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PubMed1987

[Radioimmunologic determination of aldosterone and renin in the blood in the diagnosis of different forms of arterial hypertension].

Aldosterone concentration and renin activity in the blood from the ulnar, inferior cava veins at the level of the 12th thoracic vertebra, the left and right renal veins were studied in 60 patients with arterial hypertension by means of a radioimmunoassay kit (France). The patients were divided into 4 groups: with primary and idiopathic hyperaldosteronism, renal-parenchymatous and essential arterial hypertension. A significant increase in aldosterone concentration in the blood from the ulnar vein was detected in all the groups, especially in primary and idiopathic hyperaldosteronism. Hyperaldosteronism in the patients with renal-parenchymatous and essential arterial hypertension was regarded as secondary in a stable and malignant course of arterial hypertension. The diagnosis of primary and idiopathic hyperaldosteronism was also confirmed by low blood renin activity. Renin activity in the peripheral venous blood was considerably elevated in renal-parenchymatous arterial hypertension and was within normal in essential hypertension. Aldosterone concentration in the blood from the vena cava inferior and renal veins was 1.6-2-fold as high on the affected side as on the contralateral one.

Adolescent↗
PubMed2005

Monogenic low renin hypertension.

Monogenic forms of low renin hypertension can now be identified in a large and heterogeneous family of hypertensive patients with highly specific etiologies and similar clinical manifestations. These include the following well-characterized disorders: apparent mineralocorticoid excess, Liddle's Syndrome, steroid 11beta-hydroxylase (11beta-OHD) and steroid 17-hydroxylase (17-OHD) deficiencies, glucocorticoid-remediable hyperaldosteronism (familial hyperaldosteronism type I), familial hyperaldosteronism type II, hypertension exacerbated by pregnancy and primary hyperaldosteronism (Conn's syndrome). The successful elucidation of specific DNA mutations in most of these conditions has emphasized the role of molecular genetics in hypertension, a field in which diagnosis can now be made on proven genetic evidence. The current knowledge of these genetic markers enables practitioners to make precise diagnoses, and to initiate specific therapy, in patients with these relatively uncommon but interesting and often treatable forms of hypertension.

Humans↗
PubMed1997

Angiotensin-independent mechanism for aldosterone synthesis during chronic extracellular fluid volume depletion.

Wild-type (Agt+/+) and homozygous angiotensinogen deletion mutant (Agt-/-) littermates were placed on normal (NS) or low Na diet (LS) for 2 weeks. Plasma aldosterone levels (P(aldo)) were comparable during NS, and similarly elevated during LS in Agt+/+ and Agt-/-. Moreover, in both, the elevation in P(aldo) was accompanied by marked increase in adrenal zona glomerulosa cells and adrenal P450aldo mRNA. Agt-/- mice were distinguished from Agt+/+ mice by their higher plasma K level, by approximately 1.5 and approximately 3.8 mEq/liter during NS and LS, respectively. Within the Agt-/- group, P(aldo) was directly proportional to plasma K. The importance of K for the hyperaldosteronism during dietary Na restriction was verified by the observation that superimposition of K restriction led to hypotension in Agt+/+ and uniform death in Agt-/- mice along with a reduction in P(aldo) by 75 and 90%, respectively. Thus, suppression of potassium, but not angiotensin, led to a marked attenuation of hyperaldosteronism during dietary Na restriction. Therefore, (a) a powerful angiotensin-independent mechanism exists for the hyperaldosteronism during LS; (b) high K is a central component of this mechanism; (c) contrary to current belief, the tonic effect of high K on aldosterone synthesis and release does not require an intact renin-angiotensin system; and (d) normally, intermediary feedback signals for hyperaldosteronism, i.e., both hypotension and high K, are effectively masked by aldosterone actions.

Adrenal Glands↗
PubMed2025

Perirenal Adipose Tissue and Hypertension: Observational and Genetic Analyses.

