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Hyperphosphatemia Medication

  • Author: Eleanor Lederer, MD, FASN; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Dec 16, 2015
 

Medication Summary

Oral phosphate binders are used to decrease the highly efficient gastrointestinal absorption of phosphorus. Calcium salts are widely used but may produce hypercalcemia. Aluminum salts are effective binders but may induce aluminum toxicity. Newer compounds containing iron or bile acid sequestrants are replacing calcium and aluminum binders.

Proximal diuretics are phosphuretic to the same extent that they are natriuretic. Acetazolamide is particularly efficient in promoting renal phosphate excretion.

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Diuretics

Class Summary

Diuretics lower phosphate serum levels by enhancing renal excretion.

Furosemide (Lasix)

 

Furosemide inhibits the resorption of sodium and chloride in the loop of Henle and the proximal and distal tubules of the kidney. Its onset of action is rapid after an intravenous dose. This agent increases the excretion of phosphate.

Acetazolamide (Diamox)

 

This agent inhibits carbonic anhydrase, the enzyme that catalyzes the hydration of CO2 and dehydration of carbonic acid. Inhibition reduces reabsorption of NaHCO3 in the proximal tubule, leading to natriuresis, bicarbonate, diuresis, and a decreased serum bicarbonate level. As NaHCO3 delivery to the collecting duct increases, the renal excretion of phosphate increases.

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Phosphate Binders

Class Summary

The agents bind to dietary phosphate in the gastrointestinal tract. The phosphate is then eliminated in the feces, thus limiting intestinal absorption.

Sevelamer hydrochloride (Renagel, Renvela)

 

This agent is a polymeric phosphate binder for oral administration. It does not contain aluminum; thus, aluminum intoxication not a concern.

The polymer forms ionic and hydrogen bonds with phosphates and bile acids to promote fecal excretion. It lowers serum phosphate to near normal levels in hemodialysis patients as effectively as calcium acetate without inducing hypercalcemia or increased aluminum levels. Sevelamer hydrochloride maintains stable intact PTH levels and increases alkaline phosphatase levels compared with calcium acetate.

Lanthanum carbonate (Fosrenol)

 

Lanthanum carbonate is a noncalcium, nonaluminum phosphate binder indicated for the reduction of high phosphorus levels in patients with end-stage renal disease. It directly binds dietary phosphorus in the upper gastrointestinal tract, thereby inhibiting phosphorus absorption.

Sucroferric oxyhydroxide (Velphoro)

 

Sucroferric oxyhydroxide is an iron-based, calcium-free phosphate binder. When it is taken with meals, dietary phosphate is adsorbed in the gastrointestinal tract and eliminated in the feces. It is indicated for the control of serum phosphorus levels in patients with chronic kidney disease on hemodialysis.

Ferric citrate

 

Ferric citrate is a phosphate binder. Ferric iron binds dietary phosphate in the GI tract and precipitates as ferric phosphate, which is insoluble and is excreted in the feces. It is indicated for the control of serum phosphorus levels in patients with chronic kidney disease on dialysis.

Aluminum hydroxide

 

Aluminum hydroxide, which is available in tablet or liquid form, is commonly used as an antacid. It is not a first-line therapy for hyperphosphatemia, because of the potential for aluminum intoxication with extended use.

Calcium carbonate (Caltrate 600, Os-Cal, Tums, Oysco 500)

 

This agent normalizes phosphate concentrations in patients on dialysis. Calcium carbonate combines with dietary phosphate to form insoluble calcium phosphate, which is excreted in feces. It is marketed in a variety of dosage forms and is relatively inexpensive. Calcium carbonate is available by tablet for chewing or swallowing and is sold in many sizes (250-1000 mg). It is also used as an antacid or a calcium supplement.

Calcium acetate (Calphron, PhosLo, Eliphos)

 

Calcium acetate combines with dietary phosphorus to form insoluble calcium phosphate, which is excreted in feces.

Calcium chloride

 

Calcium chloride is administered as an IV preparation; it is used in the treatment of severe symptomatic hypocalcemia. Do not confuse calcium chloride with calcium gluconate; calcium chloride contains approximately 3 times as much elemental calcium per unit weight as calcium gluconate does. In the absence of symptoms, hypocalcemia may be treated with oral supplements rather than IV infusions. Calcium chloride 10% solution contains 100 mg/mL = 1.4 mEq/mL.

Magnesium hydroxide (Milk of Magnesia)

 

Magnesium is a divalent cation that is maximally absorbed in the distal small intestine. At low concentrations, it appears to be absorbed in a saturable carrier-mediated process influenced by vitamin D. At high concentrations, absorption appears to occur largely and inefficiently through diffusion. Magnesium hydroxide reduces the absorption of dietary phosphate.

Calcium gluconate (Cal-Glu)

 

Calcium gluconate is administered as an intravenous (IV) preparation; it is used in the treatment of symptomatic hypocalcemia, being particularly employed for the treatment of tetany. In the absence of symptoms, hypocalcemia may be treated with oral supplements rather than IV infusions. Calcium gluconate 10% solution contains 100 mg/mL = 0.45 mEq elemental calcium/mL.

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Contributor Information and Disclosures
Author

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

Disclosure: Received grant/research funds from Dept of Veterans Affairs for research; Received salary from American Society