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Primary aldosteronism (PA) is the most common cause of mineralocorticoid hypertension. Different studies, using the plasma aldosterone concentration to plasma renin activity ratio (PAC/PRA) for the screening of patients with hypertension, have shown a marked increase in the detection rate of PA. Idiopathic bilateral adrenal hyperplasia (IHA) and aldosterone-producing adrenal adenoma (APA), are the leading causes of primary aldosteronism. Glucocorticoid-remediable aldosteronism (GRA), also called familial hyperaldosteronism type I, familial hyperaldosteronism type II and carcinomas are rare causes of PA. Patients with hypertension and hypokalemia, those with a family history of hypertension and stroke at an early age, or patients with medication-resistant hypertension should be screened for PA using the PAC/PRA ratio. If a high ratio is found, a sodium loading test or a captopril test is warranted to confirm the diagnosis. Adrenal gland imaging is important in subtype differentiation (APA vs IHA). Adrenal venous sampling should be used when other tests prove inconclusive. Genetic testing has facilitated detection of GRA. Surgery is considered the treatment of choice for patients with APA, while bilateral hyperplasia subtypes are treated medically. Normalization of aldosterone levels or aldosterone receptor blockade are necessary to prevent the morbidity and mortality associated with hypertension, hypokalemia, and cardiovascular damage.
Exp Clin Endocrinol Diabetes 2007 Mar
PMID:Detecting and treating primary aldosteronism: primary aldosteronism. 1742 5

Androgenetic alopecia is considered to be associated with coronary heart disease but the explanation of this association remains unknown. Hypertension is highly prevalent in patients with coronary heart disease. Essential hypertension is linked to hyperaldosteronism and spironolactone, an antihypertensive drug which is a mineralocorticoid receptor antagonist, has been used for a long time in the treatment of androgenic alopecia. We recently observed in a double transgenic mouse model that overexpression of a mineralocorticoid receptor targeted to the skin induced the development of alopecia. We prospectively studied the association of hypertension and androgenetic alopecia in Caucasian men. Two hundred and fifty Caucasian men aged 35-65 years were consecutively recruited by 5 general practitioners (50 per practitioner). Data collected included age, androgenetic alopecia score with a simplified Norwood's score (0-4), blood pressure or history of hypertension, smoking, history of diabetes mellitus or hyperlipidemia, familial history of androgenetic alopecia, and treatment. Chi-square, Fisher exact tests and linear regression model were used for statistical analysis. Hypertension was strongly associated to androgenetic alopecia (p < 0.001). Linear regression tests confirmed that this association was independent of age : odds ratio was 2.195 (95% CI : 1.1-4.3). Familial history of androgenetic alopecia was also strongly associated with androgenetic alopecia : odds ratio was 10.870 (95% CI : 4.3-27.1). Other variables (diabetes mellitus, hyperlipidemia, smoking, treatment) were not associated with androgenetic alopecia. We were limited by a relatively small study sample but in this study androgenetic alopecia was strongly associated with hypertension. Association of androgenetic alopecia and hyperaldosteronism warrants additional studies. The use of specific mineralocorticoid receptor antagonists could be of interest in the treatment of androgenetic alopecia.
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PMID:Association of androgenetic alopecia and hypertension. 1747 84

Although only recently discovered, feline adrenal disorders are becoming increasingly more recognized. Feline adrenal disorders include diseases such as hyperadrenocorticism (Cushing's syndrome) and hyperaldosteronism (Conn's syndrome). The clinical signs of feline hyperadrenocorticism, which include unregulated diabetes mellitus and severe skin atrophy, are unique to the cat. Other signs of feline hyperadrenocorticism, such as potbellied appearance, polydipsia, polyuria, and susceptibility to infections are also seen in dogs with hyperadrenocorticism. Conn's syndrome has only recently been described in the cat and is in fact more common in cats than in dogs. Characterized by severe hypokalemia, hypertension, and muscle weakness, Conn's syndrome may be misdiagnosed as renal failure. The clinician should become familiar with the clinical signs of adrenal disorders in cats and the common diagnostic tests used to diagnose these syndromes in cats as they differ from those in the dog. Treatment of feline adrenal disorders may be challenging; the clinician should become familiar with common drugs used to treat adrenal disorders in cats.
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PMID:Feline adrenal disorders. 1754 94

