Primary aldosteronism: renaissance of a syndrome

Abstract

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.

Screening for primary aldosteronism in an argentinian population: a multicenter prospective study

“…The ARR [ALD (ng/dL)/PRA (ng/mL/hour)] and the ARC [ALD (ng/dL)/PRC (pg/mL)] were calculated in hypertensive patients, ARR values were considered suspicious for PA only with ALD ≥ 15 ng/dL, in agreement with other authors (8,9).…”

“…PA was confirmed with ALD levels above 6 ng/dL in the FST (10) and above 7 ng/dL in the SIT (11). In all PA patients, adrenal computed tomography was obtained, and in two of them (1 adenoma and 1 hyperplasia) adrenal venous catheterization was performed (9).…”

Indicators of mineralocorticoid excess in the evaluation of primary aldosteronism

“…7 Therefore, in the diagnosis of PA, hypokalemia has low sensitivity and specificity and is not anymore suggested as a criterion to make the diagnosis of PA. 1,8 The plasma aldosterone-to-plasma renin activity (A PL /PRA) ratio has proved to be one of the most reliable parameters in the screening for PA. Many studies have shown superior sensitivity and specificity of the A PL /PRA ratio, as compared with measurements of A PL or renin alone.…”

Feline primary hyperaldosteronism: an emerging endocrine disease

“…In contrast to what is observed in humans, in which the primary bilateral idiopathic hyperaldosteronism (60-65% of cases), and aldosterone secretory adenoma (30-35% of cases) represent the majority of cases (YOUNG, 2003;YOUNG, 2007), in cats, hyperaldosteronism is mostly attributed to adenomas or adenocarcinomas of adrenal glands (DJAJADININGRAT-LAANEN et al, 2011). Of 25 cases in cats with histopathological confirmation described in the literature, 13 were related to carcinoma, seven to unilateral adenomas, two to bilateral adenomas and three to bilateral hyperplasia (DJAJADININGRAT-LAANEN et al, 2011).…”