Evidence map›Paper›PMID 30739536›Full record

ArticleHypertension (Dallas, Tex. : 1979)2019

Genetic Characteristics of Aldosterone-Producing Adenomas in Blacks.

Kazutaka Nanba, Kei Omata, Celso E Gomez-Sanchez, Constantine A Stratakis, Andrew P Demidowich, Mari Suzuki, Lester D R Thompson, Debbie L Cohen, James M Luther, Lan Gellert and 6 more

Open access · bronzeAbstract readMulticenter Study
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed, 1 pooled it
17.1field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

100 citing papers in PubMed, 1 synthesis or guideline pooled it, 162 citations in OpenAlex.

  1. Pooled it
  2. Evaluation of Aldosterone Suppression by Cinnarizine, a Putative Cav1.3 Inhibitor.The Journal of clinical endocrinology and metabolism · 2025
    Trial
  3. [Nature medicine · 2023
    Trial
  4. Trial
  5. Aldosterone-Producing Lesions HarboringHypertension (Dallas, Tex. : 1979) · 2026
    Article
  6. Review
  7. Article
  8. Race and Ancestry in Primary Aldosteronism.Journal of the American Heart Association · 2026
    Article
  9. Primary aldosteronism.Nature reviews. Disease primers · 2026
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Sexual dimorphism in benign adrenocortical tumours.European journal of endocrinology · 2025
    Review
  20. Review

40 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 7 institutions in 2 countries.

Kazutaka NanbaFrom the Department of Molecular and Integrative Physiology (K.N., W.E.R.), University of Michigan, Ann Arbor.
Kei OmataDepartment of Pathology (K.O., T.J.G., S.A.T.), University of Michigan, Ann Arbor.
Celso E Gomez-SanchezEndocrine and Research Service, G.V. (Sonny) Montgomery VA Medical Center, Jackson, MS (C.E.G.-S.).
Constantine A StratakisSection of Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD (C.A.S., A.P.D., M.S.).
Andrew P DemidowichSection of Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD (C.A.S., A.P.D., M.S.).
Mari SuzukiSection of Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD (C.A.S., A.P.D., M.S.).
Lester D R ThompsonDepartment of Pathology, Woodland Hills Medical Center, Southern California Permanente Medical Group (L.D.R.T.).
Debbie L CohenRenal, Electrolyte and Hypertension Division, Perelman School of Medicine, University of Pennsylvania, Philadelphia (D.L.C.).
James M LutherDivision of Clinical Pharmacology (J.M.L.), Vanderbilt University Medical Center, Nashville, TN.
Lan GellertDepartment of Pathology, Microbiology and Immunology (L.G.), Vanderbilt University Medical Center, Nashville, TN.
Anand VaidyaCenter for Adrenal Disorders, Division of Endocrinology, Diabetes, and Hypertension (A.V.), Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Justine A BarlettaDepartment of Pathology (J.A.B.), Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Tobias ElseDivision of Metabolism, Endocrine, and Diabetes, Department of Internal Medicine (T.E., T.J.G., W.E.R.), University of Michigan, Ann Arbor.
Thomas J GiordanoDepartment of Pathology (K.O., T.J.G., S.A.T.), University of Michigan, Ann Arbor.
Scott A TomlinsDepartment of Pathology (K.O., T.J.G., S.A.T.), University of Michigan, Ann Arbor.
William E RaineyFrom the Department of Molecular and Integrative Physiology (K.N., W.E.R.), University of Michigan, Ann Arbor.
University of Michigan–Ann Arbor · USEunice Kennedy Shriver National Institute of Child Health and Human Development · USVanderbilt University Medical Center · USMichigan Center for Translational Pathology · USUniversity of Mississippi Medical Center · USUniversity of Pennsylvania · USWoodland Hills Medical Center · US

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI THEODORE S LAWRENCE · 1988 to 2026
$178.2M
Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
Tracking and Evaluation CoreU54GM115428 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI GRANGER, JOEY P. · 2016 to 2025
$38.2M
Molecular Genetics of Endocrine Tumors and Related DisordersZIAHD008920 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI STRATAKIS, CONSTANTINE A. · 2012 to 2021
$25.8M
Unrecognized Primary Aldosteronism as a Pathogenic Mechanism for Chronic Kidney Disease in DiabetesR01DK115392 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI Anand Vaidya · 2018 to 2026
$6.0M
Adrenal Origins of Aldosterone ExcessR01DK106618 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI William E Rainey, Aaron Mark Udager · 2016 to 2026
$6.0M
ROLE OF MINERALOCORTICOIDS IN LOW-RENIN HYPERTENSIONR01HL027255 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI GOMEZ-SANCHEZ, CELSO ENRIQUE · 1985 to 2017
$3.9M
Endogenous Aldosterone and Glucose HomeostasisR01DK096994 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI LUTHER, JAMES MATTHEW · 2013 to 2017
$2.1M
The Genetics of Primary AldosteronismR01HL130106 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ELSE, TOBIAS · 2016 to 2020
$1.9M
NCI NIH HHS P30 CA046592NCI NIH HHS P30 CA068485NHLBI NIH HHS R01 HL027255NHLBI NIH HHS R01 HL130106NIDDK NIH HHS R01 DK096994NIDDK NIH HHS R01 DK106618NIDDK NIH HHS R01 DK115392NIGMS NIH HHS U54 GM115428
6 · The paper itself

Abstract

Somatic mutations have been identified in aldosterone-producing adenomas (APAs) in genes that include KCNJ5, ATP1A1, ATP2B3, and CACNA1D. Based on independent studies, there appears to be racial differences in the prevalence of somatic KCNJ5 mutations, particularly between East Asians and Europeans. Despite the high cardiovascular disease mortality of blacks, there have been no studies focusing on somatic mutations in APAs in this population. In the present study, we investigated genetic characteristics of APAs in blacks using a CYP11B2 (aldosterone synthase) immunohistochemistry-guided next-generation sequencing approach. The adrenal glands with adrenocortical adenomas from 79 black patients with primary aldosteronism were studied. Seventy-three tumors from 69 adrenal glands were confirmed to be APAs by CYP11B2 immunohistochemistry. Sixty-five of 73 APAs (89%) had somatic mutations in aldosterone-driver genes. Somatic CACNA1D mutations were the most prevalent genetic alteration (42%), followed by KCNJ5 (34%), ATP1A1 (8%), and ATP2B3 mutations (4%). CACNA1D mutations were more often observed in APAs from males than those from females (55% versus 29%, P=0.033), whereas KCNJ5 mutations were more prevalent in APAs from females compared with those from males (57% versus 13%, P<0.001). No somatic mutations in aldosterone-driver genes were identified in tumors without CYP11B2 expression. In conclusion, 89% of APAs in blacks harbor aldosterone-driving mutations, and unlike Europeans and East Asians, the most frequently mutated aldosterone-driver gene was CACNA1D. Determination of racial differences in the prevalence of aldosterone-driver gene mutations may facilitate the development of personalized medicines for patients with primary aldosteronism.

Indexed as

Black or African AmericanGenetic Predisposition to DiseaseMutationAdrenal Cortex NeoplasmsAdrenal GlandsAdrenocortical AdenomaAldosteroneDNA Mutational AnalysisDNA, NeoplasmHumansIncidenceUnited StatesAldosteroneDNA, Neoplasmadrenal glandsadrenocortical adenomaaldosteronehyperaldosteronismmutation

Identifiers

PMID30739536
PMCPMC6416065
OpenAlexW2913638577

What OpenQuestion holds

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Registered trials

None linked

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.