ArticleCureus2024
A Case of Primary Aldosteronism Masquerading as Bartter and Gitelman Syndromes.
Article in Cureus, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
Who cites it
1 citing paper in PubMed.
- Familial Hyperaldosteronism Type IV (FH-IV)-Clinical Phenotypes, Genetics and Management ofJournal of clinical medicine · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary aldosteronism (PA) is a common cause of secondary hypertension, with familial hyperaldosteronism (FH) contributing to a lesser number of cases. FH type IV, a rare subtype, has hardly been reported as a subtype of PA cases. We present a case of a 27-year-old female who presented to the emergency department with circumoral tingling and numbness. A diagnosis of hypocalcemia due to vitamin D deficiency was made. During hospital stay, she developed acute gastroenteritis and was treated with doxycycline, after which she experienced persistent hypokalemia. Further investigation revealed urinary potassium loss and metabolic alkalosis, although her blood pressure remained normal throughout her stay. Clinical exome sequencing identified a mutated variant in the calcium voltage-gated channel subunit alpha1 H (CACNA1H) gene associated with FH type IV. Elevated plasma aldosterone and suppressed renin confirmed PA. The administration of doxycycline for treating acute gastroenteritis likely precipitated hypokalemia by enhancing the expression of the mutated CACNA1H
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