Plasma Aldosterone Concentration In Patients Research Articles

Higher plasma aldosterone concentrations in patients with aortic diseases and hypertension: a retrospective observational study

BackgroundAortic diseases remain a highly perilous macrovascular condition. The relationship between circulating aldosterone and aortic diseases is rarely explored, thus we investigated the difference in plasma aldosterone concentration (PAC) between patients with and without aortic disease in hypertensive people.MethodsWe analyzed 926 patients with hypertension, ranging in age from 18 to 89 years, who had their PAC measured from the hospital's electronic database. The case group and control group were defined based on inclusion and exclusion criteria. The analysis included general information, clinical data, biochemical data, and medical imaging examination results as covariates. To further evaluate the difference in PAC between primary hypertension patients with aortic disease and those without, we used multivariate logistic regression analysis and also employed propensity score matching to minimize the influence of confounding factors.ResultsIn total, 394 participants were included in the analysis, with 66 individuals diagnosed with aortic diseases and 328 in the control group. The participants were predominantly male (64.5%) and over the age of 50 (68.5%), with an average PAC of 19.95 ng/dL. After controlling for confounding factors, the results showed hypertension patients with aortic disease were more likely to have high PAC levels than those without aortic disease (OR = 1.138, 95% CI [1.062 to 1.238]). Subgroup analysis revealed consistent relationship between PAC and primary hypertensive patients with aortic disease across the different stratification variables. Additionally, hypertensive patients with aortic disease still have a risk of higher PAC levels than those without aortic disease, even after propensity score matching.ConclusionsThe results of this study suggest that primary hypertensive patients with aortic diseases have elevated levels of PAC, but the causal relationship between PAC and aortic disease requires further study.

FRI128 Hiding In Plain Sight: Late Diagnosis Of Primary Hyperaldosteronism In Patient With Atypical Presentation

Abstract Disclosure: R.A. Zielinski: None. A. Syeda: None. B. Esayag-Tendler: None. Background: Primary hyperaldosteronism (PHA) can go undiagnosed in patients with primary hypertension without hypokalemia and increased plasma aldosterone concentration (PAC). Case: The patient is a 72-year-old male with a history of hypertension (HTN) diagnosed at age 55 who presented to the endocrinology clinic for further evaluation. He was asymptomatic. His antihypertensive regimen included atenolol 25 mg daily and amlodipine-benazepril 10-40 mg daily. Blood pressure (BP) was well-controlled with a goal BP under 130/80 mm Hg. Physical exam was without AV nicking in a limited retina exam, no abdominal tenderness, and no peripheral edema. Family history is notable for HTN in his father and HTN complicated by stroke in a sister and a brother, all diagnosed at an older age. Labs done 5 years prior showed potassium (K) of 4.3 mmol/L [3.6 - 5.1 mmol/L], PAC of 3.2 ng/dl [upright 4.0 - 31.0 ng/dl], and plasma renin activity (PRA) of 0.1 ng/ml/hr [upright 0.5-4.0 ng/ml/hr]. More recent labs showed K of 3.8 mmol/L, PAC of 21.5 ng/dl and PRA of 0.3 ng/ml/hr. Repeat labs 6 months later showed K of 3.4 mmol/L, PAC of 15 ng/dL and PRA of 0.2 ng/mL/hr. A 3-day dexamethasone suppression test was performed to exclude familial hyperaldosteronism or glucocorticoid remediable aldosteronism. Following the test, K was 3.6 mmol/L, PAC was 11.3 ng/dl, and cortisol was undetectable. CT abdomen showed bilateral nodular thickening of the adrenal glands without a distinct adenoma. Adrenal venous sampling was done before and after ACTH stimulation. Prior to ACTH stimulation, the mean ratio of the dominant adrenal aldosterone concentration corrected with cortisol from left to right was 1.32. Following ACTH stimulation, the ratio was 2.79. A ratio greater than 4 is consistent with a good outcome after adrenalectomy. Hence, it was decided to pursue medical management. The cause of our patient’s primary hyperaldosteronism is likely due to bilateral idiopathic hyperplasia. He was started on eplerenone 25 mg twice daily and salt restriction with a goal of increasing the PRA above 1 ng/ml/hr. Discussion and Conclusion: It was initially thought that PHA represents 1% of all patients with primary HTN. However, more recent studies indicate that the prevalence is significantly higher. Additionally, the PAC in patients with PHA can fluctuate and patients can present with normokalemia, making the diagnosis more difficult to establish. It is an important diagnosis to establish and treat appropriately because there is a higher risk of cardiovascular morbidity and mortality in patients with PHA compared to patients with primary HTN. Presentation: Friday, June 16, 2023

