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David A. Calhoun - One of the best experts on this subject based on the ideXlab platform.
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urinary sodium excretion predicts blood pressure response to spironolactone in patients with resistant hypertension independent of aldosterone status
Journal of Hypertension, 2016Co-Authors: Lama Ghazi, Suzanne Oparil, Tanja Dudenbostel, Chee Paul Lin, David A. CalhounAbstract:Objective:Resistant hypertension (RHTN), blood pressure (BP) at least 140/90 mmHg despite using at least three different medications, including a diuretic, is associated with high dietary sodium and Hyperaldosteronism. Mineralocorticoid receptor antagonists are recommended for treatment of RHTN, how
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increased dietary sodium is related to severity of obstructive sleep apnea in patients with resistant hypertension and Hyperaldosteronism
Chest, 2013Co-Authors: Eduardo Pimenta, Richard D Gordon, Michael Stowasser, Suzanne Oparil, Susan M Harding, Michel Batlouni, Bin Zhang, David A. CalhounAbstract:Background Obstructive sleep apnea (OSA) is a strong and independent risk factor for the development of hypertension, particularly resistant hypertension, and cardiovascular diseases. Patients with resistant hypertension have a high prevalence of OSA in association with elevated aldosterone levels, high salt intake, and salt-sensitive BP. The objective of this study was to determine whether dietary salt and aldosterone are associated with severity of OSA in patients with resistant hypertension. Methods Ninety-seven patients with resistant hypertension were prospectively evaluated by overnight polysomnography and 24-h urinary sodium and aldosterone levels while maintaining their usual diet. Hyperaldosteronism was defined as a plasma renin activity of Results Overall, patients' mean clinic BP was 156.3 ± 22.4/88.9 ± 13.3 mm Hg while taking an average of 4.3 ± 1.1 antihypertensive medications. Prevalence of OSA was 77.3%. Twenty-eight (28.9%) patients had Hyperaldosteronism. Urinary sodium level was an independent predictor of severity of OSA only in patients with Hyperaldosteronism. Conclusions The findings suggest that dietary salt is related to the severity of OSA in patients with resistant hypertension and Hyperaldosteronism. The results support dietary salt restriction as a treatment strategy for reduction of OSA severity in these patients.
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positive relationship of sleep apnea to Hyperaldosteronism in an ethnically diverse population
Journal of Hypertension, 2011Co-Authors: John J Sim, David A. Calhoun, Eric Yan, In Lu A Liu, Scott A Rasgon, Kamyar Kalantarzadeh, Stephen F DeroseAbstract:OBJECTIVE Approximately, 50-60% of patients with sleep apnea have hypertension. To explore a mechanism of this relationship, we compared its prevalence in a hypertensive population with and without Hyperaldosteronism. METHODS Using the Kaiser Permanente Southern California database, hypertensive individuals who had plasma aldosterone and plasma renin activity measured between 1 January 2006 and 31 December 2007 were evaluated. Hyperaldosteronism was defined as an aldosterone : renin ratio more than 30 and plasma aldosterone more than 20 ng/dl or an aldosterone : renin ratio more than 50 (ng/dl : ng/ml per h). Hypertension was identified by International Classification of Disease, Ninth Revision (ICD-9) coding and sleep apnea was defined by ICD-9 coding or procedural coding for dispensation of positive airway devices. RESULTS Of 3428 hypertensive patients, 575 (17%) had Hyperaldosteronism. Sleep apnea was present in 18% (105) with Hyperaldosteronism vs. 9% (251) without Hyperaldosteronism (P < 0.001). Odds ratio for sleep apnea in patients with Hyperaldosteronism was 1.8 (95% confidence interval 1.3-2.6) after controlling for other sleep apnea risk factors. No ethnic group was at greater risk for sleep apnea. CONCLUSION The prevalence of sleep apnea in a diverse hypertensive population is increased in patients with Hyperaldosteronism, even when controlling for other sleep apnea risk factors.
