eMedicine Specialties > Urology > Stones

Hypercalciuria: Treatment & Medication

Author: Stephen W Leslie, MD, FACS, Founder and Medical Director, Lorain Kidney Stone Research Center; Clinical Assistant Professor, Department of Urology, The University of Toledo College of Medicine
Contributor Information and Disclosures

Updated: Oct 21, 2009

Treatment

Medical Care

Medical therapy of hypercalciuria is used whenever dietary treatment guidelines alone are inadequate, ineffective, unsustainable, or intolerable for the patient. Medical therapy generally should be used together with dietary treatment guidelines for optimal results and health. Current specific medical therapies include thiazides, orthophosphates, bisphosphonates, sodium cellulose phosphate, and dipyridamole.

Absorptive hypercalciuria type I

Absorptive hypercalciuria type I is a relatively rare condition, generally characterized by elevated urinary calcium and calcium/creatinine levels except while fasting. A variant of absorptive hypercalciuria type I exists in which fasting hypercalciuria can occur due to excess serum vitamin D-3. This vitamin D–dependent variant can be diagnosed with the finding of increased serum vitamin D levels and with correction of the fasting hypercalciuria with a trial of ketoconazole therapy. (Ketoconazole is a potent P450 3A4 cytochrome inhibitor that reduces circulating vitamin D-3 levels by 30-40%.) As many as 50% of all patients with absorptive hypercalciuria type I may have increased levels of vitamin D-3. Other causes of fasting hypercalciuria can be identified by elevated PTH levels (renal calcium leak and hyperparathyroidism) or by increased urinary phosphate levels with hypophosphaturia (renal phosphate leak or absorptive hypercalciuria type III).

The diagnosis is usually clear in the traditional form of absorptive type I hypercalciuria because normocalciuria is restored only during fasting and not on the 400-mg calcium 100-mEq sodium diet. The vitamin D–dependent variant can cause fasting hypercalciuria, something generally associated only with renal leak hypercalciuria and hyperparathyroidism. Serum PTH levels are elevated in both renal leak hypercalciuria and hyperparathyroidism but normal or low in absorptive hypercalciuria type I. Serum and urinary phosphate levels are normal, as well as vitamin D-3, which differentiates it from renal phosphate leak hypercalciuria.

Treatment of absorptive hypercalciuria type I can be very difficult due to the severity of the intestinal calcium hyperabsorption. Therapy primarily consists of moderate dietary calcium restriction, thiazides, and orthophosphates.

Thiazides, such as trichlormethiazide (Naqua) or indapamide (Lozol), substantially reduce urinary calcium excretion, but they do not correct the primary defect, which is uncontrolled increased intestinal calcium absorption. Thiazides may lose their hypocalciuric effect over time and create hypokalemia, hypocitraturia, and increased uric acid levels.

Orthophosphates, such as K-Phos Neutral, Neutra-Phos K, and Uro-KP-Neutral, lower serum vitamin D-3 levels and reduce urinary calcium excretion. They are roughly equal to thiazides in their ability to reduce urinary calcium and prevent recurrent calcium stone formation. Because of the need for frequent dosing and various gastrointestinal adverse effects, orthophosphates are not the preferred agents when thiazides alone are sufficient and well tolerated. The combination of thiazides and orthophosphates used together may be necessary in difficult or resistant cases of absorptive hypercalciuria type I.

Sodium cellulose phosphate is an extremely potent intestinal calcium-binding agent. It previously was recommended as a primary therapy for absorptive hypercalciuria type I, but concerns about creating a negative calcium balance, bone demineralization, and other adverse effects currently limit its usefulness. These risks have shifted therapy away from this agent in favor of thiazides and orthophosphates.

When sodium cellulose phosphate is used as a therapy, supplemental magnesium and a dietary oxalate restriction are recommended. This is because the cellulose phosphate binds intestinal magnesium as well as calcium. Supplemental magnesium therefore must be administered to patients on cellulose phosphate therapy to avoid magnesium depletion. The dietary oxalate restriction is due to the lack of free intestinal calcium that is created with the cellulose phosphate therapy. This removes the primary intestinal oxalate-binding agent (calcium) from the digestive tract and leads directly to increased free intestinal oxalate absorption with subsequent hyperoxaluria.

Other therapies include the use of increased dietary fiber, such as rice, oat, and wheat bran supplements, as relatively mild intestinal calcium binders. Bisphosphonates, such as alendronate (Fosamax), increase bone deposition of calcium, thus removing it from the circulation before it can be excreted. This improves bone calcium density and helps reduce urinary calcium levels. The main benefit may be in protecting the bones from calcium depletion and demineralization in hypercalciuric patients.

Optimization of all other urinary stone risk factors is highly recommended, including an increase in urinary volume, reduced dietary oxalate, and potassium citrate supplements as needed. Purine intake should be restricted if uric acid levels are elevated.

Pentosan polysulphate (Elmiron) has been suggested to be of some potential use in difficult calcium oxalate stone cases. While it has no effect specifically on calcium excretion, it appears to reduce calcium oxalate crystallization and crystal aggregation, which reduces new kidney stone formation rates.^11,12,13

Absorptive hypercalciuria type I represents an extremely efficient intestinal calcium absorption mechanism. Bone density usually is normal because abundant calcium is available for bone deposition, and PTH levels are normal or low. However, in some cases, the urinary calcium excretion is even greater than the amount absorbed, resulting in a net negative calcium balance and possible decrease in bone density, which is the opposite of what would be expected. Researchers think that this could be due to elevated serum vitamin D levels or just an increased sensitivity to vitamin D and its metabolites.

Absorptive hypercalciuria type II

Absorptive hypercalciuria type II is a less severe form of absorptive hypercalciuria. By definition, the hypercalciuria is controlled by a restricted low-calcium (400 mg calcium and 100 mEq sodium) diet. Fasting hypercalciuria is not present in this disorder.

Treatment generally is with dietary modifications, whenever possible, including a diet of moderate calcium intake. Overly strict dietary calcium restrictions are discouraged because of the possibility of creating a negative calcium balance and osteoporosis. Reduced dietary calcium causes a lack of oxalate-binding sites in the intestinal tract, which increases urinary oxalate levels, negating the benefit of any reduced urinary calcium.

Patients may decide they cannot follow the recommended calcium diet, or it may prove to be ineffective. In these cases, orthophosphates and/or thiazide therapy is recommended. Some concern exists that when thiazides are used in these cases on a long-term basis, the hypocalciuric effect may become attenuated as the calcium stores in the bones become filled. If this occurs, it generally occurs at least 2 years from the time of treatment initiation. A period of alternate therapy, such as sodium cellulose phosphate or orthophosphates, can be used temporarily for approximately 6 months, and then the thiazides can be restarted. No such problem exists with orthophosphate therapy, but current formulations need to be taken frequently and often have gastrointestinal adverse effects such as diarrhea, bloating, and indigestion.