Clinical Characteristics of Obstructive Sleep Apnea and Comorbid Primary Aldosteronism

To explore the characteristics of patients with obstructive sleep apnea (OSA) and comorbid primary aldosteronism (PA) and to explore the relevant factors affecting plasma aldosterone concentration. A total of 105 patients diagnosed with PA and admitted at West China Hospital, Sichuan University between January 2016 and December 2021 were retrospectively analyzed. The subjects were divided into a PA with comorbid snoring group (n=20) and a PA with comorbid OSA group (n=85) based on the results of polysomnography (PSG). The PA with comorbid OSA group was further divided into mild, moderate, and severe subgroups according to the apnea-hypopnea index (AHI). A total of 85 outpatients diagnosed with OSA were included as the control group. Demographic, clinical, biochemical, and PSG data were compared between the groups. Compared with patients with only OSA, a significantly higher proportion of patients with OSA and comorbid PA had hypertension and elevated levels of systolic and diastolic blood pressure (P<0.05). In addition, patients with OSA and comorbid PA had significantly increased AHI and significantly decreased mean oxygen saturation and sleep efficiency (P<0.05). The more severe the OSA was, the higher levels of BMI, cholesterol, low-density lipoprotein, and uric acid the PA patients had. Linear regression analysis showed that the lowest oxygen saturation (β=－0.222, P=0.045) was negatively correlated with plasma aldosterone concentration. Comorbidity with PA can aggravate the clinical manifestations of OSA, while OSA further disrupted the metabolism of lipids and uric acid in PA patients. Plasma aldosterone concentrations in patients with comorbid OSA and PA were affected by the lowest oxygen saturation level.

Renal impairment is closely associated with plasma aldosterone concentration in patients with primary aldosteronism.

Several clinical studies have reported that renal impairments are sometimes observed in patients with primary aldosteronism (PA). We analyzed the prevalence of renal impairments in PA patients and identified parameters that increase the risk for them. This is a retrospective cross-sectional study. We assessed the PA database established by the multicenter Japan PA study (JPAS). Data were also collected from patients with essential hypertension (EHT). We compared the prevalences of proteinuria and lowered estimated glomerular filtration rate (eGFR) between patients with PA and age, sex, blood pressure and duration of hypertension-matched patients with EHT. We also performed logistic regression analysis to identify parameters that increase the risk for these renal impairments. Among 2366 PA patients, the prevalences of proteinuria and lowered eGFR were 10.3 and 11.6%, respectively. The prevalence of proteinuria was significantly higher in PA patients than matched-EHT patients (16.8 vs 4.4%), whereas there was no significant difference in the prevalence of lowered eGFR (17.2 vs 15.0%). The logistic regression analysis also showed that the plasma aldosterone concentration (PAC) significantly increases the risk of proteinuria and lowered eGFR, independent of other known risk factors. Plasma aldosterone levels are closely associated with renal impairment in patients with PA. This is contrast to our earlier finding that the PAC was not itself linearly associated with cardiovascular events such as stroke or ischemic heart disease. The mechanism underlying the kidney damage in patients with PA may differ from that affecting the cardiovascular system.

