Nephrocalcinosis Medication

  • Author: Tibor Fulop, MD; Chief Editor: Vecihi Batuman, MD, FACP, FASN   more...
 
Updated: Jan 12, 2012
 

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

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Diuretic, Thiazide

Class Summary

Thiazide diuretics are extremely helpful in decreasing calcium excretion in several conditions associated with nephrocalcinosis. Hydrochlorothiazide (HCTZ), the most commonly employed thiazide diuretic, is appropriate to use if the serum calcium level is not high; it may correct coincidental high blood pressure.[38] The usual dose range is 12.5-25 mg per day, although in rare cases it can reach up to 50 mg per day. However, if HCTZ is used, the dose should be split in 2 to cover a full 24-hour period.

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Hydrochlorothiazide (Esidrix, HydroDIURIL, Microzide)

 

Inhibits reabsorption of sodium in the distal tubules, causing increased excretion of sodium and water, as well as of potassium and hydrogen ions.

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Chlorthalidone (Thalitone [US], Apo-Chlorthalidone [Canada])

 

Inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium and water as well as potasium and hydrogen ions. Reduces calcium excretion through direct tubular effects.

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Bisphosphonates

Class Summary

These agents are used to treat hypercalcemia and to decrease calcium loss from bone.

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Pamidronate (Aredia)

 

Inhibits bone resorption via actions on osteoclasts or on osteoclast precursors, without significant effects on renal tubular calcium handling. Indicated to treat hypercalcemia.

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Calcitonins

Class Summary

Calcitonin is indicated to treat hypercalcemia. It maintains calcium homeostasis by increasing the mineral stores in bone and the renal excretion of calcium. Calcitonin also directly inhibits osteoclastic bone resorption. Because of its longer duration of action, salmon calcitonin is preferred over human calcitonin.

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Calcitonin (Miacalcin, Osteocalcin, Cibacalcin, Calcimar)

 

Lowers elevated serum calcium in patients with multiple myeloma, carcinoma, or primary hyperparathyroidism. Can expect a higher response when serum calcium levels are high. Onset of action is approximately 2 h following injection, and activity lasts for 6-8 h. May lower calcium levels for 5-8 d by about 9% if administered q12h. If administered by the IM route, use multiple injection sites with dose >2 mL.

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Vitamins

Class Summary

Pyridoxine (vitamin B-6) deficiency is a known cause of hyperoxaluria. Used to treat nephrocalcinosis, pyridoxine decreases calcium oxalate formation and the subsequent development of kidney stones.

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Pyridoxine (Nestrex)

 

Involved in synthesis of GABA within CNS.

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Antimalarial Agent

Class Summary

Hydroxychloroquine can be helpful in controlling hypercalcemia due to sarcoid and is utilized as a glucocorticoid-sparing agent.

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Hydroxychloroquine (Plaquenil)

 

May be most useful in the management of osseous involvement. Inhibits chemotaxis of eosinophils, locomotion of neutrophils, and impairs complement-dependent antigen-antibody reactions.

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Calcimimetic Agent

Class Summary

These can be used in primary hyperparathyroidism to temporarily control hypercalcemia if a patient is a poor surgical risk or if surgery is not immediately available. Experience in such settings is limited.

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Cinacalcet (Sensipar)

 

Directly lowers parathyroid hormone (PTH) levels by increasing sensitivity of calcium-sensing receptor on chief cell of parathyroid gland to extracellular calcium. Also results in concomitant serum calcium decrease. Indicated for hypercalcemia with parathyroid carcinoma.

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Alkalinizing Agent, Oral

Class Summary

These are used for urinary alkalinization.

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Sodium citrate (Bicitra, Oracit)

 

Treats metabolic acidosis and used as alkalinizing agent where long-term maintenance of an alkaline urine desirable.

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Potassium citrate (Polycitra-K)

 

Alkalinizing agent indicated for treatment of systemic metabolic acidosis, urinary alkalinization, or hypocitraturia. Administered PO and metabolized to bicarbonate in the liver.

Each 5 mL of Polycitra contains sodium citrate 500 mg, citric acid 334 mg, and potassium citrate 550 mg (each mL contains 1 mEq potassium, 1 mEq sodium, and 2 mEq bicarbonate).

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Contributor Information and Disclosures
Author

Tibor Fulop, MD  Associate Professor of Medicine, Medical Director, Outpatient Dialysis Services, Department of Medicine, Division of Nephrology, University of Mississippi Medical Center

Tibor Fulop, MD is a member of the following medical societies: American College of Physicians and American Society of Diagnostic and Interventional Nephrology

Disclosure: Nothing to disclose.

Coauthor(s)

Mahendra Agraharkar, MD, MBBS, FACP, FASN  Clinical Associate Professor of Medicine, Baylor College of Medicine; President and CEO, Space City Associates of Nephrology

Mahendra Agraharkar, MD, MBBS, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Nephrology, and National Kidney Foundation

Disclosure: South Shore DaVita Dialysis Center Ownership interest Other

Rupert Patel, MD  Physician, Division of Nephrology, Houston, Texas

Disclosure: Nothing to disclose.

Rajiv Gupta, MD  Assistant Professor, Department of Medicine, Texas A&M Health Science Center College of Medicine; Consulting Staff, Veterans Affairs Medical Center

Rajiv Gupta, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, and Society of Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Specialty Editor Board

James W Lohr, MD  Professor, Department of Internal Medicine, Division of Nephrology, Fellowship Program Director, University of Buffalo State University of New York School of Medicine and Biomedical Sciences

James W Lohr, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, and Central Society for Clinical Research

Disclosure: Alexion Salary Employment

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

Eleanor Lederer, MD  Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa

Disclosure: Dept of Veterans Affairs Grant/research funds Research

Rebecca J Schmidt, DO, FACP, FASN  Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine

Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association

Disclosure: Renal Ventures Ownership interest Other

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.

Additional Contributors

The primary author would like to thank Dr. Gurvinder Suri, Renal Fellow at the University of Mississippi Medical Center - Nephrology Division, for his valuable peer review.

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Diagram of a nephron.
Nephrocalcinosis.
Nephrocalcinosis.
Nephrocalcinosis.
Nonenhanced coronal computed tomography scans through the kidneys. These images show cortical and medullary nephrocalcinosis (left kidney). Both kidneys appear scarred. Note the thinning of the renal cortex at the upper pole of the left kidney. This patient gave a long history of chronic pyelonephritis, which is an unusual cause of nephrocalcinosis.
Axial computed tomography scans obtained from a patient with a long history of renal tubular acidosis. These images show bilateral medullary nephrocalcinosis (early arterial phase).
Ultrasonogram of the right kidney in a woman with nephrocalcinosis. This image shows hyperechoic foci in the pyramids.
Excretory urogram obtained at 15 minutes in a man with renal papillary necrosis, most likely a patient with diabetes mellitus and repeated urinary tract infections. This image shows bilateral hydronephrosis and a hydroureter due to obstruction by sloughed papillae at the lower end of the ureter.
Plain kidney, ureters, and bladder (KUB) radiograph in a man with renal papillary necrosis, most likely a patient with diabetes mellitus and repeated urinary tract infections. This image shows bilateral renal calcification. A large, sloughed, and calcified renal papilla is present in the region of left vesicoureteric junction. Note the 2 pelvic phleboliths opposite the ischial spine on the right.
 
 
 
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