BACKGROUND: Perirenal adipose tissue (PRAT) consists of white and brown adipocytes with good vascularization and dense innervation, which could influence the blood pressure. We aim to investigate the association of PRAT thickness with risks of overall and specific forms of hypertension. METHODS: We measured PRAT thickness in the UK Biobank and CONPASS (Chongqing Primary Aldosteronism Study). We prospectively examined the correlation between PRAT thickness and incident hypertension in the UK Biobank. We cross-sectionally explored associations between PRAT thickness and common forms of hypertension in CONPASS. Integrating data from GWAS (Genome-Wide Association Study), we investigated the potential causal relationship between PRAT and hypertension forms by 2-sample Mendelian randomization analyses. RESULTS: In the prospective analysis of the UK Biobank, participants whose PRAT thickness was &#x2265;46.1 mm showed a higher risk of developing hypertension than participants whose PRAT thickness was <16.4 mm (hazard ratio, 2.91 [95% CI, 1.97-4.32]). In the cross-sectional analysis of CONPASS, a 1 SD increment in PRAT thickness was associated with a 2.77-fold higher adjusted odds of low-renin essential hypertension and a 3.89-fold higher adjusted odds of idiopathic hyperaldosteronism. PRAT thickness was not significantly associated with other forms of hypertension, such as aldosterone-producing adenoma and obstructive sleep apnea. In 2-sample Mendelian randomization analyses, PRAT thickness was only significantly associated with a higher risk of idiopathic hyperaldosteronism (inverse variance weighted odds ratio, 1.33 [95% CI, 1.09-1.62]), with no evidence of significant heterogeneity or substantial directional pleiotropy. CONCLUSIONS: PRAT is causally associated with idiopathic hyperaldosteronism rather than essential hypertension and other forms of secondary hypertension.

Humans↗
PubMed1993

Unilateral renal artery stenosis seen initially as severe and symptomatic hypokalemia. Pathophysiologic assessment and effects of surgical revascularization.

Hypokalemia is an uncommon presentation of renovascular hypertension. Although renal artery stenosis has been associated with hypokalemia secondary to hyperreninemic hyperaldosteronism, few reports have actually evaluated the pathophysiologic changes in such a patient with renovascular hypertension. We studied a patient before and after surgical revascularization who presented with severe hypertension and marked, symptomatic hypokalemia. Before surgery, the patient had excessive urinary potassium secretion, markedly increased secretion of renin after captopril stimulation, and mild secondary hyperaldosteronism. Postoperatively, the patient's blood pressure decreased moderately and the serum and urinary potassium values normalized. After revascularization, plasma renin activity both before and after captopril stimulation and serum aldosterone levels decreased markedly. These findings demonstrate that renovascular hypertension may rarely present with symptomatic hypokalemia secondary to excessive aldosterone secretion. Improvement in the renal ischemic state is accompanied by rapid correction of the metabolic disturbances associated with hyperreninemic hyperaldosteronism.

Aldosterone↗
PubMed1997

Hypertensive cardiomegaly caused by an aldosterone-secreting adenoma in a newborn.

A case of primary hyperaldosteronism and cardiomegaly due to a unilateral adrenal adenoma in a newborn is presented. Some peculiarities, most likely in relation to the onset of the disease during fetal life were evident: plasma cortisol was slightly increased before surgery, plasma renin activity was elevated 9 months after surgery and mineralcorticoid receptors remained suppressed 4 months after surgery. Unilateral adrenalectomy reversed both hypertension and cardiomegaly. We speculate that cardiomegaly was related to both hyperaldosteronism and hypertension and that individual factors are involved in the pathogenesis of cardiomegaly in hyperaldosteronism.

Adenoma↗
PubMed2006

Diurnal blood pressure pattern in patients with primary aldosteronism.

