ReviewJournal of human hypertension2017
Familial hyperaldosteronism type III.
Review in Journal of human hypertension, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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
12 citing papers in PubMed, 49 citations in OpenAlex.
- Adrenal causes of endocrine hypertension in childhood or adolescence.Journal of endocrinological investigation · 2025Review
- Relevance ofInternational journal of molecular sciences · 2023Review
- Who should be screened for primary aldosteronism? A comprehensive review of current evidence.Journal of clinical hypertension (Greenwich, Conn.) · 2022Review
- Progress on Genetic Basis of Primary Aldosteronism.Biomedicines · 2021Review
- Review
- Diseases caused by mutations in the NaAmerican journal of physiology. Cell physiology · 2021Review
- Advances in Genomics Research of Blood Pressure Responses to Dietary Sodium and Potassium Intakes.Hypertension (Dallas, Tex. : 1979) · 2021Review
- Mosaicism for KCNJ5 Causing Early-Onset Primary Aldosteronism due to Bilateral Adrenocortical Hyperplasia.American journal of hypertension · 2020Article
- Overview of Monogenic Forms of Hypertension Combined With Hypokalemia.Frontiers in pediatrics · 2020Review
- Primary Aldosteronism: KCNJ5 Mutations and Adrenocortical Cell Growth.Hypertension (Dallas, Tex. : 1979) · 2019Article
- Familial hyperaldosteronism type III a novel case and review of literature.Reviews in endocrine & metabolic disorders · 2019Review
- Comparative Genomics and Transcriptome Profiling in Primary Aldosteronism.International journal of molecular sciences · 2018Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary aldosteronism is the most common form of endocrine hypertension. This disorder comprises both sporadic and familial forms. Four familial forms of primary aldosteronism (FH-I to FH-IV) have been described. FH-III is caused by germline mutations in KCNJ5, encoding the potassium channel Kir3.4 (also called GIRK4). These mutations alter the selectivity filter of the channel and lead to abnormal ion currents with loss of potassium selectivity, sodium influx and consequent increased intracellular calcium that causes excessive aldosterone biosynthesis. To date, eleven families have been reported, carrying six different mutations. Although the clinical features are variable, FH-III patients often display severe hyperaldosteronism with an early onset, associated with hypokalemia and diabetes insipidus-like symptoms. In most cases FH-III patients are resistant to pharmacological therapy and require bilateral adrenalectomy to control symptoms. In the present manuscript, we review the genetics and pathological basis of FH-III, the diagnostic work-up, clinical features and therapeutic management. Finally, we will describe a new case of FH-III of an Italian patient carrying a Gly151Arg mutation.
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Registered trials
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.