ReviewGland surgery2020
Hereditary causes of primary aldosteronism and other disorders of apparent excess mineralocorticoid activity.
Review in Gland surgery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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
4 citing papers in PubMed, 10 citations in OpenAlex.
- Functional properties of the γ-ENaC-A635V mutation in a patient with severe hyponatremia.Hormones (Athens, Greece) · 2025Article
- Clofibrate, a Peroxisome Proliferator-Activated Receptor-Alpha (PPARα) Agonist, and Its Molecular Mechanisms of Action against Sodium Fluoride-Induced Toxicity.Biological trace element research · 2022Article
- Review of the Pathophysiologic and Clinical Aspects of Hypokalemia in Children and Young Adults: an Update.Current treatment options in pediatrics · 2022Review
- Hypokalemia and hypertensive urgency in a 10-year-old boy: Answers.Pediatric nephrology (Berlin, Germany) · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Secondary hypertension is a common condition with a broad differential diagnosis. Identification of the true cause of hypertension can be critical for guiding appropriate management. Here, we review hereditary conditions underlying the most common cause of secondary hypertension, primary aldosteronism, as well as other disorders impacting various levels of mineralocorticoid action. Recently, several pathogenic variants of ion channels have been described as etiologies of familial aldosteronism. Defects in steroid hormone synthesis cause hypertension in 11β-hydroxylase deficiency and 17α-hydroxylase deficiency, two types of congenital adrenal hyperplasia. Inappropriate activation of mineralocorticoid receptors underlies the syndrome of apparent mineralocorticoid excess and constitutive activation of the mineralocorticoid receptor. Finally, Liddle syndrome and pseudohypoaldosteronism type 2 are disorders impacting the function of renal sodium channels, the endpoint of mineralocorticoid action. We discuss the pathophysiology, clinical presentation, diagnosis and management of these low renin hypertension states that ultimately result in apparent excess mineralocorticoid activity.
Indexed as
Identifiers
What OpenQuestion holds
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.