A number of pharmaceuticals may be used in an attempt to bring the polydipsia under control, including:

- Atypical antipsychotics, such as clozapine, olanzapine and risperidone

- Demeclocycline, a tetracycline antibiotic, which is effective due to the side effect of inducing nephrogenic diabetes insipidus. Demeclocycline is used for cases of psychogenic polydipsia, including those with nocturnal enuresis (bed-wetting). Its mechanism of action involves direct inhibition of vasopressin at the DCTs, thus reducing urine concentration.

There are a number of emerging pharmaceutical treatments for psychogenic polydipsia, although these need further investigation:

- ACE Inhibitors, such as enalapril

- Clonidine, an alpha-2 adrenergic agonist

- Irbesartan, an angiotensin II receptor antagonist

- Propranolol, a sympatholytic beta blocker

- Vasopressin receptor antagonists, such as conivaptan

- Acetazolamide, a carbonic anhydrase inhibitor

Lithium was previously used for treatment of PPD as a direct competitive ADH agonist, but is now generally avoided due to its toxic effects on the thyroid and kidneys.

It is important to note that the majority of psychotropic drugs (and a good many of other classes) can cause dry mouth as a side effect, but this is not to be confused with true polydipsia in which a dangerous drop in serum sodium will be seen.

Behavioural treatments may involve the use of a token economy to provide positive reinforcement to desirable behaviour. Furthermore, cognitive therapy techniques can be used to address the thought patterns that lead to compulsive drinking behaviour. Success has been seen in trials of this technique, with emphasis on the development of coping techniques (e.g. taking small sips of water, having ice cubes instead of drinks) in addition to challenging delusions leading to excessive drinking.

Psychogenic polydipsia often leads to institutionalisation of mentally ill patients, since it is difficult to manage in the community. Most studies of behavioural treatments occur in institutional settings and require close monitoring of the patient and a large degree of time commitment from staff.

Options include:

- Mild and asymptomatic hyponatremia is treated with adequate solute intake (including salt and protein) and fluid restriction starting at 500 ml per day of water with adjustments based on serum sodium levels. Long-term fluid restriction of 1,200–1,800 mL/day may maintain the person in a symptom free state.

- Moderate and/or symptomatic hyponatremia is treated by raising the serum sodium level by 0.5 to 1 mmol per liter per hour for a total of 8 mmol per liter during the first day with the use of furosemide and replacing sodium and potassium losses with 0.9% saline.

- Severe hyponatremia or severe symptoms (confusion, convulsions, or coma): consider hypertonic saline (3%) 1–2 ml/kg IV in 3–4 h. Hypertonic saline may lead to a rapid dilute diuresis and fall in the serum sodium. It should not be used in those with an expanded extracellular fluid volume.

The treatment of hyponatremia depends on the underlying cause. How quickly treatment is required depends on a persons symptoms. Fluids is typically the cornerstone of initial management. In those with severe disease an increase in sodium of about 5 mmol/L over one to four hours is recommended.

How to manage SIADH depends on whether symptoms are present, the severity of the hyponatremia, and the duration. Management of SIADH includes:

- Removing the underlying cause when possible.

- Mild and asymptomatic hyponatremia is treated with adequate solute intake (including salt and protein) and fluid restriction starting at 500 ml per day of water with adjustments based on serum sodium levels. Long-term fluid restriction of 1,200–1,800 mL/day may maintain the person in a symptom free state.

- Moderate and symptomatic hyponatremia is treated by raising the serum sodium level by 0.5 to 1 mmol per liter per hour for a total of 8 mmol per liter during the first day with the use of furosemide and replacing sodium and potassium losses with 0.9% saline.

- For people with severe symptoms (severe confusion, convulsions, or coma) hypertonic saline (3%) 1–2 ml/kg IV in 3–4 h should be given.

- Drugs

- Demeclocycline can be used in chronic situations when fluid restrictions are difficult to maintain; demeclocycline is the most potent inhibitor of Vasopressin (ADH/AVP) action. However, demeclocycline has a 2–3 day delay in onset with extensive side effect profile, including skin photosensitivity, and nephrotoxicity.

- Urea: oral daily ingestion has shown favorable long-term results with protective effects in myelinosis and brain damage. Limitations noted to be undesirable taste and is contraindicated in people with cirrhosis to avoid initiation or potentiation of hepatic encephalopathy.

- Conivaptan – an antagonist of both V and V vasopressin receptors.

- Tolvaptan – an antagonist of the V vasopressin receptor.

