Calcium is an important electrolyte that regulates vital physiologic processes in the body including hormonal secretion, cardiac contraction, and blood clotting. It also helps to grow and repair our skeletons. 

Hypercalciuria occurs in 5%-10% of the adult population. It is defined as excess calcium in the urine. This excess calcium may come from the intestines, where calcium is absorbed, or from the skeleton. Excess calcium in the urine tends to form salts that crystallize. These crystals can cause pain or other urinary symptoms, depending upon their size and location. Large crystals are known as kidney stones. Chronic hypercalciuria may lead to impairment of renal function, kidney stones, chronic kidney disease, or osteoporosis. There are two causes of hypercalciuria: 

  • Idiopathic: occurring on its own in the presence of normal serum calcium levels 
  • Secondary: occurring as a result of another condition which causes high serum calcium levels 

Patients with idiopathic hypercalciuria have a generalized increase in calcium turnover, which includes increased gut calcium absorption, decreased renal calcium reabsorption, and a tendency to lose calcium from bone. In the latter instance, it is important to complete a Dual-energy x-ray absorption (DXA or DEXA), a tool used to measure and diagnose osteoporosis to evaluate for reduction in bone mass.  

Risk Factors

Risk factors for hypercalciuria include family history of kidney stones, dehydration, diet high in sodium and protein, certain medications including but not limited to: furosemide (Lasix), corticosteroids, excessive vitamin D, methylxanthines (theophylline), obesity, diabetes mellitus, and hypertension.  

Causes and Symptoms

Causes of idiopathic hypercalciuria are largely genetic in origin without an apparent underlying etiology. Causes of secondary hypercalciuria include primary hyperparathyroidism, hyperthyroidism, Paget disease, myeloma, malignancy, and immobility. High salt (sodium) intake has also been suggested as a possible cause of hypercalciuria.  An increased sodium load leads to higher urinary excretion of sodium which decreases tubular calcium reabsorption resulting in hypercalciuria.  A high animal protein diet will produce an acid load that causes a release of calcium from the bone and inhibition of renal tubular calcium reabsorption resulting in hypercalciuria.  


Hypercalciuria is mainly diagnosed by measuring calcium in the urine using the following tests:` 

  • 24 hour urine test for calcium and other minerals. A 24-hour urinary calcium level of 250 mg is a useful initial threshold for determining hypercalciuria. 
  • Blood tests to rule out certain diseases that may cause hypercalciuria 
  • Genetic testing, especially if there is a family history of kidney stones 

Imaging studies, especially renal ultrasound which does not deliver any radiation, to look for kidney abnormalities or stones. 


Treatment for hypercalciuria includes: 

  • Addressing any secondary disease causing the hypercalciuria.  
  • Making dietary changes. If serum calcium levels are normal (which rules out hyperparathyroidism), dietary calcium is modified. A diet that is low in animal protein and salt (sodium) is recommended. Then, a repeat 24-hour urine test can be done to determine the response. If hypercalciuria persists, then medication (such as thiazides) likely will be needed.  
  • If diet changes are not enough, the doctor may need to add medicines to decrease calcium in the urine or prevent stone formation. 
  • Thiazide diuretics such as hydrochlorothiazide, chlorthalidone, and indapamide can significantly decrease urinary calcium excretion and reduce the incidence of stone formation. Thiazides also may improve bone mineralization and reduce the risk of fractures. 
  • Thiazides can induce a positive calcium balance and reduce urinary calcium by up to 50%. Hydrochlorothiazide and chlorthalidone are used most often, but indapamide also can be used. The advantage of chlorthalidone and indapamide is their longer half-life as hydrochlorothiazide would need to be given twice a day. Thiazides will not be effective unless dietary salt intake is limited.  
  • Amiloride, a potassium-sparing diuretic, is not a thiazide but when added to thiazides may further increase calcium reabsorption as well as minimizing potassium loss.  
  • Repeating 24 hour urine tests may be necessary to check how well treatment is working. 


Most often, with dietary changes—and medicine if needed—you can lower urine calcium into the normal range, lowering the risk of kidney stones. Because idiopathic hypercalciuria could be genetically inherited these individuals will always need to watch their diet to decrease the risk of developing kidney stones and other associated problems. 

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