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Resistant hypertension and Hyperaldosteronism
Current Hypertension Reports, 2008Co-Authors: Carla Castiglia Gonzaga, David A. CalhounAbstract:Resistant hypertension is defined as blood pressure that remains uncontrolled in spite of ≥ 3 antihypertensive medications at effective doses, ideally including a diuretic. Although exact prevalence is unknown, clinical trials suggest that 20% to 30% of study participants are resistant. Hyperaldosteronism, obesity, refractory volume expansion, and obstructive sleep apnea are common findings in resistant hypertension patients. Multiple studies indicate that primary aldosteronism (PA) is common (∼ 20%) in patients with resistant hypertension. Screening for PA is recommended for most patients with resistant hypertension, ideally by measurement of 24-hour urinary aldosterone excretion, or by the plasma aldosterone/plasma renin activity ratio. Successful treatment of resistant hypertension is predicated on improvement of lifestyle factors; accurate diagnosis and treatment of secondary causes of hypertension; and use of effective multidrug regimens. A long-acting diuretic, specifically chlorthalidone, is recommended as part of the treatment regimen. Recent studies demonstrate that mineralocorticoid receptor antagonists provide substantial antihypertensive benefit when added to multidrug regimens, even in patients without demonstrable aldosterone excess.
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The role of aldosterone antagonists in the management of resistant hypertension.
Current Hypertension Reports, 2005Co-Authors: Mari K. Nishizaka, David A. CalhounAbstract:Resistant hypertension is an increasingly common problem faced by primary care physicians and specialists and will undoubtedly become even more common as the adult population ages and gains weight. In the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), at least 8% of subjects were resistant to treatment based on the need for three or more antihypertensive agents. Characteristics of patients with resistant hypertension include being older, black, obese, and diabetic, and having chronic kidney disease as well as untreated sleep apnea. Hyperaldosteronism is common in patients with resistant hypertension, with a prevalence of approximately 20%. This, however, is likely an underestimation of the role aldosterone excess plays in causing drug resistance. In subjects with resistant hypertension, suppressed renin levels are common, exceeding 75% in our studies, suggesting aldosterone excess effects beyond cases of true primary Hyperaldosteronism. Recent studies indicate that aldosterone antagonists provide significant blood pressure reduction when added to antihypertensive regimens of patients with resistant hypertension. Interestingly, the blood pressure reduction with use of spironolactone is not limited to patients with Hyperaldosteronism, consistent with the concept of aldosterone excess as a continuum from low-renin hypertension with normal aldosterone levels to true primary Hyperaldosteronism.
Michael Stowasser - One of the best experts on this subject based on the ideXlab platform.
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increased dietary sodium is related to severity of obstructive sleep apnea in patients with resistant hypertension and Hyperaldosteronism
Chest, 2013Co-Authors: Eduardo Pimenta, Richard D Gordon, Michael Stowasser, Suzanne Oparil, Susan M Harding, Michel Batlouni, Bin Zhang, David A. CalhounAbstract:Background Obstructive sleep apnea (OSA) is a strong and independent risk factor for the development of hypertension, particularly resistant hypertension, and cardiovascular diseases. Patients with resistant hypertension have a high prevalence of OSA in association with elevated aldosterone levels, high salt intake, and salt-sensitive BP. The objective of this study was to determine whether dietary salt and aldosterone are associated with severity of OSA in patients with resistant hypertension. Methods Ninety-seven patients with resistant hypertension were prospectively evaluated by overnight polysomnography and 24-h urinary sodium and aldosterone levels while maintaining their usual diet. Hyperaldosteronism was defined as a plasma renin activity of Results Overall, patients' mean clinic BP was 156.3 ± 22.4/88.9 ± 13.3 mm Hg while taking an average of 4.3 ± 1.1 antihypertensive medications. Prevalence of OSA was 77.3%. Twenty-eight (28.9%) patients had Hyperaldosteronism. Urinary sodium level was an independent predictor of severity of OSA only in patients with Hyperaldosteronism. Conclusions The findings suggest that dietary salt is related to the severity of OSA in patients with resistant hypertension and Hyperaldosteronism. The results support dietary salt restriction as a treatment strategy for reduction of OSA severity in these patients.
