text: 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 hypercalcaemia, 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, hypercalcaemia 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 hypercalcaemia and hypercalciuria.
  Medullary nephrocalcinosis
  Medullary sponge kidney
  Distal renal tubular acidosis
  Hyperoxaluria