This syndrome is caused by dysregulation of the epithelial sodium channel (ENaC) due to a genetic mutation at the 16p13-p12 locus. These channels are found on the surface of epithelial cells found in the kidneys, lungs, and sweat glands. The ENaC transports sodium into cells. The mutation changes a domain in the channel so it is no longer degraded correctly by the ubiquitin proteasome system. Specifically, the PY motif in the protein is deleted or altered so the E3 ligase (Nedd4) no longer recognizes the channel. This loss of ability to be degraded leads to high amounts of the channel being chronically present in the collecting duct. This results in a hyperaldosteronism-like state, since aldosterone is typically responsible for creating and inserting these channels. The increased sodium resorption leads to increased resorption of water, and hypertension due to an increase in extracellular volume.<unk>  syndrome is inherited in an autosomal dominant fashion.
Liddle's syndrome
Renpenning's syndrome
Banti's syndrome
Satchmo's syndrome
Bertolotti's syndrome
Grisel's syndrome
Bálint's syndrome
Rowell's syndrome