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further study of chromosome 7p22 to identify the molecular basis of familial Hyperaldosteronism type ii
Journal of Human Hypertension, 2011Co-Authors: K J Carss, Richard D Gordon, Michael Stowasser, Kevin M OshaughnessyAbstract:Further study of chromosome 7p22 to identify the molecular basis of familial Hyperaldosteronism type II
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further evidence for linkage of familial Hyperaldosteronism type ii at chromosome 7p22 in italian as well as australian and south american families
Journal of Hypertension, 2008Co-Authors: Norlela Sukor, Paolo Mulatero, Franco Veglio, Richard D Gordon, David L Duffy, Chiara Bertello, Livia Kelemen, Y Jeske, Michael StowasserAbstract:Background Familial Hyperaldosteronism type II is a hereditary form of primary aldosteronism not attributable to the hybrid CYP11B1/CYP11B2 mutation that causes glucocorticoid remediable aldosteronism ( or familial Hyperaldosteronism type I). Although genetic defect(s) underlying familial Hyperaldosteronism type II have not yet been elucidated, linkage to chromosome 7p22 was previously reported in two Australian families and a South American family with familial Hyperaldosteronism type II.
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a novel genetic locus for low renin hypertension familial Hyperaldosteronism type ii maps to chromosome 7 7p22
Journal of Medical Genetics, 2000Co-Authors: Antony R Lafferty, Richard D Gordon, Michael Stowasser, David J Torpy, Susan E Taymans, Jing Ping Lin, Philip Huggard, Constantine A StratakisAbstract:Familial Hyperaldosteronism type II (FH-II) is caused by adrenocortical hyperplasia or aldosteronoma or both and is frequently transmitted in an autosomal dominant fashion. Unlike FH type I (FH-I), which results from fusion of the CYP11B1 and CYP11B2 genes, Hyperaldosteronism in FH-II is not glucocorticoid remediable. A large family with FH-II was used for a genome wide search and its members were evaluated by measuring the aldosterone:renin ratio. In those with an increased ratio, FH-II was confirmed by fludrocortisone suppression testing. After excluding most of the genome, genetic linkage was identified with a maximum two point lod score of 3.26 at θ=0, between FH-II in this family and the polymorphic markers D7S511, D7S517, and GATA24F03 on chromosome 7, a region that corresponds to cytogenetic band 7p22. This is the first identified locus for FH-II; its molecular elucidation may provide further insight into the aetiology of primary aldosteronism. Keywords: chromosome 7; aldosterone; familial Hyperaldosteronism type II; hypertension
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a new genetic test for familial Hyperaldosteronism type i aids in the detection of curable hypertension
Biochemical and Biophysical Research Communications, 1995Co-Authors: J R Jonsson, Michael Stowasser, Shelley A Klemm, T J Tunny, Richard D GordonAbstract:In Familial Hyperaldosteronism Type I (FH-I, glucocorticoid-suppressible Hyperaldosteronism), a curable form of hypertension inherited in an autosomal dominant fashion, the underlying genetic defect is a "hybrid gene" in which 11 beta-hydroxylase gene regulatory elements are fused to the coding region of the aldosterone synthase gene. The detection of this hybrid gene by Southern blotting is time consuming and involves the use of radioactive isotopes. We describe a new, long polymerase chain reaction-based method for detecting the hybrid gene which greatly reduces the time required to obtain a result, avoids exposure of laboratory workers to radioactive materials, and will thereby facilitate the screening of patients for the presence of FH-I.
Richard D Gordon - One of the best experts on this subject based on the ideXlab platform.
