Hyponatremia feedback loop is overwhelmed by increased fluid intake, 2) the feedback loop malfunctions such that ADH is always "turned on"; 3) the receptors in the kidney are always "open" regardless of there being no signal from ADH to be open; or 4) there is an increased ADH even though there is no normal stimulus (elevated serum sodium) for ADH to be increased. Hyponatremia occurs in one of two ways: either the osmoreceptor-aquaporin feedback loop is "overwhelmed", or it is "interrupted". If it is interrupted, it is either "related" or "not related" to ADH. If the feedback system is overwhelmed, this
Hypotonic hyponatremia ADH secretion. As a result, the kidneys of such patients recover water and produce a fairly concentrated urine. Treatment is simple (if not without risk) — simply restore the patient's blood volume, thereby turning off the stimulus for ongoing ADH release and water retention. It is worth considering separately, the hyponatremia that occurs in the setting of diuretic use. Patients taking diuretic medications such as furosemide (Lasix), hydrochlorothiazide, chlorthalidone, etc., become volume depleted. That is to say that their diuretic medicine, by design, has caused their kidneys to produce more urine than they would otherwise make. This extra urine represents