Classically one might find urine lytes that are very much like so:
Urine Osm 60, Una<10, UK 10 and U Crt 16.
This doesn't suggest volume depletion but suggests water intoxication. In the setting of a low Serum osm, the ADH is shut off but thirst is not shut off here and as a result the person keeps drinking water. This is classically seen in psychogenic variants but cases have been described with CNS trauma as well. It should be taken very seriously, as the amount of water ingested exceeds the amount that can be excreted by the kidneys,and can on rare occasions be life-threatening as the body's serum sodium level is diluted ( in other words dilutional hyponatremia ) to an extent that seizures and cardiac arrest can occur.
The excessive levels of fluid intake may result in a false diagnosis of diabetes insipidus since the chronic ingestion of excessive water can produce diagnostic results that closely mimic those of mild diabetes insipidus. However, in Diabetes Insipidus patients urinate excessive amounts because of a lack of ADH (central DI) or a lack of sensitivity (Nephrogenic DI).
One can differentiate between the two patients in an by a water deprivation test. In a patient with primary polydipsia, water deprivation should cause the patient patient to urinate less (because water intake was the cause of the excessive urination). In someone with primary polydipsia, once their water intake were restricted, their normal kidneys would begin to concentrate the urine again. In someone with DI, the urine would remain dilute even in the absence of water intake.
Besides free water restriction and increase solute diet, bio feedback might show some promise.
Another interesting take on treatment was a paper that described using azetazolamide for treatment. The authors reported 5 patients in whom acetazolamide was trialed for this symptom. Acetazolamide improved polydipsia and/or hyponatremia in 4 of the 5 cases. This treatment was well tolerated and allowed 3 of the patients to permanently leave isolation.