Demystifying "Steroid Withdrawal" During Remission in Cushing's Disease: Is Mineralocorticoid Replacement the Answer?

Objective:To study renin-angiotensin-aldosterone axis status (RAAS) in patients of Cushing's disease (CD) at baseline and 6 weeks after curative trans-sphenoidal surgery and evaluate the role of mineralocorticoid replacement in the resolution of “steroid withdrawal syndrome” (SWS). Postoperative RAAS status had not been evaluated in previous studies, although aldosterone levels have been shown to be suppressed during medical therapy with pasireotide and cabergoline.Materials and Methods:This was a prospective, single-center study. Patients with CD, aged between 15–75 years, undergoing curative pituitary surgery were recruited. An 8 am and 11 pm cortisol and adrenocorticotropic hormone (ACTH) were measured at baseline. An 8 am cortisol was measured 6 weeks after surgery to demonstrate remission. Plasma-renin activity and plasma-aldosterone concentration were measured at baseline and 6 weeks after curative surgery.Results:A total of 14 patients (11 female, 3 male) were recruited initially, of these 8 patients completed the study. The plasma-renin activity was not suppressed at baseline and did not rise significantly after surgery (P = 0.717). However, plasma-aldosterone concentration was in the low-normal range at baseline and had risen significantly 6 weeks after surgery (P = 0.013). No difference was noted in subgroups with or without hypertension.Conclusion:Curative pituitary surgery leads to normalization of plasma-aldosterone concentration in patients with CD just 6 weeks after surgery. Hence, mineralocorticoid replacement may not prove beneficial in alleviating the “SWS” in postsurgical CD patients who have achieved remission.

Relationship Between Visceral Fat and Plasma Aldosterone Concentration in Patients With Primary Aldosteronism.

ContextThe involvement of visceral fat in aldosterone secretion has not been reported in patients with primary aldosteronism (PA). Patients with PA are complicated by metabolic syndrome more frequently than those without PA. An excess of visceral fat has been hypothesized to cause an elevation of aldosterone secretion in patients with PA.ObjectivesTo clarify the role of visceral fat in the pathophysiology of PA, we investigated the correlation between plasma aldosterone concentration (PAC) and visceral fat parameters in patients with PA.DesignThis retrospective observational study comprised 131 patients diagnosed with PA between April 2007 and April 2017 at Sapporo City General Hospital. We divided participants into two PA subtypes, aldosterone-producing adenoma (APA; n = 47) and idiopathic hyperaldosteronism (IHA, n = 84), utilizing adrenal venous sampling. We analyzed the correlations of PAC with visceral fat percentage (VF%), visceral fat area (VFA), and subcutaneous fat area, by evaluating computed tomography studies in each subtype group.ResultsPatients with IHA showed a positive correlation of PAC with VF% (r = 0.377, P < 0.001) and VFA (r = 0.443, P < 0.001). The correlation was not evident in patients with APA.ConclusionsThis study revealed a relationship between visceral adipose tissue and aldosterone production only in patients with IHA.

Circulating pentraxin 3 is positively associated with chronic hyperglycemia but negatively associated with plasma aldosterone concentration.

Pentraxin 3 (PTX3) is reported to be a vascular inflammation marker providing prognostic information of vasculopathy. Until today, however, the effect of aldosterone or oxidative stress on the regulation of PTX3 is unknown. In present study, we investigated to find regulative factors, especially aldosterone and oxidative stress, on PTX3. Serum PTX3 levels were measured in 75 patients (45 male and 30 women, aged 55.1±13.4 year-old (mean±SD)) with various endocrine disorders including 47 with diabetes, 24 with primary aldosteronism (PA). All participants were free from cardio vascular diseases and diabetic retinopathy. Serum PTX3 level was significantly lower in patients with PA than without PA and was significantly higher in patients with diabetes than without diabetes. PTX3 was significantly correlated with glycated hemoglobin (HbA1c), urinary albumin excretion (UAE) and plasma aldosterone concentration (PAC) (r = 0.431, P<0.001; r = 0.313, P = 0.009; r = -0.375, P = 0.004). A stepwise multiple regression analysis chose HbA1c and UAE as independent determinants of PTX3 (β = 0.282, P<0.001; β = 0.783, P<0.001). On the other hand, PTX3 was not significantly correlated with HbA1c and UAE but significantly negatively correlated with PAC in patients with diabetes. Therefore, it might be suggested that PTX3 is positively regulated by chronic hyperglycemia but negatively regulated by aldosterone, and is associated with urinary albumin excretion as a micro vasculopathy.