BACKGROUND: The aim of the study was to evaluate diurnal blood pressure (BP) profiles in patients with primary aldosteronism and to compare them to those in subjects with essential hypertension. The effects of specific therapy on the circadian BP profiles have been studied. MATERIALS AND METHODS: Sixty-four patients with primary aldosteronism were included in the study. Thirty of them revealed an aldosterone-producing adenoma (APA) and 34 had idiopathic hyperaldosteronism (IHA) due to bilateral adrenal hyperplasia. RESULTS: We did not find any significant differences in ambulatory BP monitoring (ABPM) between patients with APA and IHA. However, the circadian BP variation in the patients with primary hyperaldosteronism due to APA was preserved, while the patients with IHA showed lower nocturnal decline in comparison with patients with essential hypertension. There was a significant decline in office and ambulatory BP levels after treatment in the patients with both APA and IHA. The awake-sleep BP difference in patients with APA remained unchanged after surgical treatment, while in patients with IHA the night-time systolic and diastolic BP decline was significantly higher after spironolactone treatment. CONCLUSIONS: Primary hyperaldosteronism due to APA was associated with normal circadian BP variability and the surgical treatment led to highly significant decline in all BP parameters but had no influence on the extent of nocturnal BP variation. Spironolactone therapy restored normal nocturnal BP decline in patients with IHA. Reduction of night-time BP decline in patients with IHA is more likely to be related to the duration of the disease rather than to the aldosterone levels.

Adenoma↗
PubMed1979

Dissociation in the excretion of different aldosterone metabolites and unmetabolized ('free') aldosterone in hypertension.

1. The determination of aldosterone-18-glucuronide (pH 1-labile aldosterone) was complemented by concomitant measurements of free urinary aldosterone and tetrahydroaldosterone in 307 patients, most of whom were hypertensive. In 38 cases (12.3%) the normal, aldosterone-18-glucuronide concentration was clinically misleading, but increased free aldosterone and/or tetrahydroaldosterone values suggested the presence of hyperaldosteronism, which in many of these cases was confirmed by elevated excretion of the possible major aldosterone precursor 18-hydroxycorticosterone (18-OH-B). 2. Of 224 patients with essential hypertension and normal or low plasma renin activity 18 had an elevated free aldosterone and/or tetrahydroaldosterone excretion without increased aldosterone-18-glucuronide. These cases may represent early or pre-symptomatic forms of primary hyperaldosteronism. In other cases, particularly when tetrahydroaldosterone was increased alone, abnormalities of aldosterone metabolism were suspected. 3. In two out of 15 patients with primary hyperaldosteronism, aldosterone-18-glucuronide values were frequently found to be normal, although elevations were noted in other variables. However, no relation to the morphological abnormality (adenoma versus hyperplasia) was seen.

18-Hydroxycorticosterone↗
PubMed2001

Familial varieties of primary aldosteronism.

1. Improved approaches to screening and diagnosis have revealed primary aldosteronism (PAL) to be much more common than previously thought, with most patients normokalaemic. The spectrum of this disorder has been further broadened by the study of familial varieties. 2. Familial hyperaldosteronism type I (FH-I) is a glucocorticoid-remediable form of PAL caused by the inheritance of an adrenocorticotrophic hormone (ACTH)- regulated, hybrid CYP11B1/CYP11B2 gene. Diagnosis has been greatly facilitated by the advent of genetic testing. The severity of hypertension varies widely in FH-I, even among members of the same family, and has demonstrated relationships with gender, degree of biochemical disturbance and hybrid gene crossover point position. Hormone "day curve" studies show that the hybrid gene dominates over wild-type CYP11B2 in terms of aldosterone regulation. This may be due, in part, to a defect in wild-type CYP11B2-induced aldosterone production. Control of hypertension in FH-I requires only partial suppression of ACTH and much smaller glucocorticoid doses than previously recommended. 3. Familial hyperaldosteronism type II (FH-II) is not glucocorticoid remediable and is not associated with the hybrid gene mutation. Familial hyperaldosteronism type II is clinically, biochemically and morphologically indistinguishable from apparently non-familial PAL. Linkage studies in one informative family did not show segregation of FH-II with the CYP11B2, AT1 or MEN1 genes, but a genome-wide search has revealed linkage with a locus in chromosome 7. As has already occurred in FH-I, elucidation of causative mutations is likely to facilitate earlier detection of PAL.

