Several medical treatments shift potassium ions from the bloodstream into the cellular compartment, thereby reducing the risk of complications. The effect of these measures tends to be short-lived, but may temporize the problem until potassium can be removed from the body.

- Insulin (e.g. intravenous injection of 10-15 units of regular insulin along with 50 ml of 50% dextrose to prevent the blood sugar from dropping too low) leads to a shift of potassium ions into cells, secondary to increased activity of the sodium-potassium ATPase. Its effects last a few hours, so it sometimes must be repeated while other measures are taken to suppress potassium levels more permanently. The insulin is usually given with an appropriate amount of glucose to prevent hypoglycemia following the insulin administration.

- Salbutamol (albuterol), a β-selective catecholamine, is administered by nebulizer (e.g. 10–20 mg). This medication also lowers blood levels of K by promoting its movement into cells.

- Sodium bicarbonate may be used with the above measures if it is believed the person has metabolic acidosis.

Severe cases require hemodialysis or hemofiltration, which are the most rapid methods of removing potassium from the body. These are typically used if the underlying cause cannot be corrected swiftly while temporizing measures are instituted or there is no response to these measures.

Potassium can bind to agents in the gastrointestinal tract. Sodium polystyrene sulfonate with sorbitol (Kayexalate) has been approved for this use and can be given by mouth or rectally. However, careful clinical trials to demonstrate the effectiveness of sodium polystyrene are lacking, and use of sodium polystyrene sulfonate, particularly if with high sorbitol content, is uncommonly but convincingly associated with colonic necrosis. There are no systematic studies (>6 months) looking at the long-term safety of this medication. Another medication by the name of patiromer was approved in 2015.

Loop diuretics (furosemide, bumetanide, torasemide) and thiazide diuretics (e.g., chlorthalidone, hydrochlorothiazide, or chlorothiazide) can increase kidney potassium excretion in people with intact kidney function.

Fludrocortisone, a synthetic mineralocorticoid, can also increase potassium excretion by the kidney in patients with functioning kidneys. Trials of fludrocortisone in patients on dialysis have shown it to be ineffective.

Patiromer is a selective sorbent that is taken by mouth and works by binding free potassium ions in the gastrointestinal tract and releasing calcium ions for exchange, thus lowering the amount of potassium available for absorption into the bloodstream and increasing the amount that is excreted via the feces. The net effect is a reduction of potassium levels in the blood serum.

Prevention of hypermagnesemia usually is possible. In mild cases, withdrawing magnesium supplementation is often sufficient. In more severe cases the following treatments are used:

- Intravenous calcium gluconate, because the actions of magnesium in neuromuscular and cardiac function are antagonized by calcium.

Definitive treatment of hypermagnesemia requires increasing renal magnesium excretion through:

- Intravenous diuretics, in the presence of normal kidney function

- Dialysis, when kidney function is impaired and the patient is symptomatic from hypermagnesemia

The following are the most common treatments of elevated alkaline phosphatase.

- Treatment of the underlying condition

- Once doctors identifies the cause of elevated ALP and diagnose a treatment, the levels of alkaline phosphatase fluctuates back to normal

- Removal of medication - that is associated with increased levels of alkaline phosphatase

- Birth control pills

- Anti-inflammatory medication

- Narcotic medication

- Hormonal drug

- Steroid

- Antidepressant

- Dietary changes

- Include foods rich in vitamin D

- Lifestyle change

- Healthy diet in association with physical exercise

- Exposure to sunlight which increases the production of vitamin D

Treatments for Glycerol Kinase Deficiency are targeted to treat the symptoms because there are no permanent treatments for this disease. The main way to treat these symptoms is by using corticosteroids, glucose infusion, or mineralocorticoids. Corticosteroids are steroid hormones that are naturally produced in the adrenal glands. These hormones regulate stress responses, carbohydrate metabolism, blood electrolyte levels, as well as other uses. The mineralocorticoids, such as aldosterone control many electrolyte levels and allow the kidneys to retain sodium. Glucose infusion is coupled with insulin infusion to monitor blood glucose levels and keep them stable.

