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Hypercalciuria Medication

  • Author: Stephen W Leslie, MD, FACS; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
Updated: Nov 26, 2015

Medication Summary

Thiazides are specifically indicated for patients with renal leak hypercalciuria, in whom they not only reduce the inappropriate renal calcium loss but also lower parathyroid hormone (PTH) levels and normalize other metabolic processes.[53, 54]

These agents can also be used to treat absorptive hypercalciuria, but their long-term usefulness may diminish over time, requiring approximately 6 months of an alternative regimen before they are effective again.

Thiazides also increase serum calcium and uric acid levels while decreasing urinary citrate levels. Hyperuricemia and acute gout rarely develop in individuals receiving thiazides.

Because thiazide therapy carries the risk of inducing hypokalemia and hypocitraturia, potassium citrate supplements are often prescribed with thiazides in calcium-stone formers.


Diuretics, Thiazide

Class Summary

Thiazide diuretics are used in patients with hypercalciuria that is not adequately controlled with dietary modifications alone. Thiazide diuretics are also used upon evidence of bone demineralization if a patient’s diet includes less than the DRI of calcium.

Thiazides work by increasing calcium reabsorption at the level of the distal renal tubule and, thus, lowering urinary calcium. Hydrochlorothiazide (HCTZ) is the agent most commonly used, but other thiazide or thiazide-type diuretics can be administered, including trichlormethiazide and chlorthalidone.

Despite the common use of thiazides, no long-term clinical trials have been performed documenting their efficacy and safety in children. Parents should be notified of this and understand the risks and benefits before initiating therapy.

Hydrochlorothiazide (Microzide)


HCTZ is the most frequently used thiazide in the reduction of urinary calcium levels.



This agent reduces calcium excretion through direct tubular effects.


Urinary Alkalinizing Agents

Class Summary

Potassium citrate is metabolized to bicarbonates, which increase urinary pH levels by increasing the excretion of free bicarbonate ions without producing systemic alkalosis when administered in recommended doses.

Potassium citrate (Urocit K)


This is an alkalinizing agent indicated for the treatment of systemic metabolic acidosis, urinary alkalinization, and hypocitraturia. Potassium citrate is administered orally and metabolized to bicarbonate in the liver.



Class Summary

Drugs in this class increase bone deposition of calcium, thus removing it from the circulation before it can be excreted. This improves bone calcium density and helps to reduce urinary calcium levels. Bisphosphonates, such as alendronate (Fosamax), risedronate (Actonel), or ibandronate (Boniva), should be used in men and in women when estrogen cannot be used.

Pamidronate (Aredia)


The main action of pamidronate is to inhibit the resorption of bone. The mechanism by which this inhibition occurs is not fully known. The drug is adsorbed onto calcium pyrophosphate crystals and may block the dissolution of these crystals, also known as hydroxyapatite, which are an important mineral component of bone. Evidence also suggests that pamidronate directly inhibits osteoclasts.

Alendronate (Fosamax)


Alendronate is a potent third-generation bisphosphonate that principally acts by inhibiting osteoclastic bone resorption.

Ibandronate (Boniva)


Ibandronate inhibits the resorption of bone, increases bone mineral density, and reduces the incidence of vertebral fractures.

Risedronate (Actonel, Atelvia)


Risedronate is a potent aminobisphosphonate that principally acts by inhibiting osteoclastic bone resorption. It is recommended for the treatment of Paget disease.

Etidronate (Didronel)


Etidronate was the first bisphosphonate studied in humans and approved in the United States (1978) for the treatment of Paget disease. It is the least potent of currently available bisphosphonate drugs.

Tiludronate (Skelid)


Tiludronate is a sulfur-containing bisphosphonate of intermediate potency between etidronate and newer nitrogen-containing bisphosphonates. No food, indomethacin, or calcium should be ingested within 2 hours before and 2 hours after. A 3-month posttreatment evaluation follows.


Estrogen Derivatives

Class Summary

Estrogens should be used in postmenopausal women with hypercalciuria whenever possible. Their action is similar to that of the bisphosphonates.