Absorptive hypercalciuria type III (renal phosphate leak)

Renal phosphate leak hypercalciuria is a vitamin D–dependent variant of absorptive hypercalciuria. It should be suspected in any hypercalciuric patient with a low serum phosphate level. A serum phosphate level of less than 2.9 mg/dL has been suggested as sufficient to raise the suspicion of renal phosphate leak hypercalciuria.

The etiology is an obligatory and uncontrolled loss of phosphate in the urine due to a renal defect. This produces hypophosphatemia, which stimulates the renal conversion of 25-hydroxyvitamin D to the much more active 1,25-dihydroxyvitamin D-3 (calcitriol, vitamin D-3). Vitamin D-3 increases intestinal phosphate absorption to correct the low serum phosphate levels. However, it also simultaneously increases intestinal calcium absorption. This extra calcium eventually is excreted in the urine. The diagnosis is confirmed by the following findings: (1) low serum phosphate, (2) hypercalciuria, (3) high urinary phosphate, (4) high serum vitamin D-3, and (5) normocalcemia and normal PTH levels.

Because the specific renal defect cannot be corrected, the most effective treatment is oral orthophosphate therapy. This corrects the hypophosphatemia and limits the amount of vitamin D-3 activation that occurs. The optimal orthophosphate supplement may be a slow-release neutral potassium phosphate (UroPhos-K), which has not yet been approved by the Food and Drug Administration (FDA). Dipyridamole (Persantine) also has been shown to increase the renal phosphate excretion threshold, which raises serum phosphate, normalizes high vitamin D levels, and reduces hypercalciuria.¹⁴

Renal leak hypercalciuria

Renal leak hypercalciuria occurs in about 5-10% of calcium stone formers. It is characterized by fasting hypercalciuria with secondary hyperparathyroidism but without hypercalcemia. It generally is not amenable to therapy with dietary calcium restrictions because of the obligatory calcium loss, which can easily lead to bone demineralization, especially if oral calcium intake is restricted.

The etiology is a defect in calcium reabsorption from the renal tubule that causes an obligatory excessive urinary calcium loss. This results in hypocalcemia, which causes an elevation in the serum PTH. This secondary hyperparathyroidism raises vitamin D levels and increases intestinal calcium absorption. Essentially, this means that, even in cases of undeniable renal leak hypercalciuria, an element of absorptive hypercalciuria can be present.

The diagnosis is relatively easy. Any patient who fails to control their excessive urinary calcium on dietary measures alone and demonstrates relatively high serum PTH levels without hypercalcemia or hypophosphatemia probably has renal leak hypercalciuria.

Fasting hypercalciuria typically is found in this condition, renal phosphate leak, and in hyperparathyroidism. These can be differentiated by the presence or absence of hypercalcemia and hypophosphatemia. The calcium/creatinine ratio tends to be high in renal leak hypercalciuria (>0.20), and medullary sponge kidney is more likely than in other types of hypercalciuria.

Treatment of renal leak hypercalciuria is primarily with thiazides. These medications specifically return calcium from the renal tubule to the serum. They generally reduce urinary calcium levels by 30-40% and eliminate the secondary hyperparathyroidism. This hypocalciuric effect of thiazides is diminished or eliminated if dietary sodium is not restricted. Adverse effects of thiazides include an increase in uric acid and a decrease in urinary citrate. They also can cause hypokalemia. To correct these potential problems, potassium citrate often is administered to patients on long-term thiazide therapy. When used appropriately in renal leak hypercalciuria, thiazides work extremely well and do not appear to attenuate their hypocalciuric effect over time. Thiazides chemically are sulfonamides and should be used cautiously, if at all, in patients with a known sulfa allergy.

Preferred forms of thiazide therapy include trichlormethiazide (Naqua) 2-4 mg/day and indapamide (Lozol) 1.25-2.5 mg/day. These two medications can be administered just once a day and tend to carry fewer adverse effects than shorter-acting thiazides. Potassium citrate often is added to the thiazide therapy to prevent hypokalemia and to increase urinary citrate levels. The dosage of potassium citrate should be adjusted based on serum potassium and 24-hour urinary citrate levels.

Resorptive hypercalciuria (hyperparathyroidism)

Resorptive hypercalciuria almost always is due to hyperparathyroidism. This generally accounts for 3-5% of all cases of hypercalciuria, although some reports have indicated an incidence as high as 8%. Increased PTH levels cause a release of calcium from bone stores. It also increases calcium absorption from the digestive tract by raising vitamin D-3 levels and decreases renal excretion of calcium by stimulating calcium reabsorption in the distal renal tubule. Eventually, the hypercalcemia overcomes this renal calcium conserving quality and results in an increased net loss of calcium through the urine (hypercalciuria).

Hyperparathyroidism does not always result in calcium stone disease. The reason for this is unclear but may reflect optimal levels of other urinary metabolites, such as oxalate, uric acid, sodium, phosphate, citrate, urinary volume, and serum vitamin D-3 levels among others. In some cases, the vitamin D-3 level has been suggested to be responsible for determining which patients with hyperparathyroidism actually develop kidney stones. This apparently reasonable hypothesis remains unproved. The current evidence suggests that vitamin D levels cannot be the only reason some hyperparathyroid patients develop stones while others do not.

Hyperparathyroidism produces a lower urinary calcium excretion for its level of serum calcium than hypercalcemia from other causes. In other words, for any level of serum calcium, hyperparathyroid patients have a lower urinary calcium excretion than hypercalcemic patients with normal PTH levels. This is due to the calcium-conserving effect of PTH on the kidneys.

The most common cause of hypercalcemia other than hyperparathyroidism is malignancy. Other causes include milk-alkali syndrome, Paget disease, sarcoidosis, multiple myeloma, and granulomatous diseases.

Hyperparathyroid patients who have parathyroid surgery and subsequently demonstrate normal urinary calcium levels are still at risk for developing stones at about the same rate as other calcium stone formers. Therefore, retesting with 24-hour urine determinations is recommended for calcium stone formers even after successful parathyroid surgery has normalized their serum calcium levels. Urinary cyclic AMP can be used as a substitute for serum PTH level determinations to monitor patients who have already been diagnosed.

