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

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.

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.

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.

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.

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.

Treatment consists of oral bicarbonate supplementation. However, this will increase urinary bicarbonate wasting and may well promote a bicarbonate . The amount of bicarbonate given may have to be very large to stay ahead of the urinary losses. Correction with oral bicarbonate may exacerbate urinary potassium losses and precipitate hypokalemia. As with dRTA, reversal of the chronic acidosis should reverse bone demineralization.

Thiazide diuretics can also be used as treatment by making use of contraction alkalosis caused by them.

The cornerstone of treatment is administration of free water to correct the relative water deficit. Water can be replaced orally or intravenously. Water alone cannot be administered intravenously (because of osmolarity issue), but rather can be given with addition to dextrose or saline infusion solutions. However, overly rapid correction of hypernatremia is potentially very dangerous. The body (in particular the brain) adapts to the higher sodium concentration. Rapidly lowering the sodium concentration with free water, once this adaptation has occurred, causes water to flow into brain cells and causes them to swell. This can lead to cerebral edema, potentially resulting in seizures, permanent brain damage, or death. Therefore, significant hypernatremia should be treated carefully by a physician or other medical professional with experience in treatment of electrolyte imbalance, specific treatment like ACE inhibitors in heart failure and corticosteroids in nephropathy also can be used.

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.

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.

Other conditions such as Liddle's Syndrome can mimic the clinical features of AME, so diagnosis can be made by calculating the ratio of free urinary cortisol to free urinary cortisone. Since AME patients create less cortisone, the ratio will much be higher than non-affected patients. Alternatively, one could differentiate between the two syndromes by administering a potassium-sparing diuretic. Patients with Liddle's syndrome will only respond to a diuretic that binds the ENaC channel, whereas those with AME will respond to a diuretic that binds to ENaC or the mineralcorticoid receptor.

Pseudohyperaldosteronism (also pseudoaldosteronism) is a medical condition that mimics hyperaldosteronism. Like hyperaldosteronism, it produces hypertension associated with low plasma renin activity, and metabolic alkalosis associated with hypokalemia. Unlike hyperaldosteronism, it involves aldosterone levels that are normal or low (hypoaldosteronism).

This condition is characterized by hypertension, kaliuresis and reduced plasma renin.

Glucocorticoid remediable aldosteronism (GRA), also describable as "aldosterone synthase hyperactivity", is an autosomal dominant disorder in which the increase in aldosterone secretion produced by ACTH is no longer transient.

It is a cause of primary hyperaldosteronism.

Liddle's syndrome, also called Liddle syndrome is a genetic disorder inherited in an autosomal dominant manner that is characterized by early, and frequently severe, high blood pressure associated with low plasma renin activity, metabolic alkalosis, low blood potassium, and normal to low levels of aldosterone. Liddle syndrome involves abnormal kidney function, with excess reabsorption of sodium and loss of potassium from the renal tubule, and is treated with a combination of low sodium diet and potassium-sparing diuretic drugs (e.g. amiloride). It is extremely rare, with fewer than 30 pedigrees or isolated cases having been reported worldwide as of 2008.

Primary hyperaldosteronism can be mimicked by Liddle syndrome, and by ingestion of licorice and other foods containing glycyrrhizin. In one case report, hypertension and quadriparesis resulted from intoxication with a non-alcoholic pastis (an anise-flavored aperitif containing glycyrrhizinic acid).

Familial hyperaldosteronism is a group of inherited conditions in which the adrenal glands, which are small glands located on top of each kidney, produce too much of the hormone aldosterone. Excess aldosterone causes the kidneys to retain more salt than normal, which in turn increases the body's fluid levels and causes high blood pressure. People with familial hyperaldosteronism may develop severe high blood pressure, often early in life. Without treatment, hypertension increases the risk of strokes, heart attacks, and kidney failure. There are other forms of hyperaldosteronism that are not inherited.

Familial hyperaldosteronism is categorized into three types, distinguished by their clinical features and genetic causes. In familial hyperaldosteronism type I, hypertension generally appears in childhood to early adulthood and can range from mild to severe. This type can be treated with steroid medications called glucocorticoids, so it is also known as glucocorticoid-remediable aldosteronism (GRA). In familial hyperaldosteronism type II, hypertension usually appears in early to middle adulthood and does not improve with glucocorticoid treatment. In most individuals with familial hyperaldosteronism type III, the adrenal glands are enlarged up to six times their normal size. These affected individuals have severe hypertension that starts in childhood. The hypertension is difficult to treat and often results in damage to organs such as the heart and kidneys. Rarely, individuals with type III have milder symptoms with treatable hypertension and no adrenal gland enlargement.

This condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. The various types of familial hyperaldosteronism have different genetic causes.

It is unclear how common these diseases are. All together they appear to make up less than 1% of cases of hyperaldosteronism.

The amount of potassium deficit can be calculated using the following formula:

Meanwhile, the daily body requirement of potassium is calculated by multiplying 1 mmol to body weight in kilogrammes. Adding potassium deficit and daily potassium requirement would give the total amount of potassium need to be corrected in mmol. Dividing mmol by 13.4 will give the potassium in grams.

Few women of childbearing age have high blood pressure, up to 11% develop hypertension of pregnancy. While generally benign, it may herald three complications of pregnancy: pre-eclampsia, HELLP syndrome and eclampsia. Follow-up and control with medication is therefore often necessary.

Primary hyperaldosteronism (PHA) is a disorder of the adrenal cortex that causes increased circulating aldosterone levels. There are two types of PHA. One type is caused by a unilateral aldosterone-producing adenoma or adenocarcinoma. The other type, known as idiopathic hyperaldosteronism, occurs with bilateral adrenal hyperplasia.

In those with high volume or hypervolemia:

- Intake of a hypertonic fluid (a fluid with a higher concentration of solutes than the remainder of the body) with restricted free water intake. This is relatively uncommon, though it can occur after a vigorous resuscitation where a patient receives a large volume of a concentrated sodium bicarbonate solution. Ingesting seawater also causes hypernatremia because seawater is hypertonic and free water is not available. There are several recorded cases of forced ingestion of concentrated salt solution in exorcism rituals leading to death.

- Mineralcorticoid excess due to a disease state such as Conn's syndrome usually does not lead to hypernatremia unless free water intake is restricted.

- Salt poisoning (this condition is most common in children). It has also been seen in a number of adults with mental health problems. Too much salt can also occur from drinking seawater or soy sauce.

This condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. The various types of familial hyperaldosteronism have different genetic causes. Familial hyperaldosteronism type I is caused by the abnormal joining together (fusion) of two similar genes called CYP11B1 and CYP11B2, which are located close together on chromosome 8. These genes provide instructions for making two enzymes that are found in the adrenal glands.

The CYP11B1 gene provides instructions for making an enzyme called 11-beta-hydroxylase. This enzyme helps produce hormones called cortisol and corticosterone. The CYP11B2 gene provides instructions for making another enzyme called aldosterone synthase, which helps produce aldosterone. When CYP11B1 and CYP11B2 are abnormally fused together, too much aldosterone synthase is produced. This overproduction causes the adrenal glands to make excess aldosterone, which leads to the signs and symptoms of familial hyperaldosteronism type I.

Familial hyperaldosteronism type III is caused by mutations in the KCNJ5 gene. The KCNJ5 gene provides instructions for making a protein that functions as a potassium channel, which means that it transports positively charged atoms (ions) of potassium into and out of cells. In the adrenal glands, the flow of ions through potassium channels produced from the KCNJ5 gene is thought to help regulate the production of aldosterone. Mutations in the KCNJ5 gene likely result in the production of potassium channels that are less selective, allowing other ions (predominantly sodium) to pass as well. The abnormal ion flow results in the activation of biochemical processes (pathways) that lead to increased aldosterone production, causing the hypertension associated with familial hyperaldosteronism type III.

The genetic cause of familial hyperaldosteronism type II is unknown.

Adrenocortical hyperfunction is a condition where there is an overexpression of products of the adrenal cortex.

When cortisol is overproduced, it is called Cushing's syndrome.

When aldosterone is overproduced, it is called hyperaldosteronism.

Excessive sodium and fluid intake:

- IV therapy containing sodium

- As a Transfusion reaction to a rapid blood transfusion.

- High intake of sodium

Sodium and water retention:

- Heart failure

- Liver cirrhosis

- Nephrotic syndrome

- Corticosteroid therapy

- Hyperaldosteronism

- Low protein intake

Fluid shift into the intravascular space:

- Fluid remobilization after burn treatment

- Administration of hypertonic fluids, e.g. mannitol or hypertonic saline solution

- Administration of plasma proteins, such as albumin