Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Primary aldosteronism: a new understanding

R D Gordon1

  • 1Hypertension Unit, Greenslopes Hospital, Brisbane, Australia.

Clinical and Experimental Hypertension (New York, N.Y. : 1993)
|July 1, 1997
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

ARMC5 is not implicated in familial hyperaldosteronism type II (FH-II).

Journal of human hypertension·2017
Same author

Treatment of primary aldosteronism is associated with a reduction in the severity of obstructive sleep apnoea.

Journal of human hypertension·2017
Same author

Salt, aldosterone and hypertension.

Journal of human hypertension·2012
Same author

Rapid Flush Technique for Donor Hepatectomy: Safety and Efficacy of an Improved Method of Liver Recovery for Transplantation.

Transplantation proceedings·2011
Same author

Factors affecting the aldosterone/renin ratio.

Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme·2011
Same author

Outcome after Liver Transplantation for Cystic Fibrosis.

Pediatric pulmonology. Supplement·2011
Same journal

Adiponectin improves the aortic dissection by inhibiting inflammatory cell infiltration and macrophage pyroptosis.

Clinical and experimental hypertension (New York, N.Y. : 1993)·2026
Same journal

Electroacupuncture for essential hypertension: Mechanistic insights, current clinical evidence, and translational challenges.

Clinical and experimental hypertension (New York, N.Y. : 1993)·2026
Same journal

Association of intracranial atherosclerotic stenosis with 1-year cognitive impairment after acute ischemic stroke or transient ischemic attack: a nationwide prospective cohort study.

Clinical and experimental hypertension (New York, N.Y. : 1993)·2026
Same journal

Frailty as a mediator of the association between hyperuricemia and stroke risk: A prospective cohort study.

Clinical and experimental hypertension (New York, N.Y. : 1993)·2026
Same journal

Synergistic impact of nondipper heart rate and blood pressure on left ventricular hypertrophy in essential hypertension.

Clinical and experimental hypertension (New York, N.Y. : 1993)·2026
Same journal

From clinic to home monitoring: Diagnostic strategies and evidence landscape of white-coat uncontrolled hypertension.

Clinical and experimental hypertension (New York, N.Y. : 1993)·2026
See all related articles

Primary aldosteronism (PAL) has a genetic basis, leading to increased aldosterone. Understanding the genetic cause is crucial for early diagnosis and surveillance of familial hyperaldosteronism (FHI) and other PAL forms.

Area of Science:

  • Endocrinology
  • Genetics
  • Nephrology

Background:

  • Primary aldosteronism (PAL) is increasingly recognized as a common cause of secondary hypertension.
  • PAL often has an underlying genetic etiology, influencing disease presentation and progression.

Purpose of the Study:

  • To elucidate the genetic underpinnings of primary aldosteronism.
  • To emphasize the importance of genetic diagnosis for early detection and management.

Main Methods:

  • Review of current literature on the genetics of PAL.
  • Discussion of diagnostic implications of genetic findings.
  • Emphasis on long-term follow-up and biochemical assessment.

Main Results:

  • Familial hyperaldosteronism type I (FHI) results from abnormal aldosterone biosynthesis due to genetic factors.

Related Experiment Videos

  • Other forms of PAL involve hyperplasia or adenoma, often with a genetic predisposition.
  • The distinction between hyperplasia and adenoma may be less critical than the underlying genetic cause.
  • Conclusions:

    • Genetic understanding of PAL is essential for timely diagnosis at birth and initiation of surveillance.
    • Long-term monitoring is mandatory due to the progressive nature of PAL.
    • Fludrocortisone suppression testing aids in assessing treatment outcomes and guiding further medical management.