<unk> 2 is also known as familial hyperkalaemic hypertension, or Gordon syndrome. The underlying genetic defect leads to increased sodium chloride reabsorption in the distal tubule in the kidney, leading to volume expansion, hypertension and lowered renin levels. The hyperkalemia found in<unk> 2 is proposed to be a function of diminished sodium delivery to the cortical collecting tubule (potassium excretion is mediated by the renal outer medullary potassium channel ROMK in which sodium reabsorption plays a role). Alternatively, WNK4 mutations that result in a gain of function of the Na-Cl co-transporter may inhibit ROMK activity resulting in hyperkalemia. Unlike in<unk> 1 in which aldosterone resistance is present, in<unk> 2 the volume expansion leads to relatively low aldosterone levels.
Pseudohypoaldosteronism
Glucocorticoid remediable aldosteronism
Familial hyperaldosteronism
Primary aldosteronism
Pseudohyperaldosteronism
Hypoaldosteronism
Apparent mineralocorticoid excess syndrome
Hyperaldosteronism