Raising the serum sodium concentration too rapidly may cause central pontine myelinolysis. Avoid correction by more than 12 mEq/L/day. Initial treatment with hypertonic saline may abruptly lead to a rapid dilute diuresis and fall in ADH.

Desmopressin will be ineffective in nephrogenic DI which is treated by reversing the underlying cause (if possible) and replacing the free water deficit. The diuretic hydrochlorothiazide (a thiazide diuretic) or indomethacin can be used to create mild hypovolemia which encourages salt and water uptake in proximal tubule and thus improve nephrogenic diabetes insipidus. Amiloride has additional benefit of blocking Na uptake. Thiazide diuretics are sometimes combined with amiloride to prevent hypokalemia. It seems paradoxical to treat an extreme diuresis with a diuretic, and the exact mechanism of action is unknown but the thiazide diuretics will decrease distal convoluted tubule reabsorption of sodium and water, thereby causing diuresis. This decreases plasma volume, thus lowering the glomerular filtration rate and enhancing the absorption of sodium and water in the proximal nephron. Less fluid reaches the distal nephron, so overall fluid conservation is obtained.

Lithium-induced nephrogenic DI may be effectively managed with the administration of amiloride, a potassium-sparing diuretic often used in conjunction with thiazide or loop diuretics. Clinicians have been aware of lithium toxicity for many years, and traditionally have administered thiazide diuretics for lithium-induced polyuria and nephrogenic diabetes insipidus. However, amiloride has recently been shown to be a successful treatment for this condition.

Initial therapy:

- hydration, increasing salt intake, and forced diuresis.

- hydration is needed because many patients are dehydrated due to vomiting or kidney defects in concentrating urine.

- increased salt intake also can increase body fluid volume as well as increasing urine sodium excretion, which further increases urinary potassium excretion.

- after rehydration, a loop diuretic such as furosemide can be given to permit continued large volume intravenous salt and water replacement while minimizing the risk of blood volume overload and pulmonary oedema. In addition, loop diuretics tend to depress calcium reabsorption by the kidney thereby helping to lower blood calcium levels

- can usually decrease serum calcium by 1–3 mg/dL within 24 hours

- caution must be taken to prevent potassium or magnesium depletion

The goal of therapy is to treat the hypercalcaemia first and subsequently effort is directed to treat the underlying cause.

Central DI and gestational DI respond to desmopressin which is given as intranasal or oral tablets. Carbamazepine, an anticonvulsive medication, has also had some success in this type of DI. Also, gestational DI tends to abate on its own four to six weeks following labor, though some women may develop it again in subsequent pregnancies. In dipsogenic DI, desmopressin is not usually an option.

Potassium replacement is often required as the metabolic problems are corrected. It is generally replaced at a rate 10 mEq per hour as long as there is adequate urinary output.

Treatment of HHS begins with reestablishing tissue perfusion using intravenous fluids. People with HHS can be dehydrated by 8 to 12 liters. Attempts to correct this usually take place over 24 hours with initial rates of normal saline often in the range of 1 L/h for the first few hours or until the condition stabilizes.

In GRA, the hypersecretion of aldosterone and the accompanying hypertension are remedied when ACTH secretion is suppressed by administering glucocorticoids.

Dexamethasone, spironolactone and eplerenone have been used in treatment.

Treatment of hyperglycemia requires elimination of the underlying cause, such as diabetes. Acute hyperglycemia can be treated by direct administration of insulin in most cases. Severe hyperglycemia can be treated with oral hypoglycemic therapy and lifestyle modification.

In diabetes mellitus (by far the most common cause of chronic hyperglycemia), treatment aims at maintaining blood glucose at a level as close to normal as possible, in order to avoid these serious long-term complications. This is done by a combination of proper diet, regular exercise, and insulin or other medication such as metformin, etc.

Those with hyperglycaemia can be treated using sulphonylureas or metformin or both. These drugs help by improving glycaemic control

Dipeptidyl peptidase 4 inhibitor alone or in combination with basal insulin can be used as a treatment for hyperglycemia with patients still in the hospital.

To minimise the risk of this condition developing from its most common cause, overly rapid reversal of hyponatremia, the hyponatremia should be corrected at a rate not exceeding 10 mmol/L/24 h or 0.5 mEq/L/h; or 18 m/Eq/L/48hrs; thus avoiding demyelination. No large clinical trials have been performed to examine the efficacy of therapeutic re-lowering of serum sodium, or other interventions sometimes advocated such as steroids or plasma exchange.

Alcoholic patients should receive vitamin supplementation and a formal evaluation of their nutritional status.