Hyperparathyroidism should be suspected in calcium stone–forming patients with significant hypercalciuria, even in those with only mild hypercalcemia. Failure to identify a curable cause of osteoporosis and calcium nephrolithiasis can be easily avoided just by checking the parathyroid hormone level routinely in hypercalciuric patients with relatively high serum calcium levels.¹⁵

The recommended treatment for patients who produce calcium stones with hyperparathyroidism is parathyroid surgery. For those who are unable or unwilling to undergo the surgery, medical treatment is available. Bisphosphonates now are the medical agent of choice because they correct the hypercalcemia, reduce bone resorption, and lower urinary calcium excretion. Orthophosphates and calcitonin can be used for these patients as well. Thiazides should not be used in hyperparathyroid patients even when hypercalciuria is present because of the risk of increasing the hypercalcemia. (The only exception would be a short course for testing purposes in carefully selected cases to induce a mild,controlled increase in serum calcium while monitoring the PTH level to see if it drops appropriately or is autonomous.)

Estrogens should be used in postmenopausal, hypercalciuric women whenever possible. Their action is similar to the bisphosphonates.

PTH actually stimulates both osteoblastic and osteoclastic cells. High sustained levels of PTH result in a net loss of calcium and bone mass, but intermittent injections of PTH in animals and in human studies have indicated a net increase in osteoblastic activity and bone mass. This intermittent therapy, which appears promising as a potential treatment for osteoporosis, does not appear to significantly affect hypercalciuria or serum calcium levels.

Calcimimetic agents, such as cinacalcet (Sensipar), are a new and exciting modality being studied for the medical treatment of hyperparathyroidism.^{16,17,18,19,20} Activation of specific calcium receptors on parathyroid cells by these calcimimetic agents inhibits PTH secretion. Essentially, the drug increases the sensitivity of calcium-sensing receptors. This already has been used successfully in hyperparathyroid patients, particularly in those with chronic renal failure on dialysis with secondary hyperparathyroidism. A 50-60% decrease in circulating PTH and a mild decrease in serum calcium levels have been reported, but the hypercalciuria is not significantly affected. The agent may be also useful in resistant hypercalcemias and parathyroid cancers, as well as in the medical treatment of hyperparathyroidism.

Paricalcitol is a vitamin D analog that was developed to help prevent and treat secondary hyperparathyroidism in patients with chronic renal failure. Actual vitamin D also suppresses parathyroid hormone levels but tends to cause hypercalcemia and hyperphosphatemia. Vitamin D analogues such as paricalcitol are able to significantly reduce parathyroid hormone levels without significantly changing serum levels or urinary excretion of either calcium or phosphorus.

Interestingly, the first hyperparathyroid patient treated with surgical removal of the parathyroids died of complications from his renal calculi.

