Secondary Hyperaldosteronism

Last update 08 May 2025

Basic Info

Synonyms

Aldosteronism Secondary, Aldosteronism secondary, Hyperaldosteronism, secondary

+ [13]

Introduction

A form of hyperaldosteronism caused by abnormally increased renin levels. [https://orcid.org/0000-0002-0538-4547]

Clinical Trials associated with Secondary Hyperaldosteronism

NCT02938910

/ CompletedNot ApplicableIIT

Study of Myocardial Interstitial Fibrosis in Hyperaldosteronism Noninvasive Comparative Study in Humans of the Respective Cardiovascular Effects of Hyperaldosteronism and Hypertension by Magnetic Resonance Imaging

Animal models have demonstrated the role of aldosterone in left ventricular remodeling involving fibrosis, apoptosis and hypertrophy. Myocardial fibrosis is a risk factor for serious arrhythmia and sudden death in ischemic and idiopathic hypertrophic heart disease. It is accepted that patients with primary aldosteronism have a higher prevalence of LV hypertrophy , arterial involvement and increased cardiovascular risk. In humans, a link has been demonstrated between aldosterone and heart failure as well as the benefit of the administration of an anti -aldosterone drug to lower mortality in this population , regardless of blood pressure level . The administration of spironolactone ( aldosterone ) in hypertensive rats has prevented the occurrence of aortic fibrosis . Plasma aldosteronism in humans has been associated with inflammation, fibrosis and aortic stiffness . However, primary aldosteronism is generally associated with so-called secondary hypertension . Chronic hypertension alone is a recognized etiological factor of myocardial hypertrophy ( myocardial fibrosis very advanced ) . The purpose of this study is to investigate the effects of MRI hyperaldosteronism on the heart.

Start Date01 Nov 2012

Sponsor / Collaborator

Assistance Publique des Hôpitaux de Paris SA

100 Clinical Results associated with Secondary Hyperaldosteronism

100 Translational Medicine associated with Secondary Hyperaldosteronism

0 Patents (Medical) associated with Secondary Hyperaldosteronism

679

Literatures (Medical) associated with Secondary Hyperaldosteronism

01 May 2025·Journal of Hypertension

Local release of renin unveils intrarenal arterial fibromuscular dysplasia

Article

Author: Mansueto, Giancarlo ; Contro, Alberto ; Dal Pont, Chiara ; Fava, Cristiano ; Minuz, Pietro ; Sartorio, Andrea

A previously healthy young man developed severe hypertension requiring triple antihypertensive therapy. Initial evaluation identified hyperreninemic hyperaldosteronism, mild hypokalaemia, hypodensity within the right kidney at computed tomography (CT), normal renal arteries at echography. He was referred to Verona ESH Centre were angio-CT revealed significant stenosis of an aberrant branch artery of the right kidney with hypo-perfused area colocalizing with a hypo-oxygenated area, as assessed by BOLD-MR imaging. Super-selective sampling found high plasma renin concentrations only in the vein draining the lower pole of the right kidney. Renal angiography confirmed tightened stenosis of an aberrant branch artery supplying the lower arterial segments, consistent with unifocal medial fibromuscular dysplasia, successfully treated with angioplasty. Investigating extra-renal sites, angio-MR found an S-shaped loop of extracranial left internal carotid artery, consistent with multisite fibromuscular dysplasia. This clinical case underscores the importance of comprehensive functional and imaging tests to identify elusive causes of secondary hypertension.

01 Mar 2025·Clinical Case Reports

Rare Case of Adult‐Onset Gitelman Syndrome in a Patient With Multiple Comorbidities: A Case Report

Article

Author: Hussen, Md. Deluwar ; Ony, Merazul Islam ; Sultana, Fariha ; Joba, Fabeha Akter ; Tabassum, Zareen ; Rezwana, Fareha

ABSTRACTGitelman Syndrome (GS) is a renal tubulopathy transmitted in an autosomal recessive manner. Its primary cause is mutations Of SLC12A3 (Solute Carrier Family 12 Member 3) gene that encodes the sodium‐chloride co‐transporter and is characterized by hypokalemia, hypocalciuria, hypomagnesemia, and metabolic alkalosis. It appears in most cases in adolescents or early adulthood, but with end‐organ disease in later adulthood with other comorbid conditions. The patient was a 55‐year‐old woman with refractory electrolyte disturbances comprising low potassium, calcium, and metabolic alkalosis, history of NASH (non‐alcoholic steatohepatitis) cirrhosis, benzodiazepine poisoning, and gastric polyps. Persistent electrolyte abnormalities were most likely worsening renal failure before improvement with the addition of spironolactone. Urinary magnesium/creatinine ratios above 1 were indicative of GS. Electrolyte imbalances were recurring in both her and her late mother, which even existed throughout her childhood. Persistent electrolyte abnormalities in this patient's chronic NASH cirrhosis would probably worsen due to secondary hyperaldosteronism. Supplementation of potassium, calcium, and magnesium failed to address the refractory hypokalemia and hypocalcemia, and hypomagnesemia. So spironolactone was initiated, which resulted in a successful resolution of the condition. Clinical diagnosis of GS made based on biochemical markers due to an existing strong familial pattern of similar electrolyte manifestations since a genetic test for the condition was unavailable. This case shows the issue of disease synergy and how various diseases relate and need specific methods of treatment. The patient's status requires constant observation and the investigation of the possible hereditary renal –tubular disorders.

01 Mar 2025·Redox Biology

EGR1 regulates oxidative stress and aldosterone production in adrenal cells and aldosterone-producing adenomas

Article

Author: Knösel, Thomas ; Gong, Siyuan ; Sun, Zhuolun ; Pang, Yingxian ; Wolf, Eckhard ; Kemter, Elisabeth ; Mir-Bashiri, Sanas ; Williams, Tracy Ann ; Bidlingmaier, Martin ; Reincke, Martin ; Tetti, Martina

Aldosterone-producing adenomas (APAs) are a major cause of primary aldosteronism, a common form of endocrine hypertension. Here, we demonstrate that Early Growth Response 1 (EGR1) plays a dual role in adrenal cell biology, regulating both oxidative stress and aldosterone production. Using RNA sequencing of RSL3-treated human adrenal cells and spatial transcriptomics of adrenal glands from patients with primary aldosteronism, we identify EGR1 as a key gene associated with RSL3-related oxidative stress and APAs. We show that EGR1 silencing decreases oxidative stress and increases CYP11B2 gene expression and aldosterone production in adrenal cells, while its overexpression has the opposite effects. Notably, EGR1 expression is downregulated in APAs and aldosterone-producing micronodules compared to the adjacent adrenal cortex, which correlates in part with decreased levels of oxidative stress markers. The adrenal cortex of pigs with secondary hyperaldosteronism shows decreased immunostaining of EGR1 and a marker of oxidative stress, suggesting a potential link between EGR1 expression, oxidative stress levels, and adrenocortical function. These findings reveal a novel mechanism linking EGR1 to oxidative stress regulation and aldosterone production in adrenal cells, with potential implications for the pathogenesis of APAs and other adrenocortical tumors.

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Secondary Hyperaldosteronism

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