nephrogenic diabetes insipidus) as can be seen in hypercalcemia, medullary nephrocalcinosis of any cause, or in children with Bartter syndrome in whom essential tubular salt reabsorption is compromised.There are several causes of nephrocalcinosis that are typically acute and present only with kidney failure. These include tumor lysis syndrome, acute phosphate nephropathy, and occasional cases of enteric hyperoxaluria. Cause
Nephrocalcinosis is connected with conditions that cause hypercalcemia, hyperphosphatemia, and the increased excretion of calcium, phosphate, and/or oxalate in the urine. A high urine pH can lead to  Nephrocalcinosis but only if it is accompanied by hypercalciuria and hypocitraturia, since having a normal urinary citrate usually inhibits the crystallization of calcium. In conjunction with Nephrocalcinosis, hypercalcemia and hypercalciuria the following can occur:
Primary hyperparathyroidism: Nephrocalcinosis is one of the most common symptoms of primary hyperparathyroidism. Sarcoidosis: Nephrocalcinosis is one of the most common symptoms. Vitamin D: This can cause nephrocalcinosis because of Vitamin D therapy because it increases the absorption of ingested calcium and bone resorption, resulting in hypercalcemia and hypercalciuria. Medullary nephrocalcinosis
Medullary sponge kidney
Distal renal tubular acidosis
Hyperoxaluria
Renal papillary necrosisAnd other causes of hypercalcemia (and thus hypercalciuria)
Immobilization (leading to hypercalcemia and hypercalciuria)
Milk-alkali syndrome
Hypervitaminosis D
Multiple myeloma

Hypercalciuria without hypercalcemia
These conditions can cause nephrocalcinosis in association with hypercalciuria without hypercalcemia:
Distal renal tubular acidosis
Medullary sponge kidney
Neonatal nephrocalcinosis and loop diuretics
Inherited tubulopathies
Chronic hypokalemia
Beta thalassemia

Mechanism
Nephrocalcinosis is caused by an increase in the urinary excretion of calcium, phosphate, and/or oxalate. Nephrocalcinosis is closely associated with nephrolithiasis, and patients frequently present with both conditions, however there have been cases where one occurs without the other.
Etomidate (USAN, INN, BAN; marketed as Amidate) is a short-acting intravenous anaesthetic agent used for the induction of general anaesthesia and sedation for short procedures such as reduction of dislocated joints, tracheal intubation, cardioversion and electroconvulsive therapy. It was developed at Janssen Pharmaceutica in 1964 and was introduced as an intravenous agent in 1972 in Europe and in 1983 in the United States.The most common side effects include venous pain on injection and skeletal muscle movements. Medical uses
Sedation and anesthesia
In emergency settings, etomidate can be used as a sedative hypnotic agent. It is used for conscious sedation and as a part of a rapid sequence induction to induce anaesthesia. It is used as an anaesthetic agent since it has a rapid onset of action and a safe cardiovascular risk profile, and therefore is less likely to cause a significant drop in blood pressure than other induction agents. In addition, etomidate is often used because of its easy dosing profile, limited suppression of ventilation, lack of histamine liberation and protection from myocardial and cerebral ischemia. Thus, etomidate is a good induction agent for people who are hemodynamically unstable. Etomidate also has interesting characteristics for people with traumatic brain injury because it is one of the only anesthetic agents able to decrease intracranial pressure and maintain a normal arterial pressure.In those with sepsis, one dose of the medication does not appear to affect the risk of death.