ADH (synonyms: antidiuretic hormone, vasopressin, adiuretin) is a peptide hormone produced in the hypothalamus and secreted by the pituitary gland. Antidiuretic hormone promotes water reabsorption in the kidneys. This means that the body loses as little water as possible. As part of these processes, there is also an increase in blood pressure due to vasoconstriction (narrowing of blood vessels). The main stimuli (stimuli) of ADH secretion (release) are:
- Increase in plasma osmolarity
- Decrease in blood volume
The procedure
Material needed
- Blood plasma – blood collection in the laboratory or transport in an ice bath.
Preparation of the patient
- From 12 hours before no caffeine, no alcohol, no nicotine.
- From 48 hours before do not take any medication
Interfering factors
- Blood sampling in the laboratory or transport in an ice bath.
Normal value
| Normal value in pg/ml | 6-12 |
Indications
- Diabetes insipidus – congenital or acquired disease characterized by increased urine output (polyuria) and an increased sense of thirst with polydipsia (increased drinking).
- Syndrome of inadequate ADH secretion (SIADH) (Synonym: Schwartz-Bartter syndrome) – there is an inappropriately high secretion of antidiuretic hormone (ADH; ADH excess) in relation to blood plasma osmolality; this leads to too little fluid excretion by the kidneys with the formation of a highly concentrated urine; the result is hyperhydration (overhydration) with dilutional hyponatremia (“dilutional sodium deficiency”), which can lead to cerebral edema (brain swelling). Etiology (causes): paraneoplastic in approximately 80% of cases in patients with small cell lung cancer; other possible causes include: Brain hemorrhage, brain tumor, meningitis (meningitis, encephalitis (brain inflammation), Legionella pneumonia (pneumonia caused by the pathogen Legionella pneumophilia), tuberculosis, carcinoma (diagnosis of exclusion).
Interpretation
Interpretation of increased values
- Acute intermittent porphyria (AIP) – Patients with this disease have a 50 percent reduction in the activity of the enzyme porphobilinogen deaminase (PBG-D), which is sufficient for porphyrin synthesis. Triggers of a porphyria attack, which can last a few days but also months, are infections, drugs or alcohol. The clinical picture of these attacks presents as acute abdomen or neurological deficits, which can take a lethal course. The leading symptoms of acute porphyria are intermittent (occasionally or chronically) neurologic and psychiatric disturbances. Autonomic neuropathy is often prominent, causing abdominal colic (acute abdomen), nausea (nausea), vomiting, or constipation, as well as tachycardia (heartbeat too fast, > 100 beats per minute) and labile hypertension (high blood pressure).
- Anxiety
- Blood loss
- Diabetes insipidus – congenital or acquired disease characterized by increased urine output (polyuria) and increased thirst with polydipsia (increased drinking).
- Hypothyroidism (underactive thyroid gland).
- Nicotine
- Black Bartter syndrome – see indications below.
Interpretation of lowered values
- Alcohol
- Inflammation of the central nervous system, unspecified
- Medications; atropine or phenytoin.
- Trauma, unspecified
- Tumors of the central nervous system, unspecified
- Central diabetes insipidus (synonym: diabetes insipidus neurohormonalis) – possible causes include:
- Absence or insufficient production of the antidiuretic hormone ADH in the hypothalamus.
- Lack of transport of ADH from the hypothalamus via the pituitary stalk to the posterior lobes of the pituitary gland
- Absence of storage or failure to secrete ADH in the posterior pituitary lobe.