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Familial Hyperaldosteronism Type II: Description of a Large Kindred and Exclusion of the Aldosterone
2016Co-Authors: Aldosterone Synthase Gene, Richard D Gordon, David J Torpy, See Profile, George Chrousos, Aghia Sophia, Synthase Gene, Jing Ping LinAbstract:Familial Hyperaldosteronism type II (FH-II) is characterized by autosomal dominant inheritance and hypersecretion of aldosterone due to adrenocortical hyperplasia or an aldosterone-producing ade-noma; unlike FH type I (FH-I), Hyperaldosteronism in FH-II is not suppressible by dexamethasone. Of a total of 17 FH-II families with 44 affected members, we studied a large kindred with 7 affected members that was informative for linkage analysis. Family members were screened with the aldosterone/PRA ratio test; patients with aldosterone/PRA ratio greater than 25 underwent fludrocortisone/ salt suppression testing for confirmation of autonomous aldosterone secretion. Postural testing, adrenal gland imaging, and adrenal ve-nous sampling were also performed. Individuals affected by FH-II demonstrated lack of suppression of plasma A levels after 4 days of dexamethasone treatment (0.5 mg every 6 h). All patients had neg
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increased dietary sodium is related to severity of obstructive sleep apnea in patients with resistant hypertension and Hyperaldosteronism
Chest, 2013Co-Authors: Eduardo Pimenta, Richard D Gordon, Michael Stowasser, Suzanne Oparil, Susan M Harding, Michel Batlouni, Bin Zhang, David A. CalhounAbstract:Background Obstructive sleep apnea (OSA) is a strong and independent risk factor for the development of hypertension, particularly resistant hypertension, and cardiovascular diseases. Patients with resistant hypertension have a high prevalence of OSA in association with elevated aldosterone levels, high salt intake, and salt-sensitive BP. The objective of this study was to determine whether dietary salt and aldosterone are associated with severity of OSA in patients with resistant hypertension. Methods Ninety-seven patients with resistant hypertension were prospectively evaluated by overnight polysomnography and 24-h urinary sodium and aldosterone levels while maintaining their usual diet. Hyperaldosteronism was defined as a plasma renin activity of Results Overall, patients' mean clinic BP was 156.3 ± 22.4/88.9 ± 13.3 mm Hg while taking an average of 4.3 ± 1.1 antihypertensive medications. Prevalence of OSA was 77.3%. Twenty-eight (28.9%) patients had Hyperaldosteronism. Urinary sodium level was an independent predictor of severity of OSA only in patients with Hyperaldosteronism. Conclusions The findings suggest that dietary salt is related to the severity of OSA in patients with resistant hypertension and Hyperaldosteronism. The results support dietary salt restriction as a treatment strategy for reduction of OSA severity in these patients.
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further study of chromosome 7p22 to identify the molecular basis of familial Hyperaldosteronism type ii
Journal of Human Hypertension, 2011Co-Authors: K J Carss, Richard D Gordon, Michael Stowasser, Kevin M OshaughnessyAbstract:Further study of chromosome 7p22 to identify the molecular basis of familial Hyperaldosteronism type II
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further evidence for linkage of familial Hyperaldosteronism type ii at chromosome 7p22 in italian as well as australian and south american families
Journal of Hypertension, 2008Co-Authors: Norlela Sukor, Paolo Mulatero, Franco Veglio, Richard D Gordon, David L Duffy, Chiara Bertello, Livia Kelemen, Y Jeske, Michael StowasserAbstract:Background Familial Hyperaldosteronism type II is a hereditary form of primary aldosteronism not attributable to the hybrid CYP11B1/CYP11B2 mutation that causes glucocorticoid remediable aldosteronism ( or familial Hyperaldosteronism type I). Although genetic defect(s) underlying familial Hyperaldosteronism type II have not yet been elucidated, linkage to chromosome 7p22 was previously reported in two Australian families and a South American family with familial Hyperaldosteronism type II.