Estrogens are used to increase the serum estrogen level, which, in turn, decreases the rate of bone resorption. The lowest effective dose at the shortest duration necessary should be used. Estrogen therapy reduces bone resorption and retards or halts postmenopausal bone loss. Estrogen therapy is no longer a first-line approach for the treatment of osteoporosis in postmenopausal women because of increased risk of breast cancer, stroke, venous thromboembolism, and coronary disease. The FDA recommends that other approved nonestrogen treatments be considered first for osteoporosis prevention.

Conjugated estrogens (Premarin)


Estrogens can directly affect bone mass through estrogen receptors in bone, reducing bone turnover and bone loss. Estrogens can also indirectly increase intestinal calcium absorption and renal calcium conservation and, therefore, improve calcium balance. When prescribing solely for the prevention of postmenopausal osteoporosis, therapy should be considered only for women at significant risk of osteoporosis and for whom nonestrogen medications need to be carefully considered.

Estradiol (Estrace, Estraderm, Menostar, Vivelle-Dot, Climara, Estraderm, Alora)


Estradiol restores estrogen levels to concentrations that induce negative feedback at gonadotropic regulatory centers; this, in turn, reduces the release of gonadotropins from the pituitary. Estradiol increases the synthesis of DNA, RNA, and many proteins in target tissues; it also inhibits osteoclastic activity and delays bone loss. In addition, evidence suggests a reduced incidence of fractures.

Estropipate (Ortho-Ext 0.625, Ortho-Est 1.25)


Estropipate is indicated for the prevention of osteoporosis. When estrogen therapy is discontinued, bone mass declines at a rate comparable to that of the immediate postmenopausal period. No evidence suggests that estrogen replacement therapy restores bone mass to premenopausal levels.

Contributor Information and Disclosures

Stephen W Leslie, MD, FACS Founder and Medical Director, Lorain Kidney Stone Research Center; Associate Professor of Surgery, Creighton University School of Medicine, Chief of Urology, Creighton University Medical Center

Stephen W Leslie, MD, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, National Kidney Foundation, Ohio State Medical Association

Disclosure: Nothing to disclose.


Sahar Fathallah-Shaykh, MD Associate Professor of Pediatric Nephrology, University of Alabama at Birmingham School of Medicine; Consulting Staff, Division of Pediatric Nephrology, Medical Director of Pediatric Dialysis Unit, Children's of Alabama

Sahar Fathallah-Shaykh, MD is a member of the following medical societies: American Society of Nephrology, American Society of Pediatric Nephrology

Disclosure: Nothing to disclose.

Chief Editor

Vecihi Batuman, MD, FACP, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, 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, International Society of Nephrology

Disclosure: Nothing to disclose.


Sahar Fathallah-Shaykh, MD Assistant Professor in Pediatric Nephrology, University of Alabama at Birmingham School of Medicine; Consulting Staff, Division of Pediatric Nephrology, Medical Director of Pediatric Dialysis Unit, Children's of Alabama

Sahar Fathallah-Shaykh, MD is a member of the following medical societies: American Society of Nephrology and American Society of Pediatric Nephrology

Disclosure: Medscape Reference Honoraria Other

Frederick J Kaskel, MD, PhD Director of the Division and Training Program in Pediatric Nephrology, Vice Chair, Department of Pediatrics, Montefiore Medical Center and Albert Einstein School of Medicine

Frederick J Kaskel, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association for the Advancement of Science, American Pediatric Society, American Physiological Society, American Society of Nephrology, American Society of Pediatric Nephrology, American Society of Transplantation, Eastern Society for Pediatric Research, Federation of American Societies for Experimental Biology, International Society of Nephrology, NationalKidneyFoundation, New York Academy of Sciences, Renal Physicians Association, Sigma Xi, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Craig B Langman, MD The Isaac A Abt, MD, Professor of Kidney Diseases, Northwestern University, The Feinberg School of Medicine; Division Head of Kidney Diseases, The Ann and Robert H Lurie Children's Hospital of Chicago

Craig B Langman, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, and International Society of Nephrology

Disclosure: NIH Grant/research funds None; Raptor Pharmaceuticals, Inc Grant/research funds None; Alexion Pharmaceuticals, Inc. Grant/research funds None

Richard Neiberger, MD, PhD Director of Pediatric Renal Stone Disease Clinic, Associate Professor, Department of Pediatrics, Division of Nephrology, University of Florida College of Medicine and Shands Hospital

Richard Neiberger, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Federation for Medical Research, American Medical Association, American Society of Nephrology, American Society of Pediatric Nephrology, Christian Medical & Dental Society, Florida Medical Association, International Society for Peritoneal Dialysis, International Society of Nephrology, National Kidney Foundation, New York Academy of Sciences, Shock Society, Sigma Xi, Southern Medical Association, Southern Society for Pediatric Research, and Southwest Pediatric Nephrology Study Group

Disclosure: Nothing to disclose.