Due to the multitude of varying symptoms of this disease, there is no specific treatment that will cure this disease altogether. The symptoms can be treated with many different treatments and combinations of medicines to try to find the correct combination to offset the specific symptoms. Everyone with Glycerol Kinase Deficiency has varying degrees of symptoms and thereby requires different medicines to be used in combination to treat the symptoms; however, this disease is not curable and the symptoms can only be managed, not treated fully.

Standard intravenous preparations of potassium phosphate are available and are routinely used in malnourished patients and alcoholics. Oral supplementation is also useful where no intravenous treatment are available. Historically one of the first demonstrations of this was in concentration camp victims who died soon after being re-fed: it was observed that those given milk (high in phosphate) had a higher survival rate than those who did not get milk.

Monitoring parameters during correction with IV phosphate

- Phosphorus levels should be monitored after 2 to 4 hours after each dose, also monitor serum potassium, calcium and magnesium. Cardiac monitoring is also advised.

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.

Acute adrenal insufficiency is a medical emergency and needs to be treated with injectable hydrocortisone and fluid support.

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.

American and European guidelines come to different conclusions regarding the use of medications. In the United States they are recommended in those with SIADH, cirrhosis, or heart failure who fail limiting fluid intact. In Europe they are not generally recommended.

There is tentative evidence that vasopressin receptor antagonists (vaptans), such as conivaptan, may be slightly more effective than fluid restriction in those with high volume or normal volume hyponatremia. They should not be used in people with low volume. Their use in SIADH is unclear.

Demeclocycline, while sometimes used for SIADH, has significant side effects including potential kidney problems and sun sensitivity. In many people it has no benefit while in others it can result in overcorrection and high blood sodium levels.

Daily use of urea by mouth, while not commonly used due to the taste, has tentative evidence in SIADH. It, however, is not available in many areas of the world.

The treatment is with a low sodium (low salt) diet and a potassium-sparing diuretic that directly blocks the sodium channel. Potassium-sparing diuretics that are effective for this purpose include amiloride and triamterene; spironolactone is not effective because it acts by regulating aldosterone and Liddle syndrome does not respond to this regulation. Amiloride is the only treatment option that is safe in pregnancy. Medical treatment usually corrects both the hypertension and the hypokalemia, and as a result these patients may not require any potassium replacement therapy.

Adrenal crisis is triggered by physiological stress (such as trauma). Activities that have an elevated risk of trauma are best avoided. Treatment must be given within two hours of trauma and consequently it is advisable to carry injectable hydrocortisone in remote areas.

Treatment of AIGA almost always consists of steroid pulse therapy or high-dose oral steroids and is not consistently effective. Much remains unclear regarding the reasons for recurrent anhidrosis.

Resection of the tumor is the ideal treatment and results in correction of hypophosphatemia (and low calcitriol levels) within hours of resection. Resolution of skeletal abnormalities may take many months.

If the tumor cannot be located, treatment with calcitriol (1-3 µg/day) and phosphorus (1-4 g/day in divided doses) is instituted. Tumors which secrete somatostatin receptors may respond to treatment with octreotide. If hypophosphatemia persists despite calcitriol and phosphate supplementation, administration of cinacalcet has been shown to be useful

The standard treatment is chenodeoxycholic acid (CDCA) replacement therapy. Serum cholesterol levels are also followed. If hypercholesterolemia is not controlled with CDCA, an HMG-CoA reductase inhibitor ("statins" such as simvastatin) can also be used.

As with any supplements and drugs, it is best to confer with a veterinarian as to the recommended dosages. Some drugs are not allowed in competition and may need to be withheld a few days before.

Adding potassium and salt to the diet may be beneficial to horses that suffer from recurrent bouts of ER. Horses in hard training may need a vitamin E supplement, as their requirements are higher than horses in more moderate work. The horse may also be deficient in selenium, and need a feed in supplement. Selenium can be dangerous if overfed, so it is best to have a blood test to confirm that the horse is in need of supplemental selenium.

Thyroid hormone supplementation is often beneficial for horses with low thyroid activity (only do so if the horse has been diagnosed with hypothyroidism).

