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.

Hypoaldosteronism may result in hyperkalemia and is the cause of 'type 4 renal tubular acidosis', sometimes referred to as hyperkalemic RTA or tubular hyperkalemia. However, the acidosis, if present, is often mild. It can also cause urinary sodium wasting, leading to volume depletion and hypotension.

When adrenal insufficiency develops rapidly, the amount of Na+ lost from the extracellular fluid exceeds the amount excreted in the urine, indicating that Na+ also must be entering cells. When the posterior pituitary is intact, salt loss exceeds water loss, and the plasma Na+ falls. However, the plasma volume also is reduced, resulting in hypotension, circulatory insufficiency, and, eventually, fatal shock. These changes can be prevented to a degree by increasing the dietary NaCl intake. Rats survive indefinitely on extra salt alone, but in dogs and most humans, the amount of supplementary salt needed is so large that it is almost impossible to prevent eventual collapse and death unless mineralocorticoid treatment is also instituted.

Unilateral primary hyperaldosteronism due to an adrenocortical adenoma or adrenocarcinoma can be potentially cured surgically. Unilateral adrenalectomy is the treatment of choice for unilateral PHA. Potential complications include hemorrhage and postoperative hypokalemia. With complete removal of the tumor, prognosis is excellent.

Bilateral primary hyperaldosteronism due to hyperplasia of the zona glomerulosa or metastasized adrenocortical adenocarcinoma should be treated medically. Medical therapy is aimed at normalizing blood pressure and plasma potassium concentration. Mineralocorticoid receptor blockers, such as spironolactone, coupled with potassium supplementation are the most commonly used treatments. Specific therapy for treating high blood pressure (e.g., amlodipine), should be added if necessary.

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.

The treatment for AME is based on the blood pressure control with Aldosterone antagonist like Spironalactone which also reverses the hypokalemic metabolic alkalosis and other anti-hypertensives. Renal transplant is found curative in almost all clinical cases.AME is exceedingly rare, with fewer than 100 cases recorded worldwide.

Liquorice consumption may also cause a temporary form of AME due to its ability to block 11β-hydroxysteroid dehydrogenase type 2, in turn causing increased levels of cortisol. Cessation of licorice consumption will reverse this form of AME.

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.

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).

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.

Standard therapy involves intravenous injections of glucocorticoids and large volumes of intravenous saline solution with dextrose (glucose). This treatment usually brings rapid improvement. If intravenous access is not immediately available, intramuscular injection of glucocorticoids can be used. When the patient can take fluids and medications by mouth, the amount of glucocorticoids is decreased until a maintenance dose is reached. If aldosterone is deficient, maintenance therapy also includes oral doses of fludrocortisone acetate.

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.

Treatment for Addison's disease involves replacing the missing cortisol, sometimes in the form of hydrocortisone tablets, or prednisone tablets in a dosing regimen that mimics the physiological concentrations of cortisol. Alternatively, one-quarter as much prednisolone may be used for equal glucocorticoid effect as hydrocortisone. Treatment is usually lifelong. In addition, many patients require fludrocortisone as replacement for the missing aldosterone.

People with Addison's are often advised to carry information on them (e.g., in the form of a MedicAlert bracelet or information card) for the attention of emergency medical services personnel who might need to attend to their needs. It is also recommended that a needle, syringe, and injectable form of cortisol be carried for emergencies. People with Addison's disease are advised to increase their medication during periods of illness or when undergoing surgery or dental treatment. Immediate medical attention is needed when severe infections, vomiting, or diarrhea occur, as these conditions can precipitate an Addisonian crisis. A patient who is vomiting may require injections of hydrocortisone instead.

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.

Most asymptomatic individuals with Gitelman syndrome can be monitored without medical treatment. Potassium and magnesium supplementation to normalize low blood levels of potassium and magnesium is the mainstay of treatment. Large doses of potassium and magnesium are often necessary to adequately replace the electrolytes lost in the urine. Diarrhea is a common side effect of oral magnesium which can make oral replacement difficult but dividing the dose to 3-4 times a day is better tolerated. Severe deficits of potassium and magnesium require intravenous replacement. If low blood potassium levels are not sufficiently replaced with oral replacement, aldosterone antagonists (such as spironolactone or eplerenone) or epithelial sodium channel blockers such as amiloride can be used to decrease urinary wasting of potassium.

As with other forms of CAH, the primary therapy of 11β-hydroxylase deficient CAH is lifelong glucocorticoid replacement in sufficient doses to prevent adrenal insufficiency and suppress excess mineralocorticoid and androgen production.