Once osmotic demyelination has begun, there is no cure or specific treatment. Care is mainly supportive. Alcoholics are usually given vitamins to correct for other deficiencies. The favourable factors contributing to the good outcome in CPM without hyponatremia were: concurrent treatment of all electrolyte disturbances, early Intensive Care Unit involvement at the advent of respiratory complications, early introduction of feeding including thiamine supplements with close monitoring of the electrolyte changes and input.

Research has led to improved outcomes. Animal studies suggest that inositol reduces the severity of osmotic demyelination syndrome if given before attempting to correct chronic hyponatraemia. Further study is required before using inositol in humans for this purpose.

Treatment includes spironolactone, a potassium-sparing diuretic that works by acting as an aldosterone antagonist.

Treatment is directed towards (1) correcting hypotension, hypovolemia, electrolyte imbalances, and metabolic acidosis; (2) improving vascular integrity, and (3) providing an immediate source of glucocorticoids. Rapid correction of hypovolemia is the first priority.

Most patients show dramatic improvement within 24 to 48 hours of appropriate fluid and glucocorticoid therapy. Over the ensuing 2 to 4 days, a gradual transition from IV fluids to oral water and food is undertaken, and maintenance mineralocorticoid and glucocorticoid therapy is initiated. Failure to make this transition smoothly should raise suspicion of insufficient glucocorticoid supplementation, concurrent endocrinopathy (e.g. hypothyroidism), or cocurrent illness (especially renal damage).

Simple behavioral methods are recommended as initial treatment. Enuresis alarm therapy and medications may be more effective but have potential side effects.

- Motivational therapy in nocturnal enuresis mainly involves parent and child education. Guilt should be allayed by providing facts. Fluids should be restricted 2 hours prior to bed. The child should be encouraged to empty the bladder completely prior to going to bed. Positive reinforcement can be initiated by setting up a diary or chart to monitor progress and establishing a system to reward the child for each night that he or she is dry. The child should participate in morning cleanup as a natural, nonpunitive consequence of wetting. This method is particularly helpful in younger children (<8 years) and will achieve dryness in 15-20% of the patients.

- Waiting: Almost all children will outgrow bedwetting. For this reason, urologists and pediatricians frequently recommend delaying treatment until the child is at least six or seven years old. Physicians may begin treatment earlier if they perceive the condition is damaging the child's self-esteem and/or relationships with family/friends.

- Bedwetting alarms: Physicians also frequently suggest bedwetting alarms which sound a loud tone when they sense moisture. This can help condition the child to wake at the sensation of a full bladder. These alarms are considered effective, with study participants being 13 times more likely to become dry at night. There is a 29% to 69% relapse rate, however, so the treatment may need to be repeated.

- DDAVP (desmopressin) tablets are a synthetic replacement for antidiuretic hormone, the hormone that reduces urine production during sleep. Desmopressin is usually used in the form of desmopressin acetate, DDAVP. Patients taking DDAVP are 4.5 times more likely to stay dry than those taking a placebo. The drug replaces the hormone for that night with no cumulative effect. US drug regulators have banned using desmopressin nasal sprays for treating bedwetting since the oral form is considered safer.

- DDAVP is most efficient in children with nocturnal polyuria (nocturnal urine production greater than 130% of expected bladder capacity for age) and normal bladder reservoir function (maximum voided volume greater than 70% of expected bladder capacity for age). Other children who are likely candidates for desmopressin treatment are those in whom alarm therapy has failed or those considered unlikely to comply with alarm therapy. It can be very useful for summer camp and sleepovers to prevent enuresis.

- Tricyclic antidepressants: Tricyclic antidepressant prescription drugs with anti-muscarinic properties have been proven successful in treating bedwetting, but also have an increased risk of side effects, including death from overdose. These drugs include amitriptyline, imipramine and nortriptyline. Studies find that patients using these drugs are 4.2 times as likely to stay dry as those taking a placebo. The relapse rates after stopping the medicines are close to 50%.

Aggressiveness of therapy depends on the clinical status of the patient and the nature of the insufficiency (glucocorticoid, mineralocorticoid, or both). Many dogs and cats with primary adrenal insufficiency are presented in Addisonian crisis and require immediate, aggressive therapy. In contrast, secondary insufficiency often has a chronic course.

Hypoadrenocorticism is treated with fludrocortisone (trade name Florinef) or a monthly injection of Percorten-V (desoxycorticosterone pivalate, DOCP) and prednisolone or Zycortal. Routine blood work is necessary in the initial stages until a maintenance dose is established. Most of the medications used in the therapy of hypoadrenocorticism cause excessive thirst and urination. It is absolutely vital to provide fresh drinking water for a canine suffering from this disorder.

