aldosterone excess among hypertensive patients than previously considered that could be attributed to disease heterogeneity, aldosterone level fluctuations related to an ACTH effect or inadequate sensitivity of current diagnostic means to identify apparent aldosterone excess. In addition, functioning aberrant receptors expressed in the adrenal tissue have been found in a subset of PA cases that could also be related to its pathogenesis. Recently a number of specific genetic alterations, mainly involving ion homeostasis across the membrane of zona glomerulosa, have been detected in w50% of patients with APAs. Although specific genotype/phenotype correlations have not been clearly identified, differential expression of these genetic alterations could also account for the wide clinical phenotype, variations in disease prevalence and performance of diagnostic tests. In the present review, we critically analyse the current means used to diagnose PA along with the role that ACTH, aberrant receptor expression and genetic alterations may exert, and provide evidence for an increased prevalence of aldosterone dysregulation in patients with essential hypertension and pre-hypertension.

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Section: Potential Limitations Of Currently Employed Diagnostic Testsmentioning

confidence: 99%

PROGRESS IN ALDOSTERONISM: A review of the prevalence of primary aldosteronism in pre-hypertension and hypertension

Piaditis

Markou

Papanastasiou

et al. 2015

European Journal of Endocrinology

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“…If PAC is lower than 5 ng dL −1 after the saline infusion, PA is unlikely whereas PAC >10 ng dL −1 is diagnostic for PA. PAC between 5 and 10 ng dL −1 represents a grey zone, but most clinicians consider such individuals to be affected by PA [ 4,93 ] .…”

Section: Con Fi Rmatory Testsmentioning

confidence: 99%

“…Patients should receive adequate potassium chloride supplementation to maintain plasma potassium in the normal range. Normal suppression is usually de fi ned as a 24 h urinary aldosterone concentration <12 m g day −1 on the third day (Table 1.3 ) [ 4,93,94 ] .…”

Section: Con Fi Rmatory Testsmentioning

confidence: 99%

Primary Aldosteronism: Progress in Diagnosis, Therapy, and Genetics

Mulatero

Williams

Monticone

et al. 2012

Endocrine Hypertension

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Primary aldosteronism (PA) is the most frequent cause of secondary hypertension and its prevalence increases with the severity of hypertension. The importance of PA diagnosis is not just related to offering a targeted treatment, that is, adrenalectomy, for aldosterone-producing adenoma and medical therapy with mineralocorticoid receptor antagonists for bilateral adrenal hyperplasia, but also because it has been demonstrated extensively that patients affected by PA are more susceptible to cardiovascular events and target organ damage compared to essential hypertensives. Herein, we review the pathophysiology of PA and its clinical features and potential complications; the three step approach employed in the diagnosis of PA, established by the Endocrine Society Guidelines, that is, screening, con fi rmation/exclusion, and subtype diagnosis are discussed; the rarer, familial, and sporadic genetic forms of PA are explained and we conclude with a section on targeted PA therapy.

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“…The most widely used and approved by the guidelines tests are: fludrocortisone suppression test (FST), intravenous saline load test (SLT), oral sodium loading test (OLT) and captopril challenge (CC). FST, SLT and OLT include the administration of salt and thus should be considered preferable to CC for confirming PA (Mulatero et al, 2010). CC has the advantage of being relatively cheap, safe, well tolerated and easy to perform.…”

Section: Confirmatory Testingmentioning

confidence: 99%