Aldosterone concentrations are inappropriately high in many patients with hypertension, as well as in an increasing number of individuals with metabolic syndrome and sleep apnoea. A growing body of evidence suggests that aldosterone and/or activation of the MR (mineralocorticoid receptor) contributes to cardiovascular remodelling and renal injury in these conditions. In addition to causing sodium retention and increased blood pressure, MR activation induces oxidative stress, endothelial dysfunction, inflammation and subsequent fibrosis. The MR may be activated by aldosterone and cortisol or via transactivation by the AT(1) (angiotenin II type 1) receptor through a mechanism involving the EGFR (epidermal growth factor receptor) and MAPK (mitogen-activated protein kinase) pathway. In addition, aldosterone can generate rapid non-genomic effects in the heart and vasculature. MR antagonism reduces mortality in patients with CHF (congestive heart failure) and following myocardial infarction. MR antagonism improves endothelial function in patients with CHF, reduces circulating biomarkers of cardiac fibrosis in CHF or following myocardial infarction, reduces blood pressure in resistant hypertension and decreases albuminuria in hypertensive and diabetic patients. In contrast, whereas adrenalectomy improves glucose homoeostasis in hyperaldosteronism, MR antagonism may worsen glucose homoeostasis and impairs endothelial function in diabetes, suggesting a possible detrimental effect of aldosterone via non-genomic pathways.
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PMID:Aldosterone and end-organ damage. 1768 82

To determine the prevalence of primary aldosteronism among patients with incidentally discovered adrenal adenomas ('incidentalomas') plasma concentrations of aldosterone (PA) and plasma renin activity (PRA) were determined in 269 patients (100 normotensives, 169 hypertensives) newly referred incidentaloma patients. Among the 100 normotensives a PA [ng/dl]/PRA [ng/ml.h]-ratio (A/R-R) >50 and a concomitant elevation of PA (>15 pg/ml) was initially seen in two cases but further investigations excluded the presence of primary aldosteronism in both patients suggesting a prevalence of primary aldosteronism of <1% among normotensive patients with adrenal incidentaloma. Among the 169 hypertensive incidentaloma patients 14 presented with both, an elevated PA [>15 pg/ml] and an A/R-R >50. Primary aldosteronism was confirmed in 6 of this cases resulting in a prevalence of primary aldosteronism among hypertensive incidentaloma patients of 4%. Although obtained in patients with a supposedly high pre-test probability of primary aldosteronism this percentage--while in keeping with the older literature--is surprisingly low given the recently reported large(r) prevalence of primary aldosteronism among hypertensives in general.
Exp Clin Endocrinol Diabetes 2007 Sep
PMID:Determination of the aldosterone/renin ratio in 269 patients with adrenal incidentaloma. 1785 35

Individuals with primary aldosteronism make up a substantial proportion of those with hypertension. Less well appreciated is what appears to be inappropriately elevated aldosterone secretion in hypertensive patients who do not meet the criteria for true primary aldosteronism. This finding is particularly true of African-Americans. An additional, recently described, aspect of aldosterone excess is its apparent contribution to insulin resistance as evidenced by the frequent association of primary aldosteronism with the metabolic syndrome. Thus in the management of, not only hypertension, but also certain metabolic conditions, greater consideration should be given to the participation of aldosterone.
Curr Opin Endocrinol Diabetes Obes 2007 Jun
PMID:Hyperaldosteronism: a commonly occurring underlying feature of essential hypertension and the metabolic syndrome? 1794 Apr 41

Metabolic syndrome, which is caused by obesity, is now a global pandemic. Metabolic syndrome is an aggregation of hypertension, diabetes and dyslipidaemia. Insulin resistance is a key factor in the development of these components of metabolic syndrome. Concerning the mechanism for the development of hypertension in metabolic syndrome, the lack of insulin resistance in the kidney increases sodium reabsorption by hyperinsulinaemia, leading to sodium retention in the body, and resultant salt-sensitive hypertension. Moreover, hyperaldosteronism, which is caused by adipocyte-derived aldosterone-releasing factors, induces not only salt-sensitive hypertension, but also proteinuria in obese hypertensive rats. Salt loading markedly aggravates proteinuria and induces cardiac diastolic dysfunction in obese hypertensive rats, suggesting that salt and aldosterone exert unfavourable synergistic actions on the cardiovascular system, possibly through the overproduction of oxidative stress. In turn, reactive oxygen species (ROS), which are induced by adipokines such as tumour necrosis factor-alpha, non-esterified fatty acids, angiotensinogen etc., can activate the mineralocorticoid (MR) receptor, in an aldosterone-independent fashion. Therefore, aldosterone/MR activation plays a key role not only in the development of salt-sensitive hypertension, but also in cardiovascular injury in metabolic syndrome, possibly through its function as a feed-forward system.
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PMID:Aldosterone in salt-sensitive hypertension and metabolic syndrome. 1843 32

