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PubMed1975

Effect of intravenous frusemide on plasma renin concentration: suppression of response in hypertension.

1. Intravenous frusemide produced in normal subjects a prompt rise of plasma renin concentration which correlated with urinary sodium. 2. The renin response to frusemide was suppressed in patients with primary hyperaldosteronism. 3. In patients with low-renin hypertension and normal renin essential hypertension, the renin response to frusemide was similarly suppressed. 4. Suppression of the renin response to frusemide is therefore a feature of hypertension not confined to patients with primary hyperaldosteronism and low-renin hypertension. 5. Thus low-renin hypertension does not appear to constitute a distinct diagnostic entity. 6. It is suggested that suppression of the renin response is part of a long-term renal adaptation to high blood pressure.

Adult↗
PubMed1981

Effect of angiotensin II and converting enzyme inhibitor (captopril) on blood pressure, plasma renin activity and aldosterone in primary aldosteronism.

1. Patients with idiopathic hyperaldosteronism (IHA) show a response of aldosterone to posture which is not present in patients with aldosterone-producing adenoma (APA). We have determined whether this could be explained by a different sensitivity to angiotensin II. 2. Angiotensin II was infused in gradually increasing doses in six patients with APA and in seven patients with IHA. No changes in aldosterone concentration were found at the end of each period in APA, whereas there was a significant increase in IHA; blood pressure rose by a similar extent in both groups. 3. In order to evaluate the role of endogenous angiotensin II, captopril, a converting enzyme inhibitor, was administered to six patients with APA and five patients with IHA at a dose of 75 mg/day for 1 week. There was a significant fall of mean blood pressure in IHA and only minimal changes in APA. Plasma renin activity and plasma in urinary aldosterone were unchanged in APA. In IHA there was a small increase in upright plasma renin activity and a slight decrease in both plasma and urinary aldosterone, but these changes were not significant. 4. These findings further support the idea that idiopathic hyperaldosteronism is a clinical state different from that occurring in primary aldosteronism due to adenoma, and may be more closely related to essential hypertension.

Aldosterone↗
PubMed1998

Screening for primary aldosteronism with a logistic multivariate discriminant analysis.

OBJECTIVE: Primary aldosteronism (PA) is the most common endocrine cause of curable hypertension, but no single test unequivocally identifies it. Accordingly, we investigated the usefulness of a logistic multivariate discriminant analysis (MDA) approach for PA screening. DESIGN: Generation of a logistic MDA function based on retrospective analysis of biochemical tests in a large cohort of referred patients with/without confirmed Conn's adenoma (CA), followed by prospective validation of the model. PATIENTS: We investigated 574 selected hypertensives: 206 (32 with and 174 without CA) retrospectively, 48 (with a 13% prevalence of CA) prospectively for the validation of the model, and 320 referred hypertensives (with a 3.4% prevalence of CA) similarly evaluated. Patients were referred to a specialised centre for hypertension (4th Clinica Medica--University of Padua) and to a department of Internal Medicine of a regional hospital (Reggio Emilia). MEASUREMENTS: In all patients we measured several demographic and biochemical variables and performed a captopril test. A stepwise analysis of variance, based on a model fitted with several different variables, identified baseline (sALDO) and captopril-suppressed plasma aldosterone (cALDO), supine plasma renin activity (sPRA) and K+ as the most informative. Therefore, two models of logistic MDA with sPRA, K+, and either sALDO (model A) or cALDO (model B) were developed and used. ROC analysis was also performed to assess the optimal cut-off values. RESULTS: The model B of MDA provided the best performance and identified CA with 100% sensitivity and 81% accuracy. When used prospectively it showed 100% sensitivity, both in the Padua (88% accuracy) and in the Reggio Emilia series (90% accuracy). However, at both institutions most patients with idiopathic hyperaldosteronism (IHA) were also detected. CONCLUSIONS: Thus, although developed from patients with confirmed Conn's adenoma, a strategy based on multivariate discriminant analysis can be used prospectively for accurate screening for primary aldosteronism. Furthermore, it was proven to be accurate and applicable to patients tested with similar modalities at a different institution. Although this approach did not provide a clear-cut discrimination of Conn's adenoma from idiopathic hyperaldosteronism, it may avoid unnecessary and costly further testing in patients with a low probability of primary aldosteronism.