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a novel genetic locus for low renin hypertension familial Hyperaldosteronism type ii maps to chromosome 7 7p22
Journal of Medical Genetics, 2000Co-Authors: Antony R Lafferty, Richard D Gordon, Michael Stowasser, David J Torpy, Susan E Taymans, Jing Ping Lin, Philip Huggard, Constantine A StratakisAbstract:Familial Hyperaldosteronism type II (FH-II) is caused by adrenocortical hyperplasia or aldosteronoma or both and is frequently transmitted in an autosomal dominant fashion. Unlike FH type I (FH-I), which results from fusion of the CYP11B1 and CYP11B2 genes, Hyperaldosteronism in FH-II is not glucocorticoid remediable. A large family with FH-II was used for a genome wide search and its members were evaluated by measuring the aldosterone:renin ratio. In those with an increased ratio, FH-II was confirmed by fludrocortisone suppression testing. After excluding most of the genome, genetic linkage was identified with a maximum two point lod score of 3.26 at θ=0, between FH-II in this family and the polymorphic markers D7S511, D7S517, and GATA24F03 on chromosome 7, a region that corresponds to cytogenetic band 7p22. This is the first identified locus for FH-II; its molecular elucidation may provide further insight into the aetiology of primary aldosteronism. Keywords: chromosome 7; aldosterone; familial Hyperaldosteronism type II; hypertension
Suzanne Oparil - One of the best experts on this subject based on the ideXlab platform.
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urinary sodium excretion predicts blood pressure response to spironolactone in patients with resistant hypertension independent of aldosterone status
Journal of Hypertension, 2016Co-Authors: Lama Ghazi, Suzanne Oparil, Tanja Dudenbostel, Chee Paul Lin, David A. CalhounAbstract:Objective:Resistant hypertension (RHTN), blood pressure (BP) at least 140/90 mmHg despite using at least three different medications, including a diuretic, is associated with high dietary sodium and Hyperaldosteronism. Mineralocorticoid receptor antagonists are recommended for treatment of RHTN, how
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increased dietary sodium is related to severity of obstructive sleep apnea in patients with resistant hypertension and Hyperaldosteronism
Chest, 2013Co-Authors: Eduardo Pimenta, Richard D Gordon, Michael Stowasser, Suzanne Oparil, Susan M Harding, Michel Batlouni, Bin Zhang, David A. CalhounAbstract:Background Obstructive sleep apnea (OSA) is a strong and independent risk factor for the development of hypertension, particularly resistant hypertension, and cardiovascular diseases. Patients with resistant hypertension have a high prevalence of OSA in association with elevated aldosterone levels, high salt intake, and salt-sensitive BP. The objective of this study was to determine whether dietary salt and aldosterone are associated with severity of OSA in patients with resistant hypertension. Methods Ninety-seven patients with resistant hypertension were prospectively evaluated by overnight polysomnography and 24-h urinary sodium and aldosterone levels while maintaining their usual diet. Hyperaldosteronism was defined as a plasma renin activity of Results Overall, patients' mean clinic BP was 156.3 ± 22.4/88.9 ± 13.3 mm Hg while taking an average of 4.3 ± 1.1 antihypertensive medications. Prevalence of OSA was 77.3%. Twenty-eight (28.9%) patients had Hyperaldosteronism. Urinary sodium level was an independent predictor of severity of OSA only in patients with Hyperaldosteronism. Conclusions The findings suggest that dietary salt is related to the severity of OSA in patients with resistant hypertension and Hyperaldosteronism. The results support dietary salt restriction as a treatment strategy for reduction of OSA severity in these patients.
