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.

The condition is named after Dr. Frederic Bartter, who, along with Dr. Pacita Pronove, first described it in 1960 and in more patients in 1962.

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.

Renal tuberculosis

And other causes of hypercalcemia (and thus hypercalciuria)

- Immobilization (leading to hypercalcemia and hypercalciuria)

- Milk-alkali syndrome

- Hypervitaminosis D

- Multiple myeloma

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

In the general population, the frequency of medullary sponge kidney disease is reported to be 0.02–0.005%; that is, 1 in 5000 to 1 in 20,000. The frequency of medullary sponge kidney has been reported by various authors to be 1221% in patients with kidney stones. The disease is bilateral in 70% of cases.

Most cases of FHH are associated with loss of function mutations in the calcium-sensing receptor (CaSR) gene, expressed in parathyroid and kidney tissue. These mutations decrease the receptor's sensitivity to calcium, resulting in reduced receptor stimulation at normal serum calcium levels. As a result, inhibition of parathyroid hormone release does not occur until higher serum calcium levels are attained, creating a new equilibrium. This is the opposite of what happens with the CaSR sensitizer, cinacalcet. Functionally, parathyroid hormone (PTH) increases calcium resorption from the bone and increases phosphate excretion from the kidney which increases serum calcium and decreases serum phosphate. Individuals with FHH, however, typically have normal PTH levels, as normal calcium homeostasis is maintained, albeit at a higher equilibrium set point. As a consequence, these individuals are not at increased risk of the complications of hyperparathyroidism.

Another form has been associated with chromosome 3q.

In endocrinology, the terms 'primary' and 'secondary' are used to describe the abnormality (e.g., elevated aldosterone) in relation to the defect, "i.e.", the tumor's location. Hyperaldosteronism can also be caused by plant poisoning, where the patient has been exposed to too much licorice. Licorice is a perennial herb that is used in making candies and in cooking other desserts because of its sweet taste. It contains the chemical glycyrrhizin, which has medicinal uses, but at higher levels it can be toxic. It has the potential for causing problems with sodium and potassium in the body. It also interferes with the enzyme in the kidneys that converts cortisol to cortisone.

When taking a blood test, the aldosterone-to-renin ratio is abnormally increased in primary hyperaldosteronism, and decreased or normal but with high renin in secondary hyperaldosteronism.

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.

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 evidence linking vitamin C supplements with an increased rate of kidney stones is inconclusive. The excess dietary intake of vitamin C might increase the risk of calcium oxalate stone formation, in practice this is rarely encountered. The link between vitamin D intake and kidney stones is also tenuous. Excessive vitamin D supplementation may increase the risk of stone formation by increasing the intestinal absorption of calcium; correction of a deficiency does not.

Type 4 RTA is not actually a tubular disorder at all nor does it have a clinical syndrome similar to the other types of RTA described above. It was included in the classification of renal tubular acidoses as it is associated with a mild (normal anion gap) metabolic acidosis due to a "physiological" reduction in proximal tubular ammonium excretion (impaired ammoniagenesis), which is secondary to hypoaldosteronism, and results in a decrease in urine buffering capacity. Its cardinal feature is hyperkalemia, and measured urinary acidification is normal, hence it is often called hyperkalemic RTA or tubular hyperkalemia.

Causes include:

- Aldosterone deficiency (hypoaldosteronism): Primary vs. hyporeninemic (including diabetic nephropathy)

- Aldosterone resistance

1. Drugs: NSAIDs, ACE inhibitors and ARBs, Eplerenone, Spironolactone, Trimethoprim, Pentamidine

2. Pseudohypoaldosteronism

HSH was originally believed to be an X-linked disorder due to the preponderance of affected males. With the finding that mutations in TRPM6 (on chromosome 9) are causative for the disorder this is no longer the case. Of recent interest, however, is the characterization of a patient with symptoms similar to HSH who has a translocation of the chromosomes 9 and X.

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.

Dent disease 2 (nephrolithiasis type 2) is associated with the "OCRL" gene. Both Lowe syndrome (oculocerebrorenal syndrome) and Dent disease can be caused by truncating or missense mutations in "OCRL".