Adrenocortical Adenoma↗
PubMed2004

Recurrent calcium nephrolithiasis associated with primary aldosteronism.

Typical manifestations of hyperaldosteronism include salt retention, hypokalemia, and metabolic alkalosis. However, a consequence infrequently recognized and described is hypocitraturia. In combination with hypercalciuria, aldosterone-induced hypocitraturia can trigger calcium nephrolithiasis. The authors report a case of an individual with primary hyperaldosteronism from an adrenal adenoma that resulted in hypocitraturia. The patient had severe recurrent renal calcium calculi that corrected with adrenalectomy. The clinical physiology of renal calcium and citrate handling in hyperaldosteronism is reviewed.

Adrenal Gland Diseases↗
PubMed1992

Insulin resistance in secondary hypertension.

The insulin sensitivity of five essential hypertensive patients was compared to five patients with renovascular hypertension, five patients with primary hyperaldosteronism, and five normotensive subjects, using the euglycemic hyperinsulinemic clamp technique. Essential hypertensive patients had significantly lower insulin sensitivity than patients with hyperaldosteronism and renovascular hypertensive patients (P = .0066, P = .004, respectively). Hyperaldosteronism patients also had less insulin sensitivity than renovascular hypertensive patients (P = .016). A significant negative correlation was found between body mass index and insulin sensitivity index for essential hypertension patients only (r = -0.87, P less than .003). No such correlation was found in the secondary hypertension patients. The findings suggest a causal relationship between insulin resistance and the development of essential hypertension. Secondary hypertension, on the other hand, is not such an insulin resistant state.

Adult↗
PubMed1996

Primary aldosteronism. Results of surgical treatment.

SUMMARY BACKGROUND DATA: Management of primary hyperaldosteronism has undergone dramatic changes in the past 40 years. This retrospective study was carried out to review our recent surgical experience and to identify potential factors associated with postoperative persistent hypertension. METHODS: Forty-six patients who had adrenal surgery for primary hyperaldosteronism from 1983 to 1994 were included in the study. RESULTS: Periodic paralysis occurred in 12 (26%) patients. Hypertension and hypokalemia (mean serum potassium, 2.2 + 0.5 [+ standard deviation (SD) mmol/L) were present in all patients. Postural study was diagnostic in 85% (23 of 27). Computed tomography scan correctly localized the tumor in all except 1 patient, and venous sampling was performed in 11 patients. There was no operative mortality, and complications developed in six patients (13%), including one patient requiring re-exploration for hemostasis. All patients had a histologically documented adenoma. During a mean follow-up of 51 months, 34 (77%) of the 44 patients required no further antihypertensive treatment. Two patients were lost to follow-up. Age, response to spironolactone treatment, and blood pressure on discharge were risk factors identified for persistent hypertension. CONCLUSION: Primary hyperaldosteronism due to aldosterone-producing adenoma can be diagnosed and localized expeditiously, whereas surgical treatment can be performed safely. Hypokalemia may be cured by surgical treatment, although persistent hypertension, usually of a mild degree, still occurs in selected patients.

Adrenalectomy↗
PubMed1994

Genetics of primary aldosteronism.

1. In 1991 we described a familial variety of primary hyperaldosteronism which was not glucocorticoid-suppressible and was associated with adenoma formation, and called it familial hyperaldosteronism type II (FH-II) in order to distinguish it from the glucocorticoid-suppressible variety described in 1966, familial hyperaldosteronism type I (FH-I). 2. In 1992 the genetic basis of FH-I was clarified by description of a hybrid gene. 3. Primary aldosteronism due to bilateral adrenocortical hyperplasia or to aldosterone-producing tumour can be part of the multiple endocrine neoplasia type I syndrome (MEN I), in which loss of heterozygosity has been described on chromosome 11q13. Loss of heterozygosity at the MEN I locus was found in five of 26 aldosterone-producing tumours from our series (by Japanese collaborators). These included two with adrenal cancer and two with FH-II. 4. We recently described an association of aldosterone responsiveness of aldosterone-producing adenomas with renin gene restriction fragment length polymorphisms, suggesting a possible role for renin genotype and intra-adrenal renin gene expression in the development and biochemical expression of some aldosterone-producing tumours. 5. We found abnormal karyotypes in 13 of 32 benign aldosterone-producing adenomas.