Effects of Vitamin D Supplementation on Plasma Aldosterone and Renin-A Randomized Placebo-Controlled Trial.

Increasing evidence describes a possible interplay between vitamin D insufficiency with increased aldosterone. The authors sought to evaluate the effect of vitamin D supplementation on plasma aldosterone concentration (PAC) in patients with hypertension and 25-hydroxyvitamin D[25(OH)D] insufficiency. The Styrian Vitamin D Hypertension Trial was a single-center, double-blind, placebo-controlled randomized clinical trial conducted from 2011 to 2014. Two hundred patients with arterial hypertension and 25(OH)D levels <30 ng/mL were enrolled. Study participants were randomized to receive either 2800 IU of vitamin D3 or placebo. The present investigation is a post hoc analysis using analysis of covariance adjusting for baseline differences. A total of 188 participants (mean±standard deviation age, 60.1±11.3 years; 47% women; 25(OH)D, 21.2±5.6 ng/mL) completed the trial. Mean differences between baseline and follow-up PAC in the control and intervention arm were +3.3 ng/dL and +0.9 ng/dL, respectively (P=.04). The findings indicate that vitamin D3 supplementation significantly decreases PAC in patients with arterial hypertension and 25(OH)D insufficiency.

A randomized controlled study of CPAP effect on plasma aldosterone concentration in patients with resistant hypertension and obstructive sleep apnea.

The high prevalence of obstructive sleep apnea in patients with resistant hypertension could be mediated by an activation of the renin-angiotensin-aldosterone system. This study assessed the impact of continuous positive airway pressure (CPAP) treatment on plasma aldosterone concentration (PAC). One hundred and twenty-four patients with resistant hypertension were assessed, and those who fulfilled inclusion criteria (n = 116) underwent full night polysomnography, 24-h ambulatory blood pressure monitoring, and PAC measurement. Patients with an apnea-hypopnea index above 15 (n = 102) were randomized to CPAP (n = 50) or to conventional treatment (n = 52) for 3 months. Seventy-eight patients completed the follow-up (36 CPAP, 42 conventional treatment); 58 had true resistant hypertension (74.3%), whereas 20 had white-coat resistant hypertension (25.6%). Most patients were men (70.7%), age 58.3 ± 9.4 years, and the mean apnea-hypopnea index was 50.1 ± 21.6. In patients with true resistant hypertension, CPAP achieved a significant decrease in most 24-h BP measurements and a nonsignificant decrease in PAC (25 ± 8.7 vs. 22.7 ± 9 ng/dl; P < 0.182). In patients with white-coat resistant hypertension, CPAP achieved a significant decrease in PAC (26.1 ± 11.2 vs. 18.9 ± 10.1 ng/dl; P < 0.041) and in night-time DBP. After adjustment, a weak but significant association was found between cumulative time spent with SaO2 below 90% (CT90%) and baseline PAC (P < 0.047, R 0.019), and between changes in PAC and changes in office DBP (P < 0.020, R 0.083) CONCLUSIONS:: Night-time hypoxemia and changes in DBP showed an association with baseline and changes in PAC, respectively. CPAP achieved a significant reduction in PAC only in patients with white-coat resistant hypertension, although the CPAP effect on BP was highest in patients with true resistant hypertension.