Summary of medical therapies for hypercalciuria

Thiazides
- Thiazides are currently the mainstay of medical therapy for hypercalciuria. They specifically stimulate calcium reabsorption in the distal renal tubule and can reduce urinary calcium excretion by about 30% in hypercalciuric patients. This hypocalciuric effect is reduced if sodium intake is not limited. Yendt et al first described the use of thiazides in nephrolithiasis in 1966, and they have been used extensively for kidney stone prophylaxis and as hypercalciuria therapy since then.²¹
- Thiazides are specifically indicated for renal leak hypercalciuria, in which case they not only reduce the inappropriate renal calcium loss but also lower PTH levels and correct other metabolic problems. When used appropriately in renal leak hypercalciuria, thiazides prevent secondary hyperparathyroidism and normalize vitamin D-3 synthesis, calcium absorption, and urinary calcium excretion. Stone formation rates drop more than 90% in patients with renal calcium leak who are placed on long-term thiazide therapy.
- When used for absorptive hypercalciuria, thiazides are still effective in reducing hypercalciuria, but their long-term usefulness may diminish over time as the bone stores become filled, allowing the hypercalciuria to return. Until then, bone density on thiazide therapy has been shown to increase by about 1.5% or more per year. When thiazides lose their hypocalciuric effect, which has been reported to occur at an average of about 2 years after initiating therapy, the use of an alternate regimen for a period of approximately 6 months usually restores the efficacy of the thiazide medication for use in hypercalciuria.
- Thiazides do not directly affect intestinal calcium absorption. In addition to their effect on the distal renal tubule, thiazides decrease the extracellular fluid volume and increase proximal renal tubular calcium reabsorption. Thiazides generally lower urinary calcium levels by about one third, but reductions of as much as 50% or 400 mg of calcium per day are possible and have been reported.
- Even when used in a nonselective fashion, thiazides can reduce stone recurrences from 50% (untreated) to 20% (treated) over 5 years. Thiazides are particularly well suited for hypercalciuric patients with hypertension, especially when dietary control measures alone fail to adequately normalize urinary calcium excretion.
- Thiazides have many other effects on the body. They increase serum calcium and uric acid levels while decreasing urinary citrate levels. Hyperuricemia or acute gout rarely develops in individuals receiving thiazides. A risk of dehydration, hypokalemia, and hyponatremia exists. They can cause magnesium loss and increase cholesterol. Adverse effects occur in about one third of patients but are usually mild. The most bothersome clinical adverse effect is lethargy, but muscle aches, depression, decreased libido, generalized weakness, and malaise also can occur. About 20% of patients stop thiazide therapy because of these adverse effects.
- Thiazides tend to increase urinary volume because of their diuretic effect (which is a useful feature in kidney stone formers), but this can easily lead to dehydration if oral fluid intake is not maintained. Chemically, thiazides are sulfonamides and should not generally be used or should be used cautiously in patients with a history of sulfa allergy. Drug interactions have been reported when thiazides are used together with alcohol, barbiturates, narcotics, antidiabetic drugs, steroids, pressor amines, muscle relaxants, lithium, and nonsteroidal anti-inflammatory agents.
- Thiazides increase serum calcium levels. Therefore, they can be used in a thiazide challenge for cases of borderline or subtle hyperparathyroidism to confirm the diagnosis. This involves the temporary use of thiazide therapy to create a controlled hypercalcemia. If the PTH levels drop, the patient is responding properly and hyperparathyroidism is unlikely. If the PTH level does not diminish as the serum calcium level rises, hyperparathyroidism can be diagnosed.
- The dosage depends on the specific medication used. Once-a-day drug preparations are usually preferred because of better patient compliance and tolerability. Trichlormethiazide (Naqua) is administered as a 2- or 4-mg daily tablet. Indapamide (Lozol) can be administered in either 1.25 or 2.5 mg doses once a day. If a potassium-sparing combination is desired, those that contain triamterene, such as Dyazide, should be avoided because triamterene can form its own stones. Moduretic, which uses amiloride as a potassium-sparing diuretic, would be recommended. Amiloride does not form stones and has a mild hypocalciuric effect of its own.
- Most patients do not need any potassium supplementation, but potassium and electrolyte levels need to be checked periodically. Because of the risk of both hypokalemia and hypocitraturia, potassium citrate supplements are often prescribed along with thiazides in calcium stone formers.
Orthophosphates
- In 1962, Howard et al first suggested the use of orthophosphate therapy (K-Phos Neutral, Neutra-Phos K, Uro-KP-Neutral) as a preventive treatment for kidney stones. He noted that oral orthophosphates would turn the "evil" urine of a stone former into the "good" urine of a non–stone former.²² Stone cessation rates of more than 90% have been reported with this agent. Orthophosphate therapy has been shown to decrease urinary calcium excretion by lowering serum vitamin D-3 levels (which reduces intestinal calcium absorption) and by increasing renal tubular calcium reabsorption. Orthophosphates may also have some intestinal calcium-binding capability, but the limited studies conducted on this issue have not confirmed this effect.
- Overall, orthophosphates lower 24-hour urinary calcium excretion by about 50% in patents with absorptive hypercalciuria and by about 25% in patients with other hypercalciuric states. No apparent effect on PTH levels exists in healthy individuals. Uncontrolled studies have shown kidney stone remission rates of 75-91% in recurrent stone formers on long-term orthophosphate therapy.
- Orthophosphates also increase urinary stone inhibitors such as citrate and, particularly, pyrophosphate. Many patients (40% in one series) have even noted a loss of stone mass while on orthophosphate therapy. Orthophosphates are particularly useful in cases of absorptive hypercalciuria type III (renal phosphate leak) and when thiazides cannot be used or are ineffective. The use of orthophosphates together with thiazides is extremely effective in controlling urinary calcium excretion and reducing new kidney stone formation rates, particularly in hypercalciuric calcium oxalate stone formers.
- About 60% of all dietary phosphate is absorbed in the duodenum and jejunum. Sixty-five percent of the absorbed phosphate is excreted by the kidneys; the rest is eliminated through the intestinal tract by secretion in the ileum and colon.
- To be effective, orthophosphates must be taken at regular intervals and in sufficient amounts. The neutral salt tends to have fewer adverse effects and is more effective than other preparations. Optimal levels of neutral orthophosphate are 1-2.5 g/day. Orthophosphate preparations for calcium stone formers should also be sodium free.
- Adverse effects of orthophosphate therapy include diarrhea, bloating, and gastrointestinal upset. These adverse effects usually are worst during the first 2 weeks of therapy, after which they tend to diminish. The medication must be taken 3-4 times per day, which reduces patient compliance. Do not administer to patients with struvite (magnesium ammonium phosphate) stones or to patients with renal failure because they can develop soft tissue calcifications. Use cautiously in patients with a history of predominantly calcium phosphate stones or in whom the urinary pH is consistently alkaline (which promotes calcium phosphate precipitation and stone formation). Patients with a previous history of gastrointestinal problems generally do not tolerate orthophosphate therapy well.
- Currently available orthophosphate preparations tend to be rapidly dissolving, which increases the gastrointestinal upset and diarrhea. A new slow-release form of potassium phosphate (UroPhos-K) is currently awaiting FDA approval. This new preparation uses a wax matrix to slow the release of phosphate, reducing its adverse effects. It contains no sodium and is designed to modify urinary pH to 7.0, which discourages the formation of calcium phosphate crystals and calculi. In a randomized double-blind study of this new phosphate therapy, patients with absorptive hypercalciuria type I who were administered the new slow-release phosphate preparation had an average daily urinary calcium level of only 171 mg; controls averaged 288 mg/day. Urinary inhibitor levels of citrate and pyrophosphate were increased in the group treated with orthophosphate, and no gastrointestinal adverse effects were reported.²³
Bisphosphonates
- Bisphosphonates such as alendronate (Fosamax), risedronate (Actonel), and ibandronate (Boniva) have become useful in the treatment of hypercalciuria and hypercalcemia. They are particularly helpful in cases of hyperparathyroidism in which parathyroid surgery cannot be performed or medical therapy is desired.
- Bisphosphonates are analogues of pyrophosphate with a high affinity for the hydroxyapatite of bone, especially in areas of rapid turnover and bone resorption. They inhibit osteoclast activity, which causes a net increase in bone density, calcium deposition, and mineralization. Preferential binding to osteoclasts is roughly 10 times greater than osteoblastic binding. While they are clearly helpful in cases of overt hypercalcemia and hyperparathyroidism, their usefulness in the long-term treatment of hypercalciuria in recurrent stone formers is unproved. They may be most useful in hypercalciuric stone formers in whom a history of decreased bone density or other evidence of osteoporosis, such as elevated osteocalcin levels, is present. Combination therapy with thiazides would be expected to be particularly beneficial. Bisphosphonates also can be helpful in difficult cases of hypercalciuria when other measures are unsuccessful or poorly tolerated.
Sodium cellulose phosphate
- Sodium cellulose phosphate (Calcibind) is an extremely effective intestinal calcium-binding agent. It removes about 85% of the available intestinal calcium from the digestive tract and prevents its absorption. Sodium cellulose phosphate is about 11% sodium and has a calcium-binding capacity of 1.8 mmol of calcium per gram of cellulose phosphate. In the digestive tract, the sodium ion is exchanged for calcium, which then is excreted bound to the cellulose in the stool.
- When sodium cellulose phosphate is used as a therapy, supplemental magnesium and a dietary oxalate restriction are recommended because the cellulose phosphate binds magnesium as well as calcium and results in a magnesium deficiency if supplemental magnesium is not supplied. The need for the dietary oxalate restriction (primarily of tea, colas, coffee, green leafy vegetables, chocolate, and nuts) is due to the lack of available intestinal calcium that the cellulose therapy creates. With so much intestinal calcium bound to the cellulose, intestinal oxalate-binding sites are severely lacking. This leaves an excess of free unbound intestinal oxalate available for absorption, which then increases oxaluria. To avoid this reactive enteric hyperoxaluria, a reasonable reduction in dietary oxalate is needed whenever sodium cellulose phosphate is used.
- Unfortunately, sodium cellulose phosphate causes a reduction in absorbed calcium, which helps the hypercalciuria but may cause a negative calcium balance and subsequent reduction in bone density. It still may have a role in the diagnosis of hypercalciuria as a brief, therapeutic trial and in selected cases of absorptive hypercalciuria type I when other therapies are ineffective. The benefits of its use must be judged sufficient to justify the risks. Appropriate other treatments, such as thiazides and bisphosphonates, can be used to prevent unnecessary bone demineralization and limit the dosage of cellulose required so adverse effects and complications of its use are minimized.
Dipyridamole
- Dipyridamole (Persantine) is a platelet adhesion inhibitor and vasodilator. It usually is used to lengthen platelet survival time and reduce the incidence of thromboembolic phenomenon after heart valve replacement surgery. Researchers have found that dipyridamole reduces renal phosphate excretion, which increases the serum phosphate level. This decreases the activation of vitamin D-3, resulting in reduced hypercalciuria. This is useful in patients with vitamin D–dependent hypercalciuria, such as renal phosphate leak (absorptive hypercalciuria type III), especially when orthophosphates are not tolerated or cannot be used. No direct effect on urinary calcium excretion is present. Adverse effects are minimal, but the medication must be taken frequently. Dipyridamole has been shown to reduce urinary calcium excretion in patients with vitamin D–dependent renal phosphate leak on a long-term basis.^24,14