Family↗
PubMed2005

Proliferative activity and genetic changes in adrenal cortical tumors examined by flow cytometry, fluorescence in situ hybridization and immunohistochemistry.

BACKGROUND: To determine differences in biological features among different adrenal tumors, we investigated the DNA ploidy, numerical chromosomal aberration and proliferative activity in human adrenal cortical neoplasms. METHODS: Our study included six adrenal cortical adenomas with Cushing syndrome, 12 adenomas with hyperaldosteronism, three non-functioning adenomas and three adrenal cortical carcinomas. Isolated nuclei from frozen samples were used for fluorescence in situ hybridization (FISH) analysis, and formalin-fixed, paraffin-embedded tissues from the same materials were analyzed using flow cytometry (FCM) for DNA ploidy. Sections from paraffin blocks were stained immunohistochemically with antibodies against Ki-67 and p53. For FISH analysis, we used an alpha-centromeric enumeration probe for chromosome 17. RESULTS: The mean Ki-67 labeling index (LI) of adrenal cortical carcinomas was markedly higher than that of adrenal cortical adenomas (209.4 vs 8.7). In functional adrenal cortical adenomas, the LI was significantly lower in adenomas with hyperaldosteronism than in those with Cushing syndrome (P = 0.004), although FCM results indicated that tetraploid patterns were more frequently observed in the former type. Tumor size was significantly smaller in adenomas with hyperaldosteronism than in those with Cushing syndrome (P = 0.004). Chromosome 17 showed disomy in all adrenal cortical adenomas, whereas chromosome 17 abnormalities were found in two of three adrenal cortical carcinomas. Only the latter two cases strongly expressed p53 protein. CONCLUSIONS: Our study characterized various biological features of benign and malignant adrenal cortical tumors. The use of a combination of markers might provide additional information to assist our understanding of the clinical behavior of an individual adrenal cortical tumor.

Adenoma↗
PubMed1975

Rectal potential difference in the diagnosis of aldosterone excess.

Rectal potential difference (pd) is directly related to the plasma aldosterone concentration, and rises when aldosterone is stimulated by sodium deprivation. However, when the measurement of rectal pd was tested at a screening test for hyperaldosteronism in 19 hypertensive subjects, four of the eight with primary hyperaldosteronism had a normal pd and four of the eight without aldosterone excess had an abnormally raised potential difference. The technique cannot therefore be recommended as a routine screening test for hyperaldosteronism. No relationship was found between rectal pd and hypertension associated with excess of deoxycorticosterone. Rectal pd rises in response to the mineralocorticoid-like agent carbenoxolone.

Adult↗
PubMed1985

Evidence that aldosterone influences transport in target tissues by dissimilar mechanisms.

The present study was performed to answer the question: Is the action of aldosterone on electrolyte transport and electrical properties similar in all target tissues? Studies were performed in vivo in control animals and rats with secondary hyperaldosteronism, caused by a sodium-free diet, to compare the effects of hyperaldosteronism on distal colon with hormone-induced changes in proximal colon. In distal colon aldosterone increased net sodium absorption and potassium secretion approximately threefold. Transmural potential difference increased from -15 +/- 2 to -83 +/- 3 mV (lumen negative) and ISC rose from 167 +/- 26 to 1,023 +/- 17 microA X cm-2. These aldosterone-induced responses were completely inhibited by 0.1 mM amiloride. In contrast, in proximal colon potential difference was unchanged or increased slightly in experimental animals and ISC increased only 28% above control, although increases in net sodium and potassium transport were similar to changes observed in distal colon. Amiloride did not reduce sodium absorption in proximal colon of animals with hyperaldosteronism; ISC was decreased by 43%. These studies demonstrate that rat proximal colon is an aldosterone-sensitive tissue, but that the mechanism by which aldosterone influences sodium transport is not identical in distal and proximal portions of colon.