Mineralocorticoid receptor agonists induce mouse aortic aneurysm formation and rupture in the presence of high salt.

Elevated plasma aldosterone concentrations in patients have been linked to a spectrum of cardiovascular diseases. Mineralocorticoid receptor antagonists provide additional benefits in patients with heart failure. However, whether aldosterone and the mineralocorticoid receptor are involved in aortic aneurysm is unknown. We report that administration of deoxycorticosterone acetate (DOCA) and salt or aldosterone and salt, but not DOCA or salt alone, to C57BL/6 male mice induced abdominal and thoracic aortic aneurysm formation and rupture in an age-dependent manner. DOCA and salt- or aldosterone and salt-induced aortic aneurysm mimicked human aortic aneurysm with respect to elastin degradation, inflammatory cell infiltration, smooth muscle cell degeneration and apoptosis, and oxidative stress. Aortic aneurysm formation did not correlate with the increase in blood pressure induced by DOCA and salt. Systemic administration of the angiotensin-converting enzyme inhibitor, enalapril, or angiotensin type 1 receptor antagonist, losartan, did not affect DOCA and salt-induced aortic aneurysm. In contrast, the mineralocorticoid receptor antagonists, spironolactone or eplerenone, significantly attenuated DOCA and salt- or aldosterone and salt-induced aortic aneurysm. The current study describes a novel aortic aneurysm animal model induced by mineralocorticoid receptor agonist and high salt, and reveals a previously unrecognized but potentially significant role of aldosterone in the pathogenesis of aortic aneurysm. These findings imply that mineralocorticoid receptor antagonists may be effective in the treatment of some aortic aneurysms.

Influence of plasma aldosterone on left ventricular geometry and diastolic function in treated essential hypertension.

Since aldosterone is known to promote interstitial fibrosis in cardiac tissues, it is possible that aldosterone may influence cardiac structure and function. In the present study, we investigated whether plasma aldosterone concentration (PAC) is related to the distinct patterns of left ventricular (LV) geometry and LV diastolic function in treated essential hypertension. In 92 patients with chronically treated essential hypertension, two-dimensional and Doppler echocardiographic examinations were performed and LV inflow velocities were measured for evaluation of LV diastolic function. When patients were divided into four groups by the different LV geometric patterns, PAC in patients with eccentric hypertrophy was significantly higher than in those with concentric hypertrophy (15.2+/-2.1 vs. 10.0+/-0.7 ng/dl, p<0.01). However, the ratio of the peak velocity of early diastolic filling to that of atrial filling (EIA), an index of LV diastolic function, was significantly decreased in patients with concentric hypertrophy compared with those showing normal geometry. In the relationship between PAC and LV diastolic function, PAC was negatively correlated with EIA (r=-0.35, p<0.05) only in the subgroup with normal relative wall thickness (i.e., without the concentric change in LV geometry). A multiple linear regression analysis showed that PAC was one of the independent determinants of E/A in the overall subject group. These observations indicate that PAC is associated with the eccentric change in LV geometry in patients with treated essential hypertension and also suggest that the increase in PAC participates in the impairment of LV diastolic function apart from the concentric change in LV geometry, although concentric hypertrophy clearly impairs LV diastolic function.

Therapeutic Outcome of Primary Aldosteronism: Adrenalectomy Versus Enucleation of Aldosterone-Producing Adenoma