Unilateral adrenal hyperplasia (UAH) is very rare, and shows similar endocrine features to aldosterone-producing adenoma (APA). We report a case of UAH diagnosed preoperatively as APA. Pathological analysis showed that the adrenal mass did not contradict a diagnosis of APA. However, in situ hybridization and real-time PCR indicated that the hyperplastic zona glomerulosa cells rather than the adenoma cells demonstrated intense mRNA expression of steroidogenic enzymes necessary for production of aldosterone. UAH is believed to account for less than 1% of primary aldosteronism, but it is possible that some cases of UAH may be mistakenly considered to be APA, and that the actual frequency of UAH may thus be higher than presumed. Recently, partial adrenalectomy has been attempted. It should be borne in mind that cases exist in which it is difficult to differentiate between APA and UAH only by preoperative hormonal and radiologic investigations.
Exp Clin Endocrinol Diabetes 2009 Mar
PMID:A case of unilateral adrenal hyperplasia being difficult to distinguish from aldosterone-producing adenoma. 1856 Oct 92

The field of primary aldosteronism (PA) and aldosterone-related hypertension has undergone rapid evolution. From a relatively rare curiosity PA has become a common problem particularly in selected hypertensive populations. Patients with PA and aldosterone-related hypertension appear to be at higher cardiovascular and renal risk than comparable patients with essential hypertension probably due to the pleiotropic effects of aldosterone. Aldosterone is also linked to metabolic syndrome and diabetes. The aldosterone-to-renin ratio (ARR) has allowed the widespread screening for PA, but the exact cut-off values may vary in different population groups. All patients with hypertension and hypokalaemia, and young patients with hypertension, hypertension with an incidental adrenal mass, and severe or resistant hypertension should be screened. The use of the ARR to screen all hypertensives for PA is controversial as the test lacks specificity and many patients with false-positive tests will undergo complex and expensive testing to confirm the diagnosis. The fludrocortisone suppression test, the saline infusion test or 24-hour aldosterone excretion may be used to confirm PA in patients with a positive ARR. Adrenal venous sampling is the most reliable test to detect the presence of an aldosterone-producing adenoma, but spiral CT scan or adrenocortical scintigraphy may be useful in centres without facilities for adrenal venous sampling. Spironolactone is emerging as an important antihypertensive agent in patients with resistant hypertension and aldosterone-related hypertension. The ARR may be a useful guide to drug selection in hypertensives patients, but further research is needed to make more definitive recommendations.
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PMID:Primary aldosteronism and aldosterone-associated hypertension. 1858 13

An association between primary aldosteronism and metabolism disorders has been reported. The aim of this retrospective study was to test for this association by comparison between large cohorts of patients with primary aldosteronism and with essential hypertension. We retrieved the records of 460 cases with primary aldosteronism (103 lateralized, 150 not lateralized, and 207 undetermined) and of 1363 controls with essential hypertension individually matched for age and sex. We compared clinical history; blood pressure levels; body mass index; levels of fasting plasma glucose and serum triglycerides; total, high-density lipoprotein, and low-density lipoprotein cholesterol; and the prevalence of diabetes mellitus and impaired fasting glucose among subtypes of primary aldosteronism, as well as between cases with primary aldosteronism and their matched controls. Fasting plasma glucose and serum lipid levels did not differ among the 3 subtypes of primary aldosteronism. The prevalence of impaired fasting glucose was lower in patients with primary aldosteronism than their matched controls, but the prevalence of hyperglycemia (impaired fasting glucose or diabetes mellitus) and blood levels of glucose and lipids did not differ between cases and controls. There was no significant difference between preoperative and postoperative levels of either fasting plasma glucose or serum lipids in patients who underwent adrenalectomy and had follow-up data available. The analysis of this large group of patients with primary aldosteronism and essential hypertension does not confirm a higher prevalence of carbohydrate or lipid metabolism disorders in the former. It is unlikely that the prevalence of metabolic syndrome differs significantly between patients with primary aldosteronism and those with essential hypertension.
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PMID:Fasting plasma glucose and serum lipids in patients with primary aldosteronism: a controlled cross-sectional study. 1939 50


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