Consultations

The treatment of hypercalciuria is important not only in the reduction of future kidney stone formation and the diagnosis of possible underlying metabolic disease but also in the prevention of bone demineralization and osteoporosis. Every physician who treats hypercalciuric patients may not be able to become an expert on this condition or its therapy. Physicians who are uncomfortable treating hypercalciuric patients should not hesitate to refer them, especially if the patients are highly motivated and interested in treating their calcium problem. A difficult or high-risk case that is resistant to dietary and standard medical therapy in a motivated patient would be a good case to refer to a physician expert or tertiary care center with expertise in this area.

Hyperparathyroidism cases obviously should be referred to a physician skilled in dealing with this problem. Patients with overt renal failure need the assistance of a nephrologist.

With the general availability of kidney stone prevention testing protocols from most major reference laboratories, obtaining the necessary chemical studies is not problematic in the United States. (See Nephrolithiasis: Laboratory Evaluation of Stone Formers for a detailed discussion and evaluation of the various laboratories and their protocols.)

Diet

All hypercalciuric patients are advised to follow reasonable dietary changes to help limit their urinary calcium loss, reduce stone recurrences, and improve the effectiveness of medical therapy.

Dietary Treatment Guidelines

Limit daily calcium intake to 600-800 mg/day unless otherwise instructed.
Limit dietary oxalate, especially when calcium intake is reduced. High oxalate levels are found in strong teas, nuts, chocolate, coffee, colas, green leafy vegetables (eg, spinach), and other plant and vegetable products.
Avoid excessive purines and animal protein (<1.7 g/kg of body weight).
Reduce sodium (salt) and refined sugar to the minimum possible.
Increase dietary fiber (12-24 g/d).
Limit alcohol and caffeine intake.
Increase fluid intake, especially water (sufficient to produce at least 2 L of urine per day).

Dietary Therapy for Hypercalciuria

Dietary modifications have long been the mainstay of initial therapy for hypercalciuria. While dietary changes alone may not always be successful or adequate, dietary excesses possibly can undermine or defeat even optimal medical treatments. Patients who normalize their urinary calcium excretion with dietary changes alone may still benefit from thiazides or other treatments to avoid or treat bone demineralization and osteoporosis or osteopenia. Reducing intestinal calcium inadvertently may increase oxalate absorption and contribute to hyperoxaluria, resulting in a net increase in stone formation risk rather than a reduction. This is why dietary oxalate is limited whenever calcium intake is reduced.

Dietary modifications involving reasonable restrictions of dietary calcium, oxalate, meat (purines) and sodium, have been useful in reducing the urinary supersaturation of calcium oxalate. This effect is more pronounced in hypercalciuric calcium oxalate stone formers than in calcium nephrolithiasis patients who are normocalciuric. Urinary calcium was found to decrease by 29% when reasonable dietary changes alone were used in a 2005 study by Pak and associates.²⁵

Some have suggested that three criteria need to be fulfilled for any dietary factor to be implicated in kidney stone disease. These criteria are as follows:

Intake of the dietary constituent should be increased in patients with stones compared to controls.
Restriction of the dietary factor should decrease stone formation rates.
The reason the dietary factor causes stones needs to be understood.

The main dietary contributions of calcium, sodium, potassium, animal protein, fiber, alcohol, caffeine, fluid intake, oxalate, and carbohydrates are reviewed individually below. No relationship was found with dietary fat intake.

Calcium

Avoidance of an excessively high-calcium diet is an obvious recommendation for calcium stone formers. (See Image 1 for a list of calcium rich foods.) Stone formers as a group are much more sensitive to dietary calcium than non–stone formers. For any given change in dietary calcium, urinary calcium has been shown to increase an average of only 6% in healthy controls but can increase 20% in calcium stone formers.

Calcium-rich foods.

[ CLOSE WINDOW ]

Calcium-rich foods.

Avoiding a diet that is too severely limited in calcium also is important because of the risk of a reactive hyperoxaluria and the creation of a negative calcium balance with subsequent osteopenia or actual osteoporosis. In 2 large population studies involving both men and women, patients with the highest daily calcium intake were demonstrated to have significantly fewer stones (within reasonable limits) than those with the lowest dietary calcium levels.

Any patient with kidney stones placed on a long term reduced calcium diet for any reason should have their bone density measured periodically, preferably in the spine. Urinary oxalate levels also should be checked regularly because of the risk of hyperoxaluria.

The recommended dietary calcium intake for most calcium stone formers is about 600-800 mg/day. When calcium is removed from the diet without also restricting oxalate intake, the lack of intestinal oxalate-binding sites will possibly leave too much intestinal oxalate unbound and available for easy absorption. When this occurs, urinary oxalate levels rise. Proportionately, oxalate is 15 times stronger than calcium in promoting nephrolithiasis. The net stone formation rate may actually increase if dietary oxalate intake and hyperoxaluria are not controlled.

Calcium citrate is recommended if calcium supplements are needed. This combination has been shown to be the most effective in limiting the new stone formation rate for those who require calcium supplements.

Sodium

A high sodium intake promotes various effects that enhance urinary calcium excretion and increase overall kidney stone formation rates. These effects include a rise in urinary pH, higher urinary calcium and cystine levels, and a decrease in urinary citrate excretion. In healthy adults, a high sodium intake has been associated with higher fractional intestinal calcium absorption as well as increased PTH and vitamin D-3 levels. As mentioned above, each 100-mEq increase in daily dietary sodium raises the urinary calcium level by about 50 mg.