Adult↗
PubMed2002

Severe hypomagnesaemia-induced hypocalcaemia in a patient with Gitelman's syndrome.

Gitelman's syndrome (GS) is characterized by hyperreninaemic hyperaldosteronism, hypokalaemia, metabolic alkalosis, hypomagnesaemia and hypocalciuria and is due to a defect of the Na-Cl cotransporter at the distal tubule, which may appear in a sporadic or in a familial form. It is an autosomal recessive disorder associated with normal or reduced blood pressure. We report a case of severe hypomagnesaemia-induced hypocalcaemia in a 39-year-old Caucasian woman with GS. The patient had impaired parathormone (PTH) responsiveness to peripheral stimuli, as proved by the marked PTH increase and normalization of plasma calcium levels after acute and chronic administration of magnesium salts. Secondary normotensive hyperreninaemic hyperaldosteronism with hypokalaemia and metabolic alkalosis was also present. Normal plasma renin activity (PRA) and aldosterone levels were restored by administration of an inhibitor of prostaglandin synthesis. The electrolyte imbalance was successfully corrected with chronic treatment with magnesium and potassium salts. Genetic analysis identified a compound heterozygous mutation in the Na-Cl cotransporter gene (NCCT), confirming the diagnosis of GS. The striking feature of this case of GS was impaired PTH responsiveness to peripheral stimuli determined by hypomagnesaemia and the resulting severe hypocalcaemia, which had not previously been described in this syndrome.

Adult↗
PubMed2002

Unique cases of unilateral hyperaldosteronemia due to multiple adrenocortical micronodules, which can only be detected by selective adrenal venous sampling.

Primary aldosteronism is classified as aldosterone-producing adenoma (APA), idiopathic hyperaldosteronism (IHA), unilateral adrenal hyperplasia (UAH), primary adrenal hyperplasia (PAH), adrenal cancer, and glucocorticoid-remediable aldosteronism. We describe here 4 cases of primary aldosteronism due to unilateral hyperaldosteronemia, demonstrating unique histopathologic findings, such as unilateral multiple adrenocortical micronodules in the affected adrenals. Thirty-three patients with primary aldosteronism were consecutively admitted; 27 of them were treated by unilateral adrenalectomy. Four of them also had unilateral adrenal hypersecretion of aldosterone by selective adrenal venous sampling and adrenocortical multiple micronodules without an adenoma. These patients had hyporeninemic hyperaldosteronism with normokalemic hypertension. In these patients, furosemide plus upright test failed to increase plasma renin activity (PRA); the ratio of plasma aldosterone concentration (PAC) to PRA at 90 minutes after captopril administration was similar to that in patients with IHA and APA. Aldosterone concentrations were increased in each unilateral adrenal vein, and poorly encapsulated multiple adrenocortical micronodules from 2 to 3 mm in diameter were microscopically detected in the resected adrenal glands. Immunohistochemical analysis of steroidogenic enzymes, including cholesterol side chain cleavage, 3beta-hydroxysteroid dehydrogenase, 21-hydroxylase, 17alpha-hydroxylase, and 11beta-hydroxylase, indicated that the cortical cells within these micronodules were active in aldosterone production, while the non-nodular zona glomerulosa cells were inactive. We conclude that the clinical and pathologic characteristics of our 4 cases with unilateral multiple adrenocortical micronodules (UMN) are distinct from those of APA, IHA, UAH, and PAH. Furthermore, unilateral hyperaldosteronemia induced by UMN may be frequently misdiagnosed, because standard imaging tests, which cannot always detect tiny abnormalities of adrenals, showed "normal adrenal glands" in these patients. Thus, primary aldosteronism due to UMN should be carefully examined for differential diagnosis of each form of hyperaldosteronemia.