Aldosterone↗
PubMed1979

[In vivo and in vitro studies on 18-hydroxy-11-deoxycorticosterone and 18-hydroxycorticosterone in normal subjects and in those with various adrenocortical disorders (author's transl)].

Simultaneous measurement of 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) and 18-hydroxycorticosterone (18-OH-B) in the peripheral plasma was carried out on normal subjects and in patients with adrenocortical disorders. The mean plasma levels of 18-OH-DOC at 0800h in normal males and in the follicular and luteal phases of normal females were 8.2 +/- 3.9 ng/100 ml (Mean +/- SD), 7.8 +/- 2.6 ng/100ml and 11.5 +/- 2.8 ng/100ml, respectively. The corresponding levels of 18-OH-B in normal males and in the follicular and luteal phases of normal females were 10.3 +/- 4.2 ng/100ml, 12.4 +/- 4.5 ng/100ml and 13.8 +/- 4.1 ng/100ml, respectively. No differences between the sexes nor the phases of the menstrual cycle were confirmed. ACTH stimulation increased plasma concentrations of 18-OH-DOC and 18-OH-B by 5.1 and 4.4 times respectively, while dexamethasone markedly decreased these 2 steroids. An upright posture increased these steroids significantly. In patients with Cushing syndrome, plasma levels of these 2 steroids were rarely high in cases with adrenocortical hyperplasia and adrenocortical carcinoma, while they were usually within the normal range in adrenocortical adenoma. These 2 steroid levels were increased in primary aldosteronism, idiopathic hyperaldosteronism and congenital 17 alpha-hydroxylase deficiency. They were decreased in Addison's disease and the salt-loosing type of congenital 21 alpha-hydroxylase deficiency. Patients with congenital 21 alpha-hydroxylase deficiency (simple form) showed elevated levels of 18-OH-DOC and normal levels of 18-OH-B. In vitro production of 18-OH-DOC and 18-OH-B was studied by tissue slices of the normal adrenal cortex, adrenocortical carcinoma causing Cushing syndrome, aldosteronoma and nodular hyperplasia with hyperaldosteronism. In the normal adrenal cortex, the mean production rates of 18-OH-DOC and 18-OH-B were 31 and 26 ng/g tissue/hr, respectively. ACTH and angiotensin II significantly increased the production of both 18-OH-DOC and 18-OH-B. In adrenocortical carcinoma, the production of these steroids was markedly diminished and not stimulated with either ACTH or angiotensin II. Aldosteronoma tissue produced these 2 steroids 20 to 40 times that of the normal adrenal tissue and was significantly increased with the addition of ACTH and angiotensin II. Nodular hyperplasia with hyperaldosteronism produced much 18-OH-DOC and 18-OH-B, but did not respond to ACTH and angiotensin II.

18-Hydroxycorticosterone↗
PubMed1999

Aldosterone-producing adenoma without hypertension: a report of two cases.

Normotensive primary hyperaldosteronism is exceedingly rare. We report two new cases of this syndrome in two middle-aged women, one of Asian origin. The presenting signs were tetany in one case and an adrenal mass in the other. Neither patient had hypertension, despite repeated measurements with a manual armlet. A typical biological profile of primary hyperaldosteronism was demonstrated in both patients, including hypokalemia with inappropriate kaliuresis, elevated resting plasma aldosterone, and undetectable plasma renin activity. The circadian rhythm of blood pressure was studied by ambulatory monitoring pre- and post-operatively. It confirmed the lack of hypertension, but the circadian rhythm of blood pressure was lost before surgery in one patient. Surgical removal of the histologically typical aldosterone-producing adenomas normalized the kalemia. The main finding in these two patients was spontaneously low blood pressure in the post-operative period. This suggests that excess aldosterone induced relative hypertension in these patients whose blood pressure was spontaneously very low. Genetic screening for dexamethasone-sensitive hyperaldosteronism was negative in both patients.

Adenoma↗