Increased calcium excretion is thought to be due to an increase in the extracellular fluid volume, which ultimately results in an inhibition of calcium reabsorption in the distal renal tubule. Reducing dietary sodium has been shown to decrease urinary calcium excretion in hypercalciuric stone formers, while high dietary sodium is associated with both increased urinary calcium excretion and low bone density.

The rise in urinary pH is caused by an increase in serum and urinary bicarbonate levels. High serum bicarbonate lowers urinary citrate excretion by a direct effect on citrate metabolism in proximal renal tubular cells.

Sodium intake among stone formers is equal to or higher than intake in control groups of non–stone formers. Enhanced renal calcium excretion from high dietary sodium is thought to be due to an increase in the extracellular fluid volume, which ultimately results in an inhibition of renal tubular calcium reabsorption. Sodium and calcium share common sites for reabsorption in the renal tubules. Patients with recurrent nephrolithiasis and hypercalciuria are also the most sensitive to the hypercalciuric actions of a high-sodium diet. Finally, in postmenopausal women, high sodium intake has been directly associated with low bone density in calcium stone formers.

Dietary sodium needs to be controlled during any calcium testing, such as a calcium-loading test, to avoid affecting the results.

Most experts recommend limiting dietary sodium (salt) in calcium stone formers to about 100 mEq/day, but this is difficult because salt (sodium) enhances the taste of food to many people. Patients should be aware that most restaurant meals and fast food items, such as pizza, contain a considerable amount of sodium. Many prepared foods have low-sodium varieties available. Ketchup, mustard, teriyaki, Worcestershire and soy sauces, canned soups, cold cuts, prepared vegetables, and TV dinners all have large amounts of sodium. Daily dietary salt intake should be restricted to levels sufficient to keep the urinary sodium excretion below 150-200 mEq/day.

Recommendations to reduce sodium (salt) intake include the following:

Remove the saltshaker from the dining table. Other spices, such as pepper, salt substitutes, or Mrs. Dash, can be used instead.
Use little or no salt in food preparation or cooking.
Avoid eating foods with high salt content whenever possible. Most fast food is high in sodium.
Do not add any additional salt to foods that already contain it. This would apply to most prepared or canned foods, such as soups, gravies, TV dinners, and canned vegetables.
Use fresh or frozen vegetables whenever possible. To reduce the salt content of canned vegetables, they should be drained and then rinsed with water before cooking.
Use one half or less of the specified amount of salt when following cooking recipes.
Everyone in the family should participate in the low-sodium diet so the patient does not feel singled out.

Potassium

Some evidence suggests that low potassium intake may be a risk factor for stones, but this has not been confirmed in all studies.^26,27,28 The potential influence of a low-potassium diet may be due to its relationship to sodium intake in stone formers, who generally have a higher sodium/potassium ratio than non–stone formers.

Potassium decreases urinary calcium excretion due to an induced transient sodium diuresis resulting in a temporary contraction of the extracellular fluid volume and an increase in renal tubular calcium reabsorption. Potassium also increases renal phosphate absorption, raising serum phosphate levels, which reduces serum vitamin D-3, resulting in decreased intestinal calcium absorption.

Animal protein

The possible link between high animal protein intake and kidney stones has been known since at least 1973. This link has been found in epidemiological studies first in India, then in England, Germany, Austria, Japan, Italy, and, finally, in the United States. A large prospective study in the United States found a significantly increased risk of stones in the group with the highest animal protein intake.²⁹ Additionally, known stone formers appear to be more sensitive to the stone-enhancing effects of high–animal protein diets than non–stone forming control populations.

Animal protein affects urinary calcium mainly through its acid-loading ability. Animal protein is high in purines, which are metabolized to uric acid, further contributing to the acid load. Animal protein also increases the body's acid load directly. Methionine and cystine are more common in animal protein than plant protein. Both methionine and cystine contain relatively high levels of sulfur. When the sulfur is oxidized to sulfate, additional acid is generated. Sulfate also can form a soluble complex with calcium in the renal tubules, which can reduce calcium reabsorption and contribute to hypercalciuria. Urinary sulfate levels can be used as a general marker of oral animal protein intake. Normal levels generally are 40 mg/day or less, while optimal levels in calcium stone formers would be below 25-30 mg daily.

This increased acid needs to be neutralized. This often occurs in the bone, where the extra acid is buffered, releasing calcium from the bony stores. This released calcium eventually contributes to increased urinary calcium. Acid loading directly inhibits calcium reabsorption in the distal renal tubule, which further exacerbates any hypercalciuria. The extra acid also reduces urinary citrate excretion by enhancing citrate reabsorption in the proximal renal tubule.

Each 75 g of additional dietary animal protein raises the urinary calcium level by 100 mg/day. In one study, increasing methionine ingestion by just 6 g/day was found to raise the daily urinary calcium excretion by 80 mg. Dietary animal protein intake should be less than 1.7 g/kg of body weight per day.

High protein intake has been judged second only to vitamin D ingestion in its ability to increase intestinal calcium absorption. Other effects of a high animal protein diet include increased urinary oxalate and uric acid, as well as reduced urinary citrate.

An intriguing 1996 randomized study compared the stone production rates in about 100 known calcium oxalate stone formers who differed in their dietary protein and fiber intakes. The first group was instructed just to increase fluid intake, while the second group was told to increase fluid intake and consume a high-fiber, low–animal protein diet. These groups were observed for 4.5 years. The researchers found significantly fewer stones in the group with the high-fiber, low–animal protein diet. Of course, the possibility exists that the fiber or just the combination of the high fiber and animal protein restriction was effective.³⁰ Additional studies are needed to determine exactly which dietary modifications are most efficacious and to eliminate the variables, such as uncontrolled sodium and calcium intake, which might influence the outcome.

Finally, a link between high animal protein ingestion and increased oxalate excretion may exist. For example, glycolate is an oxalate precursor whose generation is highly linked to animal protein intake. While some investigators have found a link between high animal protein intake and increased urinary oxalate, others have not. Further studies are needed to determine the presence and significance of any such correlation.

Fiber

Calcium stone formers as a group have a lower intake of dietary fiber than healthy control populations. Dietary fiber, including oat, wheat, and rice bran, can reduce hypercalciuria and lower intestinal calcium absorption by 20-33%. As much as 24 g of dietary fiber per day may be necessary. Wheat bran, for example, is rich in oxalate, which accounts in part for its ability to bind and absorb free intestinal calcium. Although no reports of significant problems with increased dietary fiber have been made, some potential risks exist.