Adenoma↗
PubMed1980

Use of computed tomography in diagnosing the cause of primary aldosteronism.

We performed computed tomography (CT) in 22 consecutive patients with primary aldosteronism to evaluate the usefulness of this technique in diagnosing and locating aldosterone-producing adenomas. Sixteen patients had severe hypokalemia, hyperaldosteronism, and elevated plasma levels of 18-hydroxycorticosterone suggestive of an adenoma. In 12 of these 16, a unilateral adrenal mass was demonstrated clearly, and in all 11 who had surgery in adenoma was confirmed. In the other four patients in this group, one adrenal gland was normal and the other was either not seen adequately or had minor abnormalities that could not be definitely classified; an adenoma was found in the poorly visualized gland in each of the two patients who had surgery. The remaining six patients, who had milder biochemical abnormalities suggestive of idiopathic hyperaldosteronism, had bilateral adrenal enlargement or normal-appearing glands on scan and were not surgically explored. We conclude that CT scans, together with appropriate biochemical measurements, are useful in diagnosing and locating aldosterone-producing adenomas.

18-Hydroxycorticosterone↗
PubMed2001

Modulation of transalveolar fluid absorption by endogenous aldosterone in adult rats.

We examined whether transalveolar fluid transport is modulated by aldosterone in adult rats. Because colocalization of mineralocorticoid receptors (MR) with 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) is important for aldosterone specific action, we first determined the immunohistochemical distribution of MR and 11betaHSD2 in the lung. We found that alveolar epithelial cells express both MR and 11betaHSD2. Reverse transcriptase polymerase chain reaction (RT-PCR) demonstrated that rat alveolar type II epithelial cells express both MR and 11betaHSD2. We then measured alveolar fluid clearance in rats treated with chronic low-sodium diet. A low-sodium diet (0.1% NaCl for 12 to 14 days) caused hyperaldosteronism accompanied by hypokalemia, whereas serum corticosterone and adrenaline levels remained normal. We found that hyperaldosteronism was associated with significantly higher alveolar fluid clearance and that this increase was related to the amiloride-sensitive component. In addition, the increase in alveolar fluid clearance was inhibited by spironolactone. Our results show that aldosterone is able to stimulate Na+ channels of alveolar epithelial cells. We conclude that alveolar epithelium is a physiological target tissue for aldosterone and transalveolar fluid absorption could in part be modulated by endogenous aldosterone acting via MR.

11-beta-Hydroxysteroid Dehydrogenase Type 2↗
PubMed2003

High prevalence of secondary hypertension and insulin resistance in patients with refractory hypertension.

OBJECTIVE: To determine causes of treatment resistance in patients with refractory hypertension, and to estimate the prevalence of true resistant hypertension. METHODS: We studied 50 consecutive patients referred with refractory hypertension after exclusion of hypokalemia and stenosis of the renal artery. Ambulatory blood pressure monitoring was performed in all patients to detect white-coat effect. The patients were hospitalized, antihypertensive drugs were withdrawn and a screening for secondary hypertension was performed. In addition, these patients, and a control group of essential hypertensives controlled with three antihypertensive drugs, underwent a OGTT with 75 g of glucose. RESULTS: Primary normokalemic hyperaldosteronism was diagnosed in seven patients. Two patients had a pheochromocytoma and six had white-coat effect. The 35 remaining patients with true resistant hypertension shown significant differences in serum insulin and HOMA IR when compared with the control group. CONCLUSIONS: These findings show that among normokalemic treatment-resistant hypertension, the presence of hyperaldosteronism and pheochromocytoma is quite high. Moreover, treatment resistance in hypertensive patients appears to be associated with insulin resistance.

Adrenal Gland Neoplasms↗
PubMed2002

Hypertension in an adolescent boy.

We report the case of an adolescent boy who presented with hypertension and hypokalemia. A systematic work-up revealed hyperreninemic hyperaldosteronism. Further study revealed Page kidney caused by trauma-associated renal hematoma. The evaluation and management of hyperaldosteronism and Page kidney are discussed.