If the owner knows about an upcoming stressful situation (shows, traveling etc.), the animals generally need an increased dose of prednisone to help deal with the added stress. Avoidance of stress is important for dogs with hypoadrenocorticism. Physical illness also stresses the body and may mean that the medication(s) need to be adjusted during this time. Most dogs with hypoadrenocorticism have an excellent prognosis after proper stabilization and treatment.

The administration of sodium bicarbonate solution to rapidly improve the acid levels in the blood is controversial. There is little evidence that it improves outcomes beyond standard therapy, and indeed some evidence that while it may improve the acidity of the blood, it may actually worsen acidity inside the body's cells and increase the risk of certain complications. Its use is therefore discouraged, although some guidelines recommend it for extreme acidosis (pH<6.9), and smaller amounts for severe acidosis (pH 6.9–7.0).

Cerebral edema, if associated with coma, often necessitates admission to intensive care, artificial ventilation, and close observation. The administration of fluids is slowed. The ideal treatment of cerebral edema in DKA is not established, but intravenous mannitol and hypertonic saline (3%) are used—as in some other forms of cerebral edema—in an attempt to reduce the swelling.

The treatment for hyperaldosteronism depends on the underlying cause. In people with a single benign tumor (adenoma), surgical removal (adrenalectomy) may be curative. This is usually performed laparoscopically, through several very small incisions. For people with hyperplasia of both glands, successful treatment is often achieved with spironolactone or eplerenone, drugs that block the effect of aldosterone. With its antiandrogen effect, spironolactone drug therapy may have a range of effects in males, including sometimes gynecomastia. These symptoms usually do not occur with eplerenone drug therapy.

In the absence of treatment, individuals with hyperaldosteronism often have poorly controlled high blood pressure, which may be associated with increased rates of stroke, heart disease, and kidney failure. With appropriate treatment, the prognosis is excellent.

While patients should be encouraged to include liberal amounts of sodium and potassium in their diet, potassium supplements are usually required, and spironolactone is also used to reduce potassium loss.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can be used as well, and are particularly helpful in patients with neonatal Bartter's syndrome.

Angiotensin-converting enzyme (ACE) inhibitors can also be used.

Persons with nephrogenic diabetes insipidus will need to consume enough fluids to equal the amount of urine produced. Any underlying cause such as high blood calcium must be corrected to treat NDI. The first line of treatment is hydrochlorothiazide and amiloride. Consider a low-salt and low-protein diet.

Thiazide is used in treatment because diabetes insipidus causes the excretion of more water than sodium (i.e. dilute urine). This condition results in a net concentrating effect on the serum (increasing its osmolarity). This high serum osmolarity stimulates excessive thirst in an attempt to dilute the serum back to normal and provide free water for excreting the excess serum solutes. However, since the patient is unable to concentrate urine to excrete the excess solutes, the resulting urine fails to decrease serum osmolarity and the cycle repeats itself, hence excessive urination. Thiazide diuretics allow increased excretion of Na+ and water, thereby reducing the serum osmolarity and eliminating volume excess. Basically, thiazides allow increased solute excretion in the urine, breaking the polydipsia-polyuria cycle.

Increase the water intake to prevent oxalates to precipitate .

Minimize dietary intake of oxalates by restricting the intake of leafy vegetables , sesame seeds , tea , cocoa , beet root , spinach , rhubarb , etc.

Food should be offered at the first signs of possible hypoglycemia. If the animal refuses it, a sugar solution (corn syrup, honey, pancake syrup, etc.) should be poured on the finger and rubbed on its gums or under the tongue (sublingually). The solution must be applied this way to prevent possible aspiration of it. Intervet suggests one tablespoon of a sugar solution rubbed onto the gums, regardless of the size of the dog. Another hypoglycemia formula is 1 gram of glucose for every kilogram (2.2 lb) of the animal's body weight. Since sugar acts quickly, a response should be seen within a minute or two.

Honey, syrup, or sugar, as simple carbohydrates, act rapidly and will make the blood glucose rise, but the rise will not last very long, as they are broken down quickly by the body. Feeding something containing complex carbohydrates when the pet is able to eat will make sure another hypoglycemia event does not overtake the rapid rise in blood glucose levels from the sugar solution. Complex carbohydrates take longer to be broken down by the body, so they do not raise blood glucose levels until some time after being eaten. A small meal should be fed and the animal taken for medical evaluation to determine if further treatment is needed. Treatment of a serious hypoglycemia episode is similar to that of diabetic humans: using glucose or glucagon infusions, depending on severity.