Salt-wasting in infancy responds to intravenous saline, dextrose, and high dose hydrocortisone, but prolonged fludrocortisone replacement is usually not necessary. The hypertension is ameliorated by glucocorticoid suppression of DOC.

Long term glucocorticoid replacement issues are similar to those of 21-hydroxylase CAH, and involve careful balance between doses sufficient to suppress androgens while avoiding suppression of growth. Because the enzyme defect does not affect sex steroid synthesis, gonadal function at puberty and long-term fertility should be normal if adrenal androgen production is controlled. See congenital adrenal hyperplasia for a more detailed discussion of androgen suppression and fertility potential in adolescent and adult women.

Life long hormone replacement therapy for the hormones that are missing.

Certain medications, including NSAIDs (Motrin/Ibuprofen) and steroids can cause hypertension. Other medications include extrogens (such as those found in oral contraceptives with high estrogenic activity), certain antidepressants (such as venlafaxine), buspirone, carbamazepine, bromocriptine, clozapine, and cyclosporine.

High blood pressure that is associated with the sudden withdrawal of various antihypertensive medications is called rebound hypertension. The increases in blood pressure may result in blood pressures greater than when the medication was initiated. Depending on the severity of the increase in blood pressure, rebound hypertension may result in a hypertensive emergency. Rebound hypertension is avoided by gradually reducing the dose (also known as "dose tapering"), thereby giving the body enough time to adjust to reduction in dose. Medications commonly associated with rebound hypertension include centrally-acting antihypertensive agents, such as clonidine and methyl-dopa.

Other herbal or "natural products" which have been associated with hypertension include ma huang, St John's wort, and licorice.

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.

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.

Secondary refers to an abnormality that indirectly results in pathology through a predictable physiologic pathway, i.e., a renin-producing tumor leads to increased aldosterone, as the body's aldosterone production is normally regulated by renin levels.

One cause is a juxtaglomerular cell tumor. Another is renal artery stenosis, in which the reduced blood supply across the juxtaglomerular apparatus stimulates the production of renin. Likewise, fibromuscular dysplasia may cause stenosis of the renal artery, and therefore secondary hyperaldosteronism. Other causes can come from the tubules: Hyporeabsorption of sodium (as seen in Bartter and Gitelman syndromes) will lead to hypovolemia/hypotension, which will activate the RAAS.

There are several causes for this condition, including adrenal insufficiency, congenital adrenal hyperplasia, and medications (certain diuretics, NSAIDs, and ACE inhibitors).

- Primary Aldosterone deficiency

1. Primary adrenal insufficiency

2. Congenital adrenal hyperplasia (21 and 11β but not 17)

3. Aldosterone synthase deficiency

- Secondary Aldosterone deficiency

1. Secondary adrenal insufficiency

2. Diseases of the pituitary or hypothalamus

- Hyporeninemic hypoaldosteronism (due to decreased angiotensin 2 production as well as intra-adrenal dysfunction)

1. Renal dysfunction-most commonly diabetic nephropathy

2. NSAIDs

3. Ciclosporin

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.

XX females with lipoid CAH may need estrogen replacement at or after puberty. Active intervention has been used to preserve the possibility of fertility and conception in lipoid CAH females. In a case report in 2009, a woman with late onset lipoid CAH due to StAR deficiency underwent hormone replacement therapy in combination with an assisted fertility technique, intracytoplasmic sperm injection. This led to ovulation and with implantation of the in vitro fertilized egg, a successful birth.

Some of the childhood management issues are similar those of 21-hydroxylase deficiency:

- Replacing mineralocorticoid with fludrocortisone

- Suppressing DHEA and replacing cortisol with glucocorticoid

- Providing extra glucocorticoid for stress

- Close monitoring and perhaps other adjunctive measures to optimize growth

- Deciding whether surgical repair of virilized female genitalia is warranted

However, unlike 21-hydroxylase CAH, children with 3β-HSD CAH may be unable to produce adequate amounts of testosterone (boys) or estradiol (girls) to effect normal pubertal changes. Replacement testosterone or estrogen and progesterone can be initiated at adolescence and continued throughout adult life. Fertility may be impaired by the difficulty of providing appropriate sex hormone levels in the gonads even though the basic anatomy is present.

Prompt treatment of some causes of azotemia can result in restoration of kidney function; delayed treatment may result in permanent loss of renal function. Treatment may include hemodialysis or peritoneal dialysis, medications to increase cardiac output and increase blood pressure, and the treatment of the condition that caused the azotemia.