Aldosterone and Metabolic Syndrome

Krug, Alexander W.; Ehrhart‐Bornstein, Monika

doi:10.1161/hypertensionaha.107.109439

Cited by 89 publications

(35 citation statements)

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“…Previous observations suggested that mineralocorticoid excess may induce abnormalities in insulin secretion and action 11 and, consequently, higher prevalence of hyperglycaemia or diabetes mellitus in patients with PA. [11][12][13] However, in a recent crosssectional study no differences in fasting plasma glucose levels were noted in patients with PA and EH. 16 This is in agreement with our present study in which we also did not find any significant differences in the fasting plasma glucose levels and prevalence of diabetes mellitus between all groups including EH.…”

Section: Discussionmentioning

confidence: 99%

“…Our results are compatible with our earlier findings that in patients with PA there are no differences in the prevalence of diabetes mellitus before and after adrenalectomy. 29 Aldosterone can also affect insulin receptor function 11,30 with adverse metabolic consequences. Potential proadipogenic role of aldosterone with subsequent negative effect on insulin sensitivity through production of cytokines (adipocytokines)/ fatty acids was reported.…”

Section: Discussionmentioning

confidence: 99%

“…Potential proadipogenic role of aldosterone with subsequent negative effect on insulin sensitivity through production of cytokines (adipocytokines)/ fatty acids was reported. 11,30 Differences between the production of various cytokines/fatty acids between two main forms of aldosterone overproduction may thus also have a role. It has been shown that metabolic parameters in PA and EH are related to adiponectin gene variants.…”

Section: Discussionmentioning

confidence: 99%

“…7,8 Indeed, as we have shown recently, patients with PA have an increased intima-media thickness of the carotid artery and higher aortic stiffness compared with EH. 9,10 Aldosterone concentrations are elevated in obese and MS patients, 11 there is an increasing body of evidence linking elevated plasma aldosterone levels to MS and its components. Clinical evidence also suggests that angiotensin II-stimulated secretion and/or stimulation of aldosterone by adipose tissue may be enhanced in obese subjects.…”

Section: Introductionmentioning

confidence: 99%

“…Clinical evidence also suggests that angiotensin II-stimulated secretion and/or stimulation of aldosterone by adipose tissue may be enhanced in obese subjects. 11,12 It was reported that prevalence of MS in patients with PA is higher compared with EH. [13][14][15] These results were, however, questioned by recent cross-sectional study of Matrozova et al, 16 in which the investigators found no significant differences in metabolic abnormalities between patients with PA and EH.…”

Section: Introductionmentioning

confidence: 99%

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The prevalence of metabolic syndrome and its components in two main types of primary aldosteronism

et al. 2010

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Metabolic syndrome (MS) is frequent clinical condition in patients with hypertension. Primary aldosteronism (PA) is a common form of secondary hypertension. This study was aimed at investigating the prevalence of the MS and its components in the two major forms of PA, in unilateral aldosterone-producing adenoma (APA) and bilateral aldosterone overproduction because of idiopathic hyperaldosteronism (IHA). The diagnosis of the particular form of PA was based on adrenal venous sampling and/or successful surgery confirmed by histopathological examination. We analyzed clinical and laboratory data from 100 patients with PA (50 patients with IHA and 50 patients with APA) and from 90 patients with essential hypertension (EH). Metabolic profiles of patients with bilateral form of PA (because of IHA) were similar to EH, but differed from those in patients with unilateral form of PA (APA). The prevalence of the MS (62% in IHA, 34% in APA and 56% in EH), the body mass index value (30 ± 4 kg m -2 in IHA, 27±5 kg m -2 in APA and 29±5 kg m -2 in EH) and triglycerides levels (1.9±0.9 mmol l -1 in IHA,1.4± 0.8 mmol l -1 in APA and 2.01 ± 1.39 mmol l -1 in EH) were all significantly (Po0.05) higher in IHA compared with APA patients. Metabolic profile of patients with bilateral form of PA (because of IHA) is similar to EH in contrast to unilateral form of PA (APA).

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The prevalence of metabolic syndrome and its components in two main types of primary aldosteronism

et al. 2010

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Aldosterone Synthase Inhibition With Lorundrostat for Uncontrolled Hypertension

Laffin,

Rodman,

Luther

et al. 2023

JAMA

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ImportanceExcess aldosterone production contributes to hypertension in both classical hyperaldosteronism and obesity-associated hypertension. Therapies that reduce aldosterone synthesis may lower blood pressure.ObjectiveTo compare the safety and efficacy of lorundrostat, an aldosterone synthase inhibitor, with placebo, and characterize dose-dependent safety and efficacy to inform dose selection in future trials.Design, Setting, and ParticipantsRandomized, placebo-controlled, dose-ranging trial among adults with uncontrolled hypertension taking 2 or more antihypertensive medications. An initial cohort of 163 participants with suppressed plasma renin (plasma renin activity [PRA] ≤1.0 ng/mL/h) and elevated plasma aldosterone (≥1.0 ng/dL) were enrolled, with subsequent enrollment of 37 participants with PRA greater than 1.0 ng/mL/h.InterventionsParticipants were randomized to placebo or 1 of 5 dosages of lorundrostat in the initial cohort (12.5 mg, 50 mg, or 100 mg once daily or 12.5 mg or 25 mg twice daily). In the second cohort, participants were randomized in a 1:6 ratio to placebo or lorundrostat, 100 mg once daily.Main Outcomes and MeasuresThe primary end point was change in automated office systolic blood pressure from baseline to study week 8.ResultsBetween July 2021 and June 2022, 200 participants were randomized, with final follow-up in September 2022. Following 8 weeks of treatment in participants with suppressed PRA, changes in office systolic blood pressure of −14.1, −13.2, −6.9, and −4.1 mm Hg were observed with 100 mg, 50 mg, and 12.5 mg once daily of lorundrostat and placebo, respectively. Observed reductions in systolic blood pressure in individuals receiving twice-daily doses of 25 mg and 12.5 mg of lorundrostat were −10.1 and −13.8 mm Hg, respectively. The least-squares mean difference between placebo and treatment in systolic blood pressure was −9.6 mm Hg (90% CI, −15.8 to −3.4 mm Hg; P = .01) for the 50-mg once-daily dose and −7.8 mm Hg (90% CI, −14.1 to −1.5 mm Hg; P = .04) for 100 mg daily. Among participants without suppressed PRA, 100 mg once daily of lorundrostat decreased systolic blood pressure by 11.4 mm Hg (SD, 2.5 mm Hg), which was similar to blood pressure reduction among participants with suppressed PRA receiving the same dose. Six participants had increases in serum potassium above 6.0 mmol/L that corrected with dose reduction or drug discontinuation. No instances of cortisol insufficiency occurred.Conclusions and RelevanceAmong individuals with uncontrolled hypertension, use of lorundrostat was effective at lowering blood pressure compared with placebo, which will require further confirmatory studies.Trial RegistrationClinicalTrials.gov Identifier: NCT05001945

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