Our followup study of 48 patients with primary aldosteronism concerns the results of 2 different operative methods. After preoperative localization of the unilateral solitary tumor 22 patients underwent unilateral adrenalectomy and 26 underwent enucleation of aldosterone-producing adenoma. Both operative methods improved hypertension, hypokalemia, the low urinary sodium-to-potassium ratio, suppressed plasma renin activity, high plasma aldosterone concentration, high urinary aldosterone excretion and high urinary kallikrein excretion in similar orders of magnitude for 5 years. Levels of plasma cortisol and plasma adrenocorticotropic hormone following respective operations were also identical. Five years postoperatively, ambulation and furosemide administration under low sodium diet stimuli remarkably enhanced plasma renin activity and plasma aldosterone concentration in the aldosterone-producing adenoma enucleation group (p less than 0.001), almost similar to that of normal subjects but increment magnitudes were slight (p less than 0.05 to less than 0.01) in the adrenalectomy group. Preoperatively, angiotensin II infusion failed to increase plasma aldosterone concentration in patients with primary aldosteronism. After respective operations, responses of plasma aldosterone concentration to angiotensin II infusion and of plasma cortisol to adrenocorticotropic hormone administration in the aldosterone-producing adenoma enucleation group were more sensitive than those in the adrenalectomy group. There was no remission of recurrent hyperaldosteronism in either group throughout the study. These results suggest that angiotensin II induces aldosterone release by an activation of tumor uninvolved cortical cells and that the enucleation of aldosterone-producing adenoma is more preferable than unilateral adrenalectomy.

Subclinical hormone secretion by incidentally discovered adrenal masses.

To determine the frequency of subclinical hormone secretion in incidentally discovered adrenal masses. We reviewed the radiologic reports of 1779 consecutive computed tomographic scans of the chest, abdomen, and pelvis. Regional referral medical center. Eighty-nine patients with abnormalities of one or both adrenal glands were identified. Patients with nonadrenal gland malignant neoplasms, primary aldosteronism, adrenal hemorrhage, and death or severe illness were not investigated. The final study group consisted of 26 patients with incidentally discovered adrenal masses. Aldosterone secretion was assessed by measuring plasma renin activity and the plasma aldosterone concentration in patients with unexplained hypokalemia. We evaluated cortisol secretion by performing a 1-mg overnight dexamethasone suppression test and by measuring the corticotropin concentration at 8 AM by a sensitive method. In patients with low corticotropin values, we also measured the 24-hour urinary excretion of free cortisol and 17-ketosteroids and assessed diurnal variation by measuring plasma cortisol concentrations at 8 AM and 4 PM. Adrenal medullary function was studied by measuring urinary free catecholamines. One patient had unrecognized primary aldosteronism, two patients had elevated free catecholamine excretion, and three patients (12%) had subclinical Cushing's syndrome. Based on our observations and a review of the literature, we conclude that subclinical hormone secretion, especially cortisol secretion, is more common in patients with incidentally discovered adrenal masses than previously appreciated. Surgeons and anesthesiologists must be alert to the possibility that adrenal insufficiency or a hypertensive crisis may develop in the perioperative period in patients with incidentally discovered adrenal masses.

Abnormality of circulatory reflex and aldosterone response during head-up tilting in patients with primary aldosteronism.

Abnormality of the circulatory reflexes has been reported in patients with primary aldosteronism. However, changes in blood pressure, heart rate, plasma renin activity (PRA), and plasma aldosterone concentration (PAC) after head-up tilting in primary aldosteronism have not yet been reported. Seven patients with primary aldosteronism were tilted to a 65 degree head-up position which was maintained for 30 min. Systolic blood pressure decreased significantly 5 min after tilting and remained at this level during the period of tilting. Diastolic blood pressure did not change during the tilting. Heart rate increased after 5 min of tilting and this level of heart rate was maintained for 30 min. Plasma renin activity was low and did not change during tilting. However, plasma aldosterone concentration increased significantly 20 min after tilting. Plasma cortisol concentration and plasma ACTH concentration also increased significantly. These results suggest that primary aldosteronism causes abnormalities of the circulatory reflexes. The increase of endogenous ACTH may increase plasma aldosterone concentration in patients with primary aldosteronism.

Effects of various doses of captopril on plasma aldosterone concentrations in patients with essential hypertension.