Dietary fiber may reduce intestinal magnesium, resulting in a deficit. Patients on a very high-fiber diet should be checked periodically for magnesium deficiency. A magnesium supplement, such as magnesium oxide, can be added if necessary.

Another potential problem is a reactive enteric hyperoxaluria. Whenever intestinal calcium is reduced, fewer intestinal oxalate-binding sites are available. This leads to more free intestinal oxalate, which is absorbed easier than oxalate bound to calcium or other agents. The increased free intestinal oxalate is absorbed and eventually is excreted in the urine, increasing urinary oxalate levels. Because oxalate is proportionately about 15 times stronger than calcium with regards to stone promotion, limiting oxalate absorption in known stone formers makes sense. The easiest way to accomplish this is to limit dietary oxalate any time intestinal oxalate-binding sites (such as dietary calcium intake) are reduced. Dietary oxalate can be lowered by limiting such foods as iced tea, coffee, colas, green leafy vegetables, collard greens, spinach, chocolate, nuts, and rhubarb. Another approach is to use an alternate oxalate-binding agent, such as iron supplements.

Alcohol

Acute alcohol ingestion causes hypoparathyroidism with hypercalciuria and hypocalcemia. PTH levels can drop by 70% after acute alcohol intoxication. Prolonged but moderate alcohol intake eventually raises PTH levels. People with chronic alcoholism develop low serum vitamin D levels, which cause impaired intestinal calcium absorption and hypocalciuria. A direct inhibitory effect on osteoblast activity by alcohol ingestion also appears to exist. This effect is enhanced in smokers. Urinary calcium excretion during periods of alcohol consumption can increase by over 200% over controls. Osteopenia also has been linked to alcohol consumption.

Caffeine

Caffeine has been shown to increase urinary calcium excretion, but the clinical importance is relatively small unless very large amounts of caffeine are ingested. As noted earlier, ingestion of 34 ounces of caffeine is necessary to cause the loss of 1.6 mmol of total calcium. This caffeine-induced hypercalciuria seems to parallel changes in urinary prostaglandin F_2-alpha (PGF2-alpha), which suggests that prostaglandins may play a role in this entity.

Fluids

Several studies have shown that, on average, stone formers have a lower overall fluid intake than non-stone formers. Not surprisingly, the highest incidence of kidney stone formation was in the group with the lowest overall fluid intake.

The need for a high fluid intake to increase urinary fluid volume seems obvious because extra water decreases urinary concentration and reduces the likelihood of stones even if the total calcium excretion is unchanged. The amount of extra water to be consumed is variable. In general, the author suggests an amount of water that produces a 24-hour urinary volume of 2000 cc or more. This amount may need to be increased in selected cases.

Citrus

Potassium rich citrus fruits and juices, such as oranges, grapefruit, and cranberries, are recommended. Orange juice, for example, has natural potassium citrate. Lemon juice also has a very high citrate content, so lemonade made from real lemon juice is recommended. In contrast, lime juice contains mostly citric acid and does not increase urinary citrate substantially.

Oxalate

Oxalate is an organic acid found primarily in the leaves, bark, and fruit of plants. Its only known function in plants is to bind tightly with calcium. This is useful because it allows the plant to extract unwanted calcium from the internal circulation. The leaves containing the calcium-oxalate complex then can be discarded or shed by the plant. Humans absorb oxalate when the oxalate-containing leaves and other vegetable products are eaten. Oxalate has no known useful function in human nutrition.

A relatively mild restriction of foods that contain high amounts of oxalate enables the body to avoid a reactive hyperoxaluria when intestinal oxalate-binding sites are reduced from a drop in oral calcium intake. Common foods with relatively high oxalate content include nuts, chocolate, colas, green leafy vegetables, rhubarb, spinach, collard greens, and tea.

Carbohydrates (refined)

Several large population studies have investigated the issue of the potential contribution of a high-carbohydrate diet to stone production. For example, Curhan found that carbohydrates were not a significant risk factor for stone formation in men but were associated with an increased stone production in women. Some investigators have found that stone formers tend to have a higher carbohydrate intake than non-stone formers, but other researchers have failed to confirm such an association.

Good evidence indicates that a high-carbohydrate diet causes an increase in urinary calcium excretion because of decreased distal renal tubular calcium reabsorption and an increase in intestinal calcium absorption. Evidence also indicates that excessive carbohydrate loading can increase endogenous oxalate production. This seems reasonable because glucose is involved in oxalate metabolism through a series of chemical interactions with glyoxylate. (Glyoxylate is involved not only in the metabolism of endogenous oxalate but also in the gluconeogenesis pathway and urea metabolism.)

Ketogenic diet

The ketogenic diet sometimes is used to treat intractable seizure disorders in children. It involves an initial period of fluid restriction and starvation until ketone bodies appear in the urine. This is followed by a low-protein, low-carbohydrate, and fluid-restricted diet. This tends to cause chronic metabolic acidosis with hypocitraturia and relatively low urinary volumes, which induce kidney stone formation. Elevated uric acid levels also have been reported. The average time from initiation of the diet until stone presentation is about 18 months, so patients who are started on this diet should be checked for stone formation at about 12 months after diet application. Fluid liberalization and citrate supplements can be used to prevent kidney stone formation in these patients.

Medication

Medications used in the treatment of hypercalciuria include diuretics (thiazides, indapamide, amiloride), orthophosphates (neutral phosphate), bisphosphonates (alendronate), and, rarely, calcium-binding agents (sodium cellulose phosphate). Ketoconazole and dipyridamole occasionally are useful in lowering vitamin D levels in selected cases. These therapies should be used together with dietary treatment guidelines. Combination therapy with multiple medicines is possible and recommended in unusual or difficult cases.

Thiazides and related drugs

These medications originally were intended solely for use as diuretics for hypertension. They have become the primary medical treatment for hypercalciuria because of their unique ability to remove calcium from the urine and return it to the general circulation. They can be used in virtually any type of hypercalciuria, with the possible exception of resorptive hypercalciuria, in which they can exacerbate hypercalcemia. They particularly are useful in renal leak hypercalciuria and in patients who also are hypertensive or osteoporotic. All thiazides chemically are sulfonamides, so they all have the potential of producing allergic reactions in patients with sulfa allergies.

Trichlormethiazide (Naqua)

Long-acting thiazide that can be taken only once per day.