The condition is due to:

- Bilateral idiopathic (micronodular) adrenal hyperplasia (66%)

- Adrenal adenoma (Conn's syndrome) (33%)

- Primary (unilateral) adrenal hyperplasia—2% of cases

- Aldosterone-producing adrenocortical carcinoma—<1% of cases

- Familial Hyperaldosteronism (FH)

- Glucocorticoid-remediable aldosteronism (FH type I)—<1% of cases

- FH type II (APA or IHA)—<2% of cases

- Ectopic aldosterone-producing adenoma or carcinoma—< 0.1% of cases

There are no conclusive data demonstrating a cause-and-effect relationship between alcoholic beverage consumption and kidney stones. However, some have theorized that certain behaviors associated with frequent and binge drinking can lead to dehydration, which can, in turn, lead to the development of kidney stones.

The American Urological Association has projected that global warming will lead to an increased incidence of kidney stones in the United States by expanding the "kidney stone belt" of the southern United States.

People with lymphoproliferative/myeloproliferative disorders who were treated with chemotherapy developed symptomatic kidney stones 1.8% of the time in one study.

Complications associated with medullary sponge kidney include the following:

- Kidney stones

- Urinary tract infection (UTI)

- Blood in the urine

- Distal renal tubular acidosis (Type 1 RTA)

- Chronic kidney disease (rarely)

- Marked chronic pain

Results from a longitudinal study with end-stage renal disease suggest that hypermagnesemia may retard the development of arterial calcifications in end-stage renal disease. Significantly lower values of carotid intima-media thickness and aortic pulse wave velocity values, which are surrogate markers for vascular calcification, were observed in chronic kidney disease patients with high serum magnesium levels (0.90–1.32 mmol/L or 2.18–3.21 mg/dL) indicating a lower arteriosclerotic burden associated with a lower risk of cardiovascular events and mortality. Consequently, people with CKD with mildly elevated magnesium levels could have a survival advantage over those with lower magnesium levels.

Distal renal tubular acidosis (dRTA) or Type 1 renal tubular acidosis (RTA) is the classical form of RTA, being the first described. Distal RTA is characterized by a failure of acid secretion by the alpha intercalated cells of the cortical collecting duct of the distal nephron. This failure of acid secretion may be due to a number of causes, and it leads to an inability to acidify the urine to a pH of less than 5.3.

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.

In some patients, RTA shares features of both dRTA and pRTA. This rare pattern was observed in the 1960s and 1970s as a transient phenomenon in infants and children with dRTA (possibly in relation with some exogenous factor such as high salt intake) and is no longer observed. This form of RTA has also been referred to as juvenile RTA.

Combined dRTA and pRTA is also observed as the result of inherited carbonic anhydrase II deficiency. Mutations in the gene encoding this enzyme give rise to an autosomal recessive syndrome of osteopetrosis, renal tubular acidosis, cerebral calcification, and mental retardation. It is very rare and cases from all over the world have been reported, of which about 70% are from the Magreb region of North Africa, possibly due to the high prevalence of consanguinity there.

The kidney problems are treated as described above. There is no treatment for the osteopetrosis or cerebral calcification.

Type 3 is rarely discussed. Most comparisons of RTA are limited to a comparison of types 1, 2, and 4.

The most common cause of primary hyperparathyroidism is a sporadic, single parathyroid adenoma resulting from a clonal mutation (~97%). Less common are parathyroid hyperplasia (~2.5%), parathyroid carcinoma (malignant tumor), and adenomas in more than one gland (together ~0.5%).

Primary hyperparathyroidism is also a feature of several familial endocrine disorders: Multiple endocrine neoplasia type 1 and type 2A (MEN type 1 and MEN type 2A), and familial hyperparathyroidism.

Genetic associations include:

In all cases, the disease is idiopathic, but is thought to involve inactivation of tumor suppressor genes (Menin gene in MEN1), or involve gain of function mutations (RET proto-oncogene MEN 2a).

Recently, it was demonstrated that liquidators of the Chernobyl power plant are faced with a substantial risk of primary hyperparathyroidism, possibly caused by radioactive strontium isotopes.

Primary hyperparathyroidism can also result from pregnancy. It is apparently very rare, with only about 110 cases have so far been reported in world literature, but this is probably a considerable underestimate of its actual prevalence in pregnant women.

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