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What is Nephrocalcinosis and explain in detail?
Nephrocalcinosis, once known as Albrights calcinosis after Fuller Albright, is a term originally used to describe deposition of calcium salts in the renal parenchyma due to hyperparathyroidism. The term nephrocalcinosis is used to describe the deposition of both calcium oxalate and calcium phosphate. It may cause acute kidney injury. It is now more commonly used to describe diffuse, fine, renal parenchymal calcification in radiology. It is caused by multiple different conditions and is determined progressive kidney dysfunction.  These outlines eventually come together to form a dense mass. During its early stages, nephrocalcinosis is visible on x-ray, and appears as a fine granular mottling over the renal outlines. It is most commonly seen as an incidental finding with medullary sponge kidney on an abdominal x-ray.
It may be severe enough to cause (as well as be caused by) renal tubular acidosis or even end stage kidney disease, due to disruption of the kidney tissue by the deposited calcium.

Signs and symptoms
Though this condition is usually asymptomatic, if symptoms are present they are usually related to the causative process, (e.g. hypercalcemia). Some of the symptoms that can happen are blood in the urine, fever and chills, nausea and vomiting, severe pain in the belly area, flanks of the back, groin, or testicles.
These include renal colic, polyuria and polydipsia:
Renal colic is usually caused by pre-existing nephrolithiasis, as may occur in patients with chronic hypercalciuria. Less commonly, it can result from calcified bodies moving into the calyceal system.
Nocturia, polyuria, and polydipsia from reduced urinary concentrating capacity (i.e. 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. Calcium oxalate and calcium phosphate crystals form when the concentration of the reactants exceeds the limit. The deposits are collected in the inner medullary interstitium in the basement membranes of the thin limbs of the loop of Henle. The calcium phosphate plaques can enlarge into the surrounding interstitial tissue, or even rupture into the tubule lumen and can promote calcium oxalate stone formation.

Diagnosis
Nephrocalcinosis is diagnosed for the most part by imaging techniques. The imagings used are ultrasound (US), abdominal plain film and CT imaging. Of the 3 techniques CT and US are the more preferred. Nephrocalcinosis is considered present if at least two radiologists make the diagnosis on US and/or CT. In some cases a renal biopsy is done instead if imaging is not enough to confirm nephrocalcinosis. Once the diagnosis is confirmed additional testing is needed to find the underlying cause because the underlying condition may require treatment for reasons independent of nephrocalcinosis. These additional tests will measure serum, electrolytes, calcium, and phosphate, and the urine pH. If no underlying cause can be found then urine collection should be done for 24 hours and measurements of the excretion of calcium, phosphate, oxalate, citrate, and creatinine are looked at.

Stages of nephrocalcinosis
Chemical or Molecular nephrocalcinosis: Defined as a measurable increase in intracellular calcium concentrations, however, it is not visible through X-ray or microscopically.
Microscopic nephrocalcinosis: Occurs when depositis are visible by light microscope by obtaining a tissue sample from a biopsy. However, this cannot be seen in an X-ray.
Macroscopic nephrocalcinosis: Occurs when calcification can be seen through X-ray imaging.

Treatment
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 a 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.

Prognosis
The prognosis of nephrocalcinosis is determined by the underlying cause