Adolescent↗
PubMed1993

Carcinosarcoma of the adrenal cortex presenting with mineralocorticoid excess.

An adrenal carcinosarcoma is reported in a 79-year-old woman presenting with clinical signs of hyperaldosteronism. The tumor weighed 199 g and consisted of areas typical of adrenal carcinoma and areas of sarcoma. The sarcomatous component of the tumor showed osteogenic and chondroid differentiation. Vimentin stained both the carcinomatous and sarcomatous regions. Four months after resection, the patient developed metastases. This is the third reported case of adrenal carcinosarcoma and the only case in which hyperaldosteronism or bony differentiation was observed.

Adrenal Cortex Neoplasms↗
PubMed1985

Body-sodium and blood volume in a patient with licorice-induced hypertension.

A 68-year-old man a nine-year history of licorice ingestion had moderate hypertension and low plasma potassium. Exchangeable sodium and blood volume were increased to 128 and 111%, respectively of the expected values; plasma renin and aldosterone levels were suppressed. Plasma norepinephrine concentration was distinctly elevated but the pressor response to infused norepinephrine was normal. After licorice withdrawal, blood pressure, plasma potassium and blood volume reverted to normal levels within three weeks, exchangeable sodium and plasma renin within four months. Exchangeable sodium in our patient with licorice-induced hypertension was increased to a comparable extent as in primary hyperaldosteronism. Moreover, blood pressure in relation to body sodium or plasma potassium did not differ between the exogenous or the endogenous types of mineralocorticoid excess. This observation does not support the possibility that in primary hyperaldosteronism excess aldosterone secretion per se could play an important pressor role independently from sodium retention.

Aged↗
PubMed1990

Functional relationships between platelet alpha 2-adrenoceptors and sympathetic nerve activity in clinical hypertensive states.

Tritiated yohimbine binding was used to estimate platelet membrane alpha 2-adrenoceptor characteristics in normal subjects (n = 12) and patients with essential hypertension (n = 30), primary hyperaldosteronism (n = 10) and phaeochromocytoma (n = 10). There was a 20-fold increase in mean levels of resting norepinephrine and epinephrine in the phaeochromocytoma group. Total binding sites (Bmax) and dissociation constant (Kd) for 3H-yohimbine did not differ significantly among the four groups. Following curative surgery for phaeochromocytoma, plasma catecholamine levels were normalized but the Bmax remained unchanged. Following surgery for primary hyperaldosteronism, levels of plasma norepinephrine rose but Bmax was not changed. In all but the phaeochromocytoma patients, Bmax values correlated positively (r = 0.437, n = 48, P less than 0.01) with resting plasma norepinephrine. A significant negative correlation was observed between the change in plasma norepinephrine in response to postural change and resting Bmax. Treatment for 2-4 weeks with guanabenz or bethanidine induced a parallel fall in both Bmax and plasma norepinephrine. Treatment with reserpine was followed by a comparable fall in plasma norepinephrine, but Bmax values were unchanged. The findings support the view that platelet alpha 2-adrenoceptor density is functionally regulated in parallel with sympathetic nerve activity rather than circulating catecholamine levels, although it is not known which neuronal substance(s) may participate in this regulation.

Adrenal Gland Neoplasms↗
PubMed1988

Are calcium antagonists helpful in the management of primary aldosteronism?

