Anti-Diuretic Hormone, a.k.a. ADH, is one of the key hormones that helps regulate kidney function. If the kidneys were not precisely regulated you would either make gallons of urine per day and would rapidly dehydrate, or alternatively, make minimal urine and consequently develop water intoxication.
Diuretic refers to a chemical or medication that causes increased urine production, e.g. hydrochlorothiazide (Hydrodiuril), furosemide (Lasix), etc. ADH, manufactured in the hypothalamus and released in the pituitary gland of the brain, functions as an anti-diuretic that restricts urine production to maintain blood volume and blood pressure. ADH can be thought of as the kidneys’ “brakes.” ADH is also known as “vasopressin” since it causes arterial muscle to contract and thus increases blood pressure.
On the other hand, the hormone atrial natriuretic peptide, a.k.a. ANP, manufactured in the heart, functions to increase urine production and inhibit ADH to decrease blood volume and blood pressure. ANP can be thought of as the kidneys’ “accelerator.”
With ADH and ANP functioning as the brakes and accelerator of the kidney, respectively, urine production is precisely and tightly regulated. This keeps one’s fluid balance in check, avoiding dehydration and water intoxication and maintaining blood volume and blood pressure.
SNORING YOUR WAY TO FREQUENT NIGHTTIME PEEING
Interestingly, the reason those who suffer with obstructive sleep apnea (OSA) make so much urine at night is that the collapse of the soft tissues of the throat and neck (that causes the snoring) decreases pressure within the chest, increasing venous return of blood to the heart with the heart falsely sensing fluid overload, resulting in the release of ANP that accelerates urine production in an attempt to overcome the falsely sensed fluid overload. Treat the OSA and the nocturnal urinating goes away! Physiology magic!
TOO MUCH ADH
Certain cancers and other disorders can cause excessive ADH production, called Syndrome of Inappropriate Secretion of ADH (SIADH). The excessive restraint on urine production results in over-concentration of urine, causing fluid and electrolyte imbalance, muscle cramps, confusion and convulsions from water intoxication.
TOO LITTLE ADH
There is a natural biorhythmic pattern to ADH production, with decreased ADH production while sleeping, which can cause excessive urine production during sleep hours, nocturnal polyuria in medical speak. The elderly population is particularly susceptible to suppressed ADH production while asleep and therefore may produce copious volumes of urine during sleep hours with only modest urine production while awake. This clinically presents as full-volume urinary frequency that only occurs during sleep hours and not during daytime hours.
THERAPEUTIC USES OF ADH: FROM BEDWETTING TO BLEEDING
ADH can be used to treat a variety of medical conditions — central diabetes insipidus, caused by a lack of ADH due to destruction of part or all of the hypothalamus or pituitary gland, bleeding abnormalities from esophageal varices, hemophilia and von Willebrand’s diseases, hypovolemic septic shock, bedwetting, and nocturnal polyuria.
Both full volume nocturnal urinary frequency as well as bedwetting in children can be managed with synthetic ADH, a.k.a. desmopressin. There are numerous ways to administer synthetic ADH including oral pills, sub-lingual tablets and nasal sprays. Since ADH results in decreased urine output and fluid retention, a possible consequence is electrolyte dilution, so it is imperative for serum sodium levels to be checked periodically because of the possibility of low sodium levels that may give rise to a variety of symptoms.
FORMULATIONS OF SYNTHETIC ADH
NOCTIVA (desmopressin acetate) is available as an oil-in-water emulsion at two dose strengths, 0.83 mcg and 1.66 mcg of desmopressin acetate per spray, for nasal administration.
NOCDURNA (desmopressin acetate) is available as a pill in two dose strengths, 27.7 mcg and 55.3 mcg of desmopressin acetate per pill, for sub-lingual administration.
DESMOPRESSIN ACETATE is available as a pill in two dose strengths, 0.1 and 0.2 mg, for oral administration. The recommended initial dose for patients age 6 years and older is 0.2 mg at bedtime that may be titrated up to 0.6 mg to achieve the desired response.
The great variety in dosing strength has to do with the different absorption capabilities of the nasal mucosa, oral mucosa and stomach as well as the bioavailability of the drug.