Various doses (5 mg, 12.5 mg and 25 mg) of angiotensin I converting enzyme inhibitor (SQ 14,255, captopril) were administered to 8 patients with essential hypertension on a three-crossover study design, and the time course of mean blood pressure (MBP), plasma renin activity (PRA), plasma angiotensin converting enzyme activity (ACE-A), plasma cortisol (PC) and plasma aldosterone (PA) were determined following administration of the drug. MBP fell in a dose dependent manner, and PRA showed a minor but significant increases in cases receiving 5 and 12.5 mg of the drug. A large and significant increase in PRA was observed following 25 mg of captopril. ACE-A was also reduced in a dose dependent manner. There was no difference between changes in PC at any of the three dose levels. The serum potassium concentration was determined before and 3 hr after 25 mg of captopril treatment and no significant change was observed. In spite of the dose dependent and theoretical changes in the above parameters, lowered responses of PA to each dose of the drug were shown in reverse order against an increasing dose. That is to say, the grade of fall in PA following 25 of captopril was smaller than that following the other doses of the drug, and 5 mg induced a greater decrease in PA than 12.5 mg. Based on these findings, the relatively high dose of captopril in the present study was apparently more effective in increasing some factors which suppressed reduction of PA by a fall in angiotensin II than a low dose of the drug.

Plasma aldosterone during extracellular fluid volume expansion in patients on regular haemodialysis

The influence of extracellular fluid volume expansion on the plasma aldosterone concentration (PAC) was investigated in five anephric and six non-nephrectomized patients on regular haemodialysis, and compared to a control group of four anephric and four non-nephrectomized patients. Plasma-renin activity, cortisol, Na+, and K+ were measured together with the PAC during the investigation. In anephric patients the PAC remained constant during the control period as well as during extracellular fluid volume expansion by infusion of 350 mmol of 20% mannitol. In the non-nephrectomized patients PAC diminished after mannitol infusion. The decline in PAC was correlated with the basal levels of PAC and the plasma renin activity. It is concluded that 5% extracellular fluid volume expansion has no direct influence on the regulation of PAC in patients without the renal renin-angiotensin system and that the regulation of PAC in anephric patients in the present investigation is probably mediated by changes in potassium and ACTH.

Studies on the Simultaneous Measurement of Plasma Renin Activity and Plasma Aldosterone Concentration in Patients with Various Endoxrine, Hypertensitve, and Edematous Diseases; its Clinical Evaluation and Significance

Studies on the Simultaneous Measurement of Plasma Renin Activity and Plasma Aldosterone Concentration in Patients with Various Endoxrine, Hypertensitve, and Edematous Diseases; its Clinical Evaluation and Significance

Circadian Rhythm of Plasma Aldosterone Concentration in Patients with Primary Aldosteronism

Plasma aldosterone, cortisol, and renin activity were measured in nine recumbent patients with hyperaldosteronism, including seven with adenomas, one with idiopathic hyperplasia, and one with glucocorticoid suppressible hyperplasia. All had peak values of plasma aldosterone concentration from 3 a.m. to noon and lowest values at 6 p.m. or midnight. This rhythm was similar to the circadian pattern of plasma cortisol in the same patients. When these data were normalized to eliminate the wide variation in ranges of plasma aldosterone and cortisol between individuals, there was an excellent correlation (r = + 0.87, P < 0.005) between the two hormones. In contrast, plasma aldosterone concentrations did not correlate with plasma renin activity before or after normalization of data. Short term suppression of ACTH by administration of dexamethasone eliminated the circadian variation of plasma aldosterone in both patients with hyperplasia and in four of five patients with adenomas, while it markedly altered the rhythm in the fifth. Similar doses of dexamethasone were administered to four normal subjects and did not flatten the circadian rhythm of plasma aldosterone. These data suggest that patients with primary aldosteronism have a circadian rhythm of plasma aldosterone mediated by changes in ACTH.