The chronic effect of the calcium antagonist nitrendipine, a 1,4-dihydropyridine derivative, on blood pressure (BP), plasma aldosterone concentration (PAC), plasma renin activity (PRA), and serum potassium was investigated in six patients with primary aldosteronism, either due to an (unilateral) aldosterone-producing adenoma (APA) (n = 3; age 44 +/- 4 years; PAC: 312 +/- 96 pg/ml; PRA: less than 0.1 ng/L/h; serum potassium: 2.8 +/- 0.3 mmol/L) or to bilateral idiopathic hyperaldosteronism (IHA): (n = 3; age 49 +/- 1 years; PAC: 212 +/- 32 pg/ml; PRA: 0.1 +/- 0.1 ng/L/h; serum potassium: 3.3 +/- 0.2 mmol/L). After withdrawal of antihypertensive medications 2 weeks prior to the study, nitrendipine was given orally in a daily dosage of 40-60 mg. BP, PAC, PRA, and serum potassium were determined before and after 4 weeks of nitrendipine therapy. After 4 weeks, blood pressure was significantly reduced (178 +/- 10 to 165 +/- 6 mm Hg systolic, 109 +/- 7 to 101 +/- 6 mm Hg diastolic) in three patients with APA and in two with IHA. No significant changes of PAC, PRA, and serum potassium were observed in these patients. However, one patient with clinical characteristics of IHA and a long-term history of diuretic therapy showed a complete normalization of BP, PAC, PRA, and serum potassium, suggesting that the etiology of autonomous hyperaldosteronism in this patient might differ from typical primary aldosteronism. From these findings, we follow that calcium antagonists do not normalize BP, PAC, PRA, and serum potassium in patients with APA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Long-term medical management of aldosterone-producing adenoma.

This case of Conn's syndrome demonstrates long-term (seven years) efficacy of triamterene-thiazide therapy in controlling both hypertension and hypokalemia. Studies done before the adrenal tumor was removed surgically showed that the tumor had increased in size and function since the first studies were done before triamterene-thiazide therapy. The resolution of hypertension after nine years of hyperaldosteronism suggests that surgery is effective even after chronic hyperaldosteronism has been present for some time.

Adenoma↗
PubMed1986

Primary aldosteronism due to a malignant ovarian tumour.

The case of a woman with autonomous aldosteronism, hypertension, and malignant ovarian tumour is reported. Hormone studies revealed high plasma aldosterone levels, and low plasma renin concentration. Following surgical removal of a malignant sex cord stromal tumour, the hyperaldosteronism regressed, and the hypertension improved. Subsequently the tumour recurred, as did hyperaldosteronism.

Aldosterone↗
PubMed1987

Adrenocortical carcinoma presenting as primary aldosteronism in a young man.

A young Polynesian man presented with severe hypertension complicated by an intracerebral hemorrhage. The hypertension was found to be secondary to hyperaldosteronism from a well differentiated adrenocortical carcinoma. Surgical removal of the tumor has resulted in a near normal blood pressure with no evidence of tumour recurrence of hyperaldosteronism after one year.

Adrenal Cortex Neoplasms↗
PubMed2006

Diuretic-induced hypokalaemia in patients with hypertension.

We describe a 55 year-old woman with longstanding hypertension who developed hypokalaemia following diuretic treatment. Investigations revealed primary hyperaldosteronism due to an adrenal adenoma, and normal blood pressure was restored after surgical removal of the tumour. Primary hyperaldosteronism is a potentially curable cause of hypertension and should be considered in hypertensive patients who present with diuretic - induced hypokalaemia.

Adrenal Cortex Neoplasms↗
PubMed2006

QT interval is prolonged but QT dispersion is maintained in patients with primary aldosteronism.

The relationship between QT duration and its dispersion in patients with primary hyperaldosteronism is not clearly known. We studied 26 patients (nine males and 17 females) with primary hyperaldosteronism. The serum potassium levels were low (2.32 +/- 0.52 mmol/l), did not correlate with serum renin or aldosterone levels, or aldosterone/renin ratio (ARR). The maximum QT intervals (QTmax) were prolonged (502 +/- 62 ms), correlated well with ARRs (p = 0.005) and aldosterone levels (p = 0.019), but not to renin (p = 0.517) or potassium levels (p = 0.196). The QT dispersions (QTd) were small (60 +/- 28.8 ms) and did not correlate with potassium, renin or aldosterone levels. QTmax but not QTd correlate with aldosterone levels in patients with primary aldosteronism. The maintenance of repolarisation homogeneity with relatively unchanged QT dispersion may contribute to our understanding of the clinical observation that ventricular tachydysrhythmia is rare among patients with primary aldosteronism.

Adult↗