ArticleHypertension (Dallas, Tex. : 1979)2018
Cellular and Genetic Causes of Idiopathic Hyperaldosteronism.
Article in Hypertension (Dallas, Tex. : 1979), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
104 citing papers in PubMed, 1 synthesis or guideline pooled it, 193 citations in OpenAlex.
- Identification of risk loci for primary aldosteronism in genome-wide association studies.Nature communications · 2022Pooled it
- Evaluation of Aldosterone Suppression by Cinnarizine, a Putative Cav1.3 Inhibitor.The Journal of clinical endocrinology and metabolism · 2025Trial
- A controlled trial of percutaneous adrenal arterial embolization for hypertension in patients with idiopathic hyperaldosteronism.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Trial
- [Nature medicine · 2023Trial
- ACTH Stimulation Maximizes the Accuracy of Peripheral Steroid Profiling in Primary Aldosteronism Subtyping.The Journal of clinical endocrinology and metabolism · 2021Trial
- Aldosterone-Producing Lesions HarboringHypertension (Dallas, Tex. : 1979) · 2026Article
- Gut microbiome dysbiosis is associated with aldosterone overproduction in idiopathic hyperaldosteronism.iScience · 2026Article
- From bench to bedside: primary aldosteronism revisited.Endocrine connections · 2026Article
- Rare germline variants in canonical and candidate genes in apparently sporadic bilateral primary aldosteronism.Journal of the Endocrine Society · 2026Article
- Primary aldosteronism.Nature reviews. Disease primers · 2026Review
- Integrated Transcriptomics Reveals Evolutionary Trajectories and Cell Density-Dependent Mechanisms in Aldosterone-Producing Adenomas.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Partially Successful Adrenal Vein Sampling With and Without Cross-Sectional Imaging in Primary Aldosteronism Subtyping.Hypertension (Dallas, Tex. : 1979) · 2026Article
- Increased Frequency and Distinct Genotypic Patterns of Somatic Aldosterone-Driver Mutations in Aldosterone-Producing Micronodules from Primary Aldosteronism Patients.Endocrine pathology · 2026Article
- The role of arachidonic acid metabolites in the subtype classification and pathogenesis of primary aldosteronism.iScience · 2026Article
- The genetics of hypertension.Nature reviews. Nephrology · 2026Review
- Emerging methods for subtype differentiation in primary aldosteronism.Journal of internal medicine · 2026Review
- Case Report: SomaticFrontiers in medicine · 2026Article
- Bilateral adrenal heterogeneity in contrast-enhanced CT for differentiating nodule-negative primary aldosteronism.Abdominal radiology (New York) · 2025Article
- Subclinical primary aldosteronism.Archives of endocrinology and metabolism · 2025Review
- Cosyntropin-Stimulated Aldosterone Reserve of the Nondominant Adrenal Predicts Surgical Outcomes in Primary Aldosteronism.Hypertension (Dallas, Tex. : 1979) · 2025Article
44 more citing papers are in PubMed but not listed here.
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12 authors at 3 institutions in 2 countries.
Funding
Abstract
Primary aldosteronism affects ≈5% to 10% of hypertensive patients and has unilateral and bilateral forms. Most unilateral primary aldosteronism is caused by computed tomography-detectable aldosterone-producing adenomas, which express CYP11B2 (aldosterone synthase) and frequently harbor somatic mutations in aldosterone-regulating genes. The cause of the most common bilateral form of primary aldosteronism, idiopathic hyperaldosteronism (IHA), is believed to be diffuse hyperplasia of aldosterone-producing cells within the adrenal cortex. Herein, a multi-institution cohort of 15 IHA adrenals was examined with CYP11B2 immunohistochemistry and next-generation sequencing. CYP11B2 immunoreactivity in adrenal glomerulosa harboring non-nodular hyperplasia was only observed in 4/15 IHA adrenals suggesting that hyperplasia of CYP11B2-expressing cells may not be the major cause of IHA. However, the adrenal cortex of all IHA adrenals harbored at least 1 CYP11B2-positive aldosterone-producing cell cluster (APCC) or micro-aldosterone-producing adenomas. The number of APCCs per case (and individual APCC area) in IHA adrenals was significantly larger than in normotensive controls. Next-generation sequencing of DNA from 99 IHA APCCs demonstrated somatic mutations in genes encoding the L-type calcium voltage-gated channel subunit α 1-D ( CACNA1D, n=57; 58%) and potassium voltage-gated channel subfamily J-5 ( KCNJ5, n=1; 1%). These data suggest that IHA may result from not only hyperplasia but also the accumulation or enlargement of computed tomography-undetectable APCC harboring somatic aldosterone-driver gene mutations. The high prevalence of mutations in the CACNA1D L-type calcium channel provides a potential actionable therapeutic target that could complement mineralocorticoid blockade and inhibit aldosterone overproduction in some IHA patients.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.