by Jesús Ramón Girando and Julio Libman 

Polydipsia is defined as the increase in thirst that leads to increased fluid intake.

Physiology and pathophysiology 

The balance of the water metabolism in the organism is the result of the factors that intervene in its entry »constituted by thirst, the production of metabolic water and the water contained in the ingested food, on the one hand, and the discharge of the same through the skin, the lungs, the gastrointestinal tract and the kidneys, on the other.

Thirst is the subjective feeling that leads to water intake. The physiological factors that determine this sensation would be related to the greater osmolarity of the extracellular fluid determined by an excess of salt or a deficit of water, also involving the decrease in circulating vascular volume. Body water deficit can be a consequence of decreased supply or increased loss. Conscious desire to drink appears when plasma osmolarity reaches 295 mOsm / kg. The appearance of this desire is also influenced by factors related to the habits of consuming salt and water. A basic component of stimulation is the feeling of dryness of the mucous membranes of the mouth and pharynx. Drugs such as anticholinergics act in this way. However,

Causes of polydipsia 

The causes that can induce polydipsia are the following:

  1. Lack of water intake due to lack or vomiting.
  2. Greater loss that can occur by various routes and mechanisms:
    1. Skin. Excessive sensitive perspiration induced by heat, physical activity, or fever is made up of a hypotonic fluid that can reach a volume of 2 liters per hour.
    2. Digestive system. Loss occurs through vomiting and diarrhea.
    3. Polyuria. It includes the causes that are detailed below:
      1. Poor tubular absorption of filtered water due to lack of vasopressin, as occurs in central diabetes insipidus. In these circumstances, the onset of polyuria and polydipsia are abrupt, and the patient shows a marked predilection for ingesting cold water. Diabetes insipidus can be primary (idiopathic or hereditary, dominant or recessive), or secondary to head injuries, surgery and primary pituitary or supraselar and metastatic tumors of adenocarcmomas of the breast and lung, mainly. There are other causes that can induce diabetes insipidus, including sarcoidosis, histiocytosis, tuberculosis, syphilis, and encephalitis.
      2. Poor tubular reinsertion of the filtered water despite the existence of adequate amounts of antidiuretic hormone, due to the lack of response of the renal tubules to said hormone. Includes congenital nephrogenic diabetes insipidus and acquired forms. The latter include that produced by drugs (lithium, demethylchlortetracycin, etc.), chronic kidney diseases, obstructive uropathy, multiple myeloma, amyloidosis, hypokalemia, hypercalcemia, sickle cell anemia and the polyuric phase of acute tubular necrosis.
      3. Osmotic diuresis, as in diabetes mellitus. When hyperglycemia reaches a critical level, the so-called renal threshold, which varies from patient to patient, the amount of glucose filtered by the glomerulus exceeds the maximum capacity of tubular reinsertion (Tm), and then the excessive filtered load acts as a diuretic, producing polyuria with simultaneous loss of Na + Cl-. This leads to decreased extracellular fluid volume, dehydration, thirst, and polydipsia.
      4. Diuretics. They act at the level of the renal tubules, increasing the excretion of Na + and water. Primary or psychogenic polydipsia, rarely postencephalitic hypothalamic lesions, and certain drugs such as chlorpromazine induce excessive water intake, without there being a real deficit of water in the organism.

Interrogation and study methodology

The questioning is aimed at determining the form of acute or progressive onset of polydipsia, its evolution time, and its magnitude. An acute-onset polydipsia, accompanied by polyuria of several liters a day, with a tendency to ingest cold water, leads to the existence of central diabetes insipidus. Confirmed the diagnosis through the determination of the urinary and plasma osmolarity in the course of an aqueous deprivation test, the cause of the same must be determined. X-rays and a computed axial tomography of the skull will rule out the presence of tumors. Family history and age of onset, as well as lack of response to vasopressin, will be ascertained to assess the existence of nephrogenic diabetes insipidus. The evaluation of the secondary forms will look for a history of drug intake or the existence of kidney or systemic conditions. The possibility of primary hyperaldosteronism (hypokalemia) or hyperparathyroidism (hypercalcemia and hypercalciuria) will also be evaluated. A pathological personality will suggest the presence of psychogenic polydipsia in a compulsive drinker of water. In this case, there is generally a decrease in plasma osmolarity.

High blood glucose with positive blood glucose confirms the diagnosis of diabetes mellitus as the cause of polydipsia. The presence of a constant density of 1,010, accompanied by pathological elements in the urine, suggests the existence of a renal pathology.