Deogracias Pena, MD Medical Director of Dialysis, Department of Pediatrics, Cook Children's Medical Center; Clinical Associate Professor, Texas Tech University Health Sciences Center

Deogracias Pena, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, and American Society of Pediatric Nephrology

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Martha K Terris, MD, FACS Professor, Department of Surgery, Section of Urology, Director, Urology Residency Training Program, Medical College of Georgia; Professor, Department of Physician Assistants, Medical College of Georgia School of Allied Health; Chief, Section of Urology, Augusta Veterans Affairs Medical Center

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 Society of Clinical Oncology, American Urological Association, Association of Women Surgeons, New York Academy of Sciences, Society of Government Service Urologists, Society of University Urologists, Society of Urology Chairpersons and Program Directors, and Society of Women in Urology

Disclosure: Nothing to disclose.

Taylor S Troischt, MD Clinical Assistant Professor of Pediatrics, West Virginia University Hospitals; Medical Director, Cheat Lake Physicians

Taylor S Troischt, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Calcium-rich foods.
Table 1. Definitions of Hypercalciuria
Diet Definition
Regular diet (unrestricted) Women: Urinary excretion >250 mg calcium (6.2 mmol/24 h)

Men: Urinary excretion >275-300 mg calcium (7.5 mmol/24 h)

Urinary excretion >4 mg calcium (0.1 mmol) per kilogram of body weight per day

Urinary concentration >200 mg calcium per liter

Restricted diet (400 mg calcium, 100 mEq sodium) Urinary excretion >200 mg calcium per day
Urinary excretion >3 mg calcium per kilogram of body weight per day
Table 2. Hypercalciuria Simplified Test Guideline
Hypercalciuria Diagnosis Urinary Calcium on 400-mg Calcium Diet

(Normal = < 200 mg/24 h)

Fasting Calcium/Creatinine Ratio

(Normal = < 0.11)

Post–Calcium Load Calcium/Creatinine Ratio

(Normal = < 0.20)

Normal Normal Normal Normal
Absorptive type I High Normal High
Absorptive type II Normal Normal High
Absorptive type III (renal phosphate leak) High High High
Renal leak High High High
Resorptive (hyperparathyroidism) High High High
Table 3. Calcium-Loading Test Interpretation Guide
Criteria Absorptive Type I

Vitamin D–Dependent (Classic Form)

Absorptive Type I

Vitamin D–Dependent (Variant Form)

Absorptive Type II

Dietary Calcium Responsive

Absorptive Type III

(Renal Phosphate Leak)

Renal Calcium Leak Resorptive
Urinary calcium on regular diet* High High High High High High
Urinary calcium on low-calcium diet High High NL High High High
Urinary calcium fasting NL High NL High High High
Urinary calcium after 1-g calcium load§ High High NL High High High
Serum PO4 (fasting) NL NL NL Low NL or high Low
Serum calcium (fasting) NL NL or high NL NL or high NL or low High
Serum PTH NL or low NL or low NL Low High High
Serum PTH after 1-g calcium load NL or low NL or low NL Low High High
Serum vitamin D-3 (calcitriol) NL High NL High High High
Fasting normocalciuria while on ketoconazole No Yes No Yes No No
Bone calcium density NL NL or low NL NL or low Low Low
NL = normal; PO4 = phosphate; PTH = parathyroid hormone.

* Regular diet is unrestricted calcium and sodium intake. Normal upper limit calciuria is < 4 mg/kg body weight per day.

Low-calcium diet is 400 mg calcium and 100 mEq of sodium per day. Normal upper limit calciuria is < 200 mg/day.

Fasting is a 12-hour fast. Normal upper limit is < 0.11 mg calcium/mg creatinine.

§ After 1-g calcium load, normal upper limit is < 0.20 mg calcium/mg creatinine.

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