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.

The limited prognostic information available suggests that early diagnosis and appropriate treatment of infants and young children with classic Bartter Syndrome may improve growth and perhaps neurointellectual development. On the other hand, sustained hypokalemia and hyperreninemia can cause progressive tubulointerstitial nephritis, resulting in end-stage kidney disease (kidney failure). With early treatment of the electrolyte imbalances, the prognosis for patients with classic Bartter Syndrome is good.

This is relatively straightforward. It involves correction of the acidemia with oral sodium bicarbonate, sodium citrate or potassium citrate. This will correct the acidemia and reverse bone demineralisation. Hypokalemia and urinary stone formation and nephrocalcinosis can be treated with potassium citrate tablets which not only replace potassium but also inhibit calcium excretion and thus do not exacerbate stone disease as sodium bicarbonate or citrate may do.

As of today, no agreed-upon treatment of Dent's disease is known and no therapy has been formally accepted. Most treatment measures are supportive in nature:

- Thiazide diuretics (i.e. hydrochlorothiazide) have been used with success in reducing the calcium output in urine, but they are also known to cause hypokalemia.

- In rats with diabetes insipidus, thiazide diuretics inhibit the NaCl cotransporter in the renal distal convoluted tubule, leading indirectly to less water and solutes being delivered to the distal tubule. The impairment of Na transport in the distal convoluted tubule induces natriuresis and water loss, while increasing the reabsorption of calcium in this segment in a manner unrelated to sodium transport.

- Amiloride also increases distal tubular calcium reabsorption and has been used as a therapy for idiopathic hypercalciuria.

- A combination of 25 mg of chlorthalidone plus 5 mg of amiloride daily led to a substantial reduction in urine calcium in Dent's patients, but urine pH was "significantly higher in patients with Dent’s disease than in those with idiopathic hypercalciuria (P < 0.03), and supersaturation for uric acid was consequently lower (P < 0.03)."

- For patients with osteomalacia, vitamin D or derivatives have been employed, apparently with success.

- Some lab tests on mice with CLC-5-related tubular damage showed a high-citrate diet preserved kidney function and delayed progress of kidney disease.

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

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.

Treatment of HSH involves administration of high doses of magnesium salts. These salts may be taken orally or otherwise (e.g. subcutaneously). This treatment works by increasing magnesium absorption through the non-TRPM6 mediated paracellular uptake pathways. This treatment must be continued throughout life.

Increasing fluid intake to yield a urine output of greater than 2 liters a day can be advantageous for all patients with nephrocalcinosis. Patients with hypercalciuria can reduce calcium excretion by restricting animal protein, limiting sodium intake to less than 100 meq a day and being lax of potassium intake. If changing ones diet alone does not result in an suitable reduction of hypercalciuria, a thiazide diuretic can be administered in patients who do not have hypercalcemia. Citrate can increase the solubility of calcium in urine and limit the development of nephrocalcinosis. Citrate is not given to patients who have urine pH equal to or greater than 7.

Often, aggressive treatment is unnecessary for people with MSK disease that does not cause any symptoms (asymptomatic). In such cases, treatment may consist of maintaining adequate fluid intake, with the goal of decreasing the risk of developing kidney stones (nephrolithiasis). Cases of recurrent kidney stone formation may warrant evaluation for possible underlying metabolic abnormalities.

In patients with low levels of citrate in the urine (hypocitraturia) and incomplete distal renal tubular acidosis, treatment with potassium citrate helps prevent the formation of new kidney stones. Urinary tract infections, when they occur, should also be treated.

Patients with the more rare form of MSK marked by chronic pain typically require pain management. Non-obstructing stones in MSK can be associated with significant and chronic pain even if they're not passing. The pain in this situation can be constant. It is not certain what causes this pain but researchers have proposed that the small numerous stones seen in MSK may cause obstruction of the small tubules and collecting ducts in the kidney which could lead to the pain. This pain can often be debilitating and treatment is challenging. Narcotic medication even with large quantities is sometimes not adequate. Some success with pain control has been reported using laser lithotripsy (called “ureteroscopic laser papillotomy”).

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

For people with hyperuricosuria and calcium stones, allopurinol is one of the few treatments that have been shown to reduce kidney stone recurrences. Allopurinol interferes with the production of uric acid in the liver. The drug is also used in people with gout or hyperuricemia (high serum uric acid levels). Dosage is adjusted to maintain a reduced urinary excretion of uric acid. Serum uric acid level at or below 6 mg/100 ml) is often a therapeutic goal. Hyperuricemia is not necessary for the formation of uric acid stones; hyperuricosuria can occur in the presence of normal or even low serum uric acid. Some practitioners advocate adding allopurinol only in people in whom hyperuricosuria and hyperuricemia persist, despite the use of a urine-alkalinizing agent such as sodium bicarbonate or potassium citrate.

One of the recognized medical therapies for prevention of stones is the thiazide and thiazide-like diuretics, such as chlorthalidone or indapamide. These drugs inhibit the formation of calcium-containing stones by reducing urinary calcium excretion. Sodium restriction is necessary for clinical effect of thiazides, as sodium excess promotes calcium excretion. Thiazides work best for renal leak hypercalciuria (high urine calcium levels), a condition in which high urinary calcium levels are caused by a primary kidney defect. Thiazides are useful for treating absorptive hypercalciuria, a condition in which high urinary calcium is a result of excess absorption from the gastrointestinal tract.

There is no known treatment at present, although some investigators have tried to lessen the hypercalcemia with various forms of bisphosphonates.

Treatment including addressing the cause, such as improving the diet, treating diarrhea, or stopping an offending medication. People without a significant source of potassium loss and who show no symptoms of hypokalemia may not require treatment.