Other drugs that have been used with success include phenytoin, dantrolene, and dimetyl glycine.

Bicarbonate and NSAIDs are of no use in preventing ER.

A horse may need fluids, especially if his urine is colored, the horse is receiving NSAIDs, or if he is dehydrated. Fluids will increase the production of urine that will in turn help flush out the excess, and potentially damaging, myoglobin from the kidneys and will reduce NSAID-produced kidney damage. Fluids should be administered until the urine is clear, which usually takes from a few hours to a few days.

Vasodilators, such as acepromazine, can help improve blood flow to the muscles. However, the owner should only give acepromazine if it is prescribed by the horse's veterinarian, as it can lower the animal's blood pressure and can cause collapse in a severely dehydrated horse. The human drug dantrolene is sometimes given to alleviate the muscle spasms and prevent further degeneration of muscle tissue.

Vitamin E is an anti-oxidant, and so may help prevent further cell degeneration in the affected muscles. However, vitamin E products must be used with caution if they also contain selenium.

Bicarbonate will not help offset any lactic acid in the bloodstream, as lactic acid generally only accumulates in the affected muscles.

Except to get a horse to his stall, a horse showing signs of severe ER should not be moved until he is comfortable enough to do so eagerly. This may take several days. After this point, it is important to either hand-walk the horse a few times each day, or provide him with a few hours of turnout in a pasture or paddock.

No treatment is generally required, as bone demineralisation and kidney stones are relatively uncommon in the condition.

In common forms of MTHFR deficiency, elevated plasma homocysteine levels have sometimes been treated with Vitamin B12 and low doses of folic acid. Although this treatment significantly decreases the serum levels of homocysteine, this treatment is not thought to improve health outcomes.

Due to the ineffectiveness of these treatments, it is no-longer considered clinically useful to test for MTHFR in most cases of thrombophilia or recurrent pregnancy loss.

Medications that are sometimes required include estrogen replacement therapy in postmenopausal women and bisphosphonates. Bisphosphonates may improve bone turnover.

Newer medications termed "calcimimetics" used in secondary hyperparathyroidism are now being used in primary hyperparathyroidism. Calcimimetics reduce the amount of parathyroid hormone released by the parathyroid glands. They are recommended in patients in whom surgery is inappropriate.

In people with secondary hyperparathyroidism, the high PTH levels are an appropriate response to low calcium and treatment must be directed at the underlying cause of this (usually vitamin D deficiency or chronic kidney failure). If this is successful PTH levels should naturally return to normal levels unless PTH secretion has become autonomous (tertiary hyperparathyroidism)

Treatment is usually surgical removal of the gland(s) containing adenomas, but medication may also be required.

People with primary hyperparathyroidism who are symptomatic benefit from surgery to remove the parathyroid tumor (parathyroid adenoma). Indications for surgery are as follows:

- Symptomatic hyperparathyroidism

- Asymptomatic hyperparathyroidism with any of the following:

- 24-hour urinary calcium > 400 mg (see Foot Note, below)

- serum calcium > 1 mg/dL above upper limit of normal

- Creatinine clearance > 30% below normal for patient's age

- Bone density > 2.5 standard deviations for below peak (i.e., T-score of -2.5)

- People age < 50

Surgery can rarely result in hypoparathyroidism.

In season 2 of the USA Network series Royal Pains, Reshma Shetty (as Divya Katdare) diagnoses a storm chaser (Jamie Ray Newman) with recurring fractures to have tumor-induced osteomalacia.

These treatments have been used to help treat or manage toxicity in animals. Although not considered part of standard treatment, they might be of some benefit to humans.

- Vitamin E appears to be an effective treatment in rabbits, prevents side effects in chicks

- Taurine significantly reduces toxic effects in rats. Retinoids can be conjugated by taurine and other substances. Significant amounts of retinotaurine are excreted in the bile, and this retinol conjugate is thought to be an excretory form, as it has little biological activity.

- Cholestin - significantly reduces toxic effects in rats.

- Vitamin K prevents hypoprothrombinemia in rats and can sometimes control the increase in plasma/cell ratios of vitamin A.