Familial hyperaldosteronism

Summary

Familial hyperaldosteronism (MONDO:0016525) is a disease (an umbrella term covering 5 Mondo subtypes). A subtype of primary aldosteronism — broader associated-gene and molecular evidence is on the parent page (see Disease family below).

At a glance

• Prevalence: Unknown (Europe)
• Umbrella term: 5 Mondo subtypes

Clinical features

No curated clinical features (Orphanet) for this disease.

Identifiers

Disease identifiers

Field	Value
Canonical name	familial hyperaldosteronism
Mondo ID	MONDO:0016525
MeSH	C580087
OMIM	103900
Orphanet	235936, 371861
DOID	DOID:0061247
ICD-11	1586992015
NCIT	C127160
SNOMED CT	703231005
UMLS	C3713420
MedGen	780028
GARD	0020630
Is cancer (heuristic)	no

Also known as: FH · genetic hyperaldosteronism · hereditary hyperaldosteronism

Disease family

This is a subtype of primary aldosteronism. Genetic, therapeutic, and trial evidence is largely curated at the broader-term level — see the parent page for the associated-gene cohort and molecular evidence.

Classification path: disease › human disease › disease by body system or component › endocrine system disorder › adrenal gland disorder › adrenal cortex disorder › adrenal gland hyperfunction › hyperaldosteronism › primary aldosteronism › familial hyperaldosteronism

Related subtypes (3): primary unilateral adrenal hyperplasia, aldosterone-producing adrenal cortex adenoma, ectopic aldosterone-producing tumor

Subtypes (5): glucocorticoid-remediable aldosteronism, familial hyperaldosteronism type II, familial hyperaldosteronism type III, aldosterone-producing adenoma with seizures and neurological abnormalities, hyperaldosteronism, familial, type IV

Genetics & variants

GWAS landscape

No GWAS associations recorded — common-variant (GWAS) studies don’t cover this disease (typical for Mendelian / rare diseases). See the curated gene cohort and Mendelian overlap below.

Variant details and genetic-evidence tiers

No tiered GWAS variants or ClinVar records for this disease.

Genes & proteins

No associated-gene cohort resolved for this disease. Atlas builds the molecular and therapeutic sections — associated genes, protein families, druggability, pathways, interactions, and drug associations — by aggregating over a disease’s associated genes (resolved via GWAS / GenCC / ClinVar / CIViC), and none resolved here. This is expected for antibody-mediated, autoimmune, or otherwise non-gene-defined conditions; the curated evidence for this disease is its clinical features, GWAS susceptibility, and clinical trials (above).

Function

No pathway enrichment — requires an associated-gene cohort.

Therapeutics

No druggable-target or therapeutic data for this disease’s cohort.

Clinical trials & evidence

Clinical trials

Clinical trials: 0.