Mild hypokalemia (>3.0 meq/l) may be treated with oral potassium chloride supplements (Klor-Con, Sando-K, Slow-K). As this is often part of a poor nutritional intake, potassium-containing foods may be recommended, such as leafy green vegetables, avocados, tomatoes, coconut water, citrus fruits, oranges, or bananas. Both dietary and pharmaceutical supplements are used for people taking diuretic medications.

Severe hypokalemia (<3.0 meq/l) may require intravenous supplementation. Typically, a saline solution is used, with 20–40 meq/l KCl per liter over 3–4 hours. Giving IV potassium at faster rates (20–25 meq/hr) may predispose to ventricular tachycardias and requires intensive monitoring. A generally safe rate is 10 meq/hr. Even in severe hypokalemia, oral supplementation is preferred given its safety profile. Sustained-release formulations should be avoided in acute settings.

Difficult or resistant cases of hypokalemia may be amenable to a potassium-sparing diuretic, such as amiloride, triamterene, spironolactone, or eplerenone. Concomitant hypomagnesemia will inhibit potassium replacement, as magnesium is a cofactor for potassium uptake.

When replacing potassium intravenously, infusion by a central line is encouraged to avoid the frequent occurrence of a burning sensation at the site of a peripheral infusion, or the rare occurrence of damage to the vein. When peripheral infusions are necessary, the burning can be reduced by diluting the potassium in larger amounts of fluid, or mixing 3 ml of 1% lidocaine to each 10 meq of KCl per 50 ml of fluid. The practice of adding lidocaine, however, raises the likelihood of serious medical errors.

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

The prognosis of nephrocalcinosis is determined by the underlying cause. Most cases of nephrocalcinosis do not progress to end stage renal disease, however if not reated it can lead to renal dysfunction this includes primary hyperoxaluria, hypomagnesemic hypercalciuric nephrocalcinosis and Dent's disease. Once nephrocalcinosis is found, it is unlikely to be reversed, however, partial reversal has been reported in patients who have had successful treatment of hypercalciuria and hyperoxaluria following corrective intestinal surgery.

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

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.

Carbamazepine is at least partly effective at reducing the number or severity of attacks in the majority of PEPD patients. High doses of this drug may be required, perhaps explaining the lack of effect in some individuals. While other anti-epileptic drugs, gabapentin and topiramate, have limited effect in some patients, they have not been shown to be generally effective. Opiate derived analgesics are also largely ineffective, with only sporadic cases of beneficial effect.

For treatment of type II, dietary modification is the initial approach, but many patients require treatment with statins (HMG-CoA reductase inhibitors) to reduce cardiovascular risk. If the triglyceride level is markedly raised, fibrates (peroxisome proliferator-activated receptor-alpha agonists) may be preferable due to their beneficial effects. Combination treatment of statins and fibrates, while highly effective, causes a markedly increased risk of myopathy and rhabdomyolysis, so is only done under close supervision. Other agents commonly added to statins are ezetimibe, niacin, and bile acid sequestrants. Dietary supplementation with fish oil is also used to reduce elevated triglycerides, with the greatest effect occurring in patients with the greatest severity. Some evidence exists for benefit of plant sterol-containing products and omega-3 fatty acids.

Most patients with thin basement membrane disease need only reassurance. Indeed, this disease was previously referred to as "benign familial hematuria" because of its usually benign course. Angiotensin converting enzyme inhibitors have been suggested to reduce the episodes of hematuria, though controlled studies are lacking. Treating co-existing hypercalciuria and hyperuricosuria will also be helpful in reducing hematuria.

The molecular basis for thin basement membrane disease has yet to be elucidated fully; however, defects in the gene encoding the a4 chain of type IV collagen have been reported in some families.

Weight loss and dietary modification are effective first-line lifestyle modification treatments for hypertriglyceridemia. For people with mildly or moderately high levels of triglycerides lifestyle changes including weight loss and dietary modification are recommended. This may include restriction of carbohydrates (specifically fructose) and fat in the diet. Medications are recommended in those with high levels of triglycerides that are not corrected with the aforementioned lifestyle modifications, with fibrates being recommended first.

The decision to treat hypertriglyceridemia with medication depends on the levels and on the presence of other risk factors for cardiovascular disease. Very high levels that would increase the risk of pancreatitis is treated with a drug from the fibrate class. Niacin and omega-3 fatty acids as well as drugs from the statin class may be used in conjunction, with statins being the main medication for moderate hypertriglyceridemia when reduction of cardiovascular risk is required.

Management of hematuria is aimed at treating secondary causes of hematuria. If hematuria is a result of a UTI, treatment with antibiotics is usually initiated and urine testing repeated after 6 weeks. If hematuria is secondary to a kidney stone, then management depends on the size of the kidney stone. If the stone is small enough, usually less than 1 cm, then conservative management with analgesics and fluid hydration may be sufficient, however stones that are too bid may require removal by a urologist. Another common cause of hematuria is benign enlargement of the prostate (BPH), treatment is aimed at reducing the size of the bladder with medications like finasteride and symptomatic management with drugs like terazonsin or tamsulosin.

For people with exercise induced hematuria, management is conservative and involves cessation of strenuous activities and keeping hydrated. If the cause of hematuria is a result of malignancy, treatment and management depends on the type and stage of cancer and can involve chemotherapy, radiation or surgical resection of the tumor or organ involved.

The affected animal should be left in the pasture, and not forced to come back to stall because excitation can darken the prognosis, even after adequate treatment.

Intravenous mixed calcium and magnesium injection are used. Subcutaneous injection of magnesium sulfate (200 ml of 50% solution) is also recommended.

Magnesium supplements are used to prevent the disease when ruminants, for obvious economic reasons, must have access to dangerous pastures.