Adult

2-4 mg/d PO

Pediatric

Documented hypersensitivity; infected phosphate or struvite stones; renal failure; hyperphosphatemia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adverse effects include GI distress, osteomalacia, bone/joint pain

Bisphosphonates

Specifically inhibit osteoclast activity, resulting in a net increase of calcium deposition in bone. Chemically, bisphosphonates are synthetic analogues of pyrophosphate that bind to the hydroxyapatite found in bone, especially in areas of rapid bone turnover. This is useful in the therapy and prophylaxis of osteoporosis and osteopenia. Bisphosphonates also are used as a second-line therapy in hypercalciuria and as a first-line medical treatment for hypercalcemia and Paget disease.

Alendronate (Fosamax)

Adult

5-10 mg/d PO with water 0.5 h before first food, beverage, or medication of the day to avoid risk of decreased absorption or esophageal irritation; do not lie down for at least 0.5 h after taking medication and first food of the day

Pediatric

Not established

Decreased absorption with vitamin/mineral supplements and medications containing calcium, aluminum, or magnesium; enhanced suppression of bone turnover with estrogen; increased GI distress with H2 blockers and gastric mucosal agents; NSAIDs, aspirin

Documented hypersensitivity; esophageal abnormalities (stricture, achalasia) that delay transit; inability to stand or sit upright for at least 0.5 h after taking; hypocalcemia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Esophageal, gastric, and duodenal ulcers have occurred; correct preexisting hypocalcemia

Risedronate (Actonel)

By decreasing osteoclast activity, alendronate and risedronate cause a net calcium deposition in bone. This leaves less calcium in the blood, thus treating both hypercalcemia and hypercalciuria. Chemically, they are synthetic analogs of pyrophosphate that bind to the hydroxyapatite found in bone. This binding takes place preferentially at sites of active bone resorption, primarily under osteoclasts. Studies have shown that alendronate and risedronate are effective in the medical treatment of hypercalcemia and hypercalciuria. Usually takes 6-12 mo for maximum effectiveness when used for osteoporosis.

Adult

5 mg PO qd; take with water 0.5 h before first food, beverage, or medication of the day to avoid risk of decreased absorption or esophageal irritation; do not lie down for at least 0.5 h after taking medication and first food of the day

Pediatric

Not established

Documented hypersensitivity; esophageal abnormalities (stricture, achalasia) that delay transit; inability to stand or sit upright for at least 0.5 h after taking; hypocalcemia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor hypercalcemia-related parameters (eg, serum levels of calcium, phosphate, magnesium, potassium); maintain adequate intake of calcium and vitamin D to prevent severe hypocalcemia; caution if active upper GI problems; not to administer with alendronate for osteoporosis in postmenopausal women; adverse effects include diarrhea, headache, and arthralgia; may cause upper GI disorders (eg, dysphagia, esophagitis, or esophageal or gastric ulcer; take first thing in the morning before eating or drinking anything except plain water; swallow whole (do not chew or dissolve in mouth)

Ibandronate (Boniva)

Adult

2.5 mg PO qd; administer with water at least 1 h prior to first food or beverages (other than water) of the day

Alternatively, 150 mg PO once monthly on the same date each month or 3 mg IV push (infuse over 15-30 sec) q3mo

Pediatric

Not established

Overview: Hypercalciuria

Differential Diagnoses & Workup: Hypercalciuria

Treatment & Medication: Hypercalciuria

Follow-up: Hypercalciuria

Multimedia: Hypercalciuria

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Keywords

absorptive hypercalciuria, calcium-loading test, calcium stone disease, calcium stones, Dent disease, elevated urinary calcium, high urinary calcium, hyperparathyroidism, geriatric hypercalciuria, idiopathic hypercalciuria, ketogenic diet, medullary sponge kidney, MSK, nephrolithiasis, osteoporosis, pediatric hypercalciuria, renal calculi, renal leak hypercalciuria, renal phosphate leak, resorptive hypercalciuria, sarcoid, urolithiasis

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Contributor Information and Disclosures

Author

Stephen W Leslie, MD, FACS, Founder and Medical Director, Lorain Kidney Stone Research Center; Clinical Assistant Professor, Department of Urology, The University of Toledo College of Medicine
Stephen W Leslie, MD, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, National Kidney Foundation, and Ohio State Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Martha K Terris, MD, FACS, Professor, Department of Surgery, Medical College of Georgia
Martha K Terris, MD, FACS is a member of the following medical societies: American Cancer Society, American College of Surgeons, American Institute of Ultrasound in Medicine, American Urological Association, New York Academy of Sciences, and Society of University Urologists
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

CME Editor

J Stuart Wolf Jr, MD, FACS, David A Bloom Professor of Urology, Director of Division of Minimally Invasive Urology, Department of Urology, University of Michigan
J Stuart Wolf Jr, MD, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, Catholic Medical Association, Endourological Society, Society for Urology and Engineering, Society of Laparoendoscopic Surgeons, Society of University Urologists, and Society of Urologic Oncology
Disclosure: Terumo Corporation Consulting fee Consulting; Gyrus-ACMI Honoraria Speaking and teaching

Chief Editor

Vecihi Batuman, MD, FACP, FASN, Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System
Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology
Disclosure: Nothing to disclose.

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eMedicine Specialties > Urology > Stones

Hypercalciuria: Treatment & Medication

Treatment

Medical Care

Consultations

Diet

Dietary Treatment Guidelines

Dietary Therapy for Hypercalciuria

Calcium-rich foods.

Calcium-rich foods.

Medication

Thiazides and related drugs

Trichlormethiazide (Naqua)

Adult

Pediatric

Pregnancy

Precautions

Indapamide (Lozol)

Adult

Pediatric

Pregnancy

Precautions

Potassium-sparing diuretics

Amiloride (Midamor, Moduretic)

Adult

Pediatric

Pregnancy

Precautions

Orthophosphates

Neutral orthophosphates (K-Phos Neutral, Uro-KP-Neutral, Neutra-Phos K)

Adult

Pediatric

Pregnancy

Precautions

Bisphosphonates

Alendronate (Fosamax)

Adult

Pediatric

Pregnancy

Precautions

Risedronate (Actonel)

Adult

Pediatric

Pregnancy

Precautions

Ibandronate (Boniva)

Adult

Pediatric

Pregnancy

Precautions

Calcium-binding agents

Sodium cellulose phosphate (Calcibind)

Adult

Pediatric

Pregnancy

Precautions

Vitamin D suppressors

Ketoconazole (Nizoral)

Adult

Pediatric

Pregnancy

Precautions

Dipyridamole (Persantine)

Adult

Pediatric

Pregnancy

Precautions

Urinary macromolecules

Pentosan polysulphate (Elmiron)

Adult

Pediatric

Pregnancy

Precautions

More on Hypercalciuria

References

Further Reading

Keywords

Contributor Information and Disclosures

Author

Medical Editor