[2] Pseudohypoaldosteronism type 1 (PHA1) is characterized by the body's inability to respond adequately to aldosterone, a hormone crucial for regulating electrolyte levels.

This condition often manifests with dehydration as the kidneys struggle to retain sufficient salt, leading to symptoms like increased thirst and dry mouth.

In the kidney, aldosterone plays an important role of regulating sodium and potassium homeostasis by its actions on distal nephron cells.

[7] Individuals with PHA1B can have additional symptoms such as cardiac arrhythmia, shock, recurrent lung infections, or lesions on the skin due to imbalanced salts in the body especially in infancy.

[8] PHA2 also known as Familial hyperkalemic hypertension or Gordon syndrome is a rare disorder characterized by abnormalities in how the body regulates sodium and potassium levels.

These genes regulate the Sodium-chloride symporter (NCC) transporter, which is involved in controlling the levels of sodium and chloride in the body.

Normally, the NCC transporter reabsorbs sodium and chloride in a part of the kidney called the distal convoluted tubule (DCT), however in PHA2 this process is dysregulated.

People with PHA2 may experience other nonspecific symptoms including nausea, vomiting, extreme fatigue, muscle weakness, and hypercalcuria.

PHA2 requires salt restriction and use of thiazide diuretics to block sodium chloride reabsorption and normalise blood pressure and serum potassium.

[25] Later, the severe form of PHA was discovered to be due to mutations in the genes SCNN1A, SCNN1B, and SCNN1G that code for the epithelial sodium channel subunits, α, β, and γ, respectively.