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rapid reversal of left ventricular hypertrophy and intracardiac volume overload in patients with resistant hypertension and Hyperaldosteronism a prospective clinical study
Hypertension, 2010Co-Authors: Krishna K Gaddam, Cecilia Corros, Eduardo Pimenta, Mustafa I Ahmed, Thomas S Denney, Inmaculada Aban, Seidu Inusah, Himanshu Gupta, Steven G Lloyd, Suzanne OparilAbstract:We have shown previously that patients with resistant hypertension and Hyperaldosteronism have increased brain natriuretic peptide suggestive of increased intravascular volume. In the present study, we tested the hypothesis that Hyperaldosteronism contributes to cardiac volume overload. Thirty-seven resistant hypertensive patients with Hyperaldosteronism (urinary aldosterone ≥12 μg/24 hours and plasma renin activity ≤1.0 ng/mL per hour) and 71 patients with normal aldosterone status were studied. Both groups had similar blood pressure and left ventricular mass, whereas left and right ventricular end-diastolic volumes measured by cardiac MRI were greater in high versus normal aldosterone subjects ( P
Paula Weissmann - One of the best experts on this subject based on the ideXlab platform.
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Hyperaldosteronism among black and white subjects with resistant hypertension
Hypertension, 2002Co-Authors: David A. Calhoun, Mari K. Nishizaka, Mohammad A Zaman, Roopal B Thakkar, Paula WeissmannAbstract:Recent reports suggesting that the prevalence of primary Hyperaldosteronism may be higher than historically thought have relied on an elevated plasma aldosterone concentration/plasma renin activity ratio to either diagnose or identify subjects at high risk of having primary Hyperaldosteronism and have not included suppression testing of all evaluated subjects. In this prospective study of 88 consecutive patients referred to a university clinic for resistant hypertension, we determined the 24-hour urinary aldosterone excretion during high dietary salt ingestion, baseline plasma renin activity, and plasma aldosterone in all subjects. Primary Hyperaldosteronism was confirmed if plasma renin activity was 12 μg/24-hour during high urinary sodium excretion (>200 mEq/24-hour). Eighteen subjects (20%) were confirmed to have primary Hyperaldosteronism. The prevalence of Hyperaldosteronism was similar in black and white subjects. Of the 14 subjects with confirmed Hyperaldosteronism who have been treated with spironolactone, all have manifested a significant reduction in blood pressure. In this population, an elevated plasma aldosterone/plasma renin activity ratio (>20) had a sensitivity of 89% and a specificity of 71% with a corresponding positive predictive value of 44% and a negative predictive value of 96%. These data provide strong evidence that Hyperaldosteronism is a common cause of resistant hypertension in black and white subjects. The accuracy of these results is strengthened by having done suppression testing of all evaluated subjects.
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Hyperaldosteronism among black and white subjects with resistant hypertension
Hypertension, 2002Co-Authors: David A. Calhoun, Mohammad A Zaman, Roopal B Thakkar, Mari Nishizaka, Paula WeissmannAbstract:Recent reports suggesting that the prevalence of primary Hyperaldosteronism may be higher than historically thought have relied on an elevated plasma aldosterone concentration/plasma renin activity ratio to either diagnose or identify subjects at high risk of having primary Hyperaldosteronism and have not included suppression testing of all evaluated subjects. In this prospective study of 88 consecutive patients referred to a university clinic for resistant hypertension, we determined the 24-hour urinary aldosterone excretion during high dietary salt ingestion, baseline plasma renin activity, and plasma aldosterone in all subjects. Primary Hyperaldosteronism was confirmed if plasma renin activity was 12 microg/24-hour during high urinary sodium excretion (>200 mEq/24-hour). Eighteen subjects (20%) were confirmed to have primary Hyperaldosteronism. The prevalence of Hyperaldosteronism was similar in black and white subjects. Of the 14 subjects with confirmed Hyperaldosteronism who have been treated with spironolactone, all have manifested a significant reduction in blood pressure. In this population, an elevated plasma aldosterone/plasma renin activity ratio (>20) had a sensitivity of 89% and a specificity of 71% with a corresponding positive predictive value of 44% and a negative predictive value of 96%. These data provide strong evidence that Hyperaldosteronism is a common cause of resistant hypertension in black and white subjects. The accuracy of these results is strengthened by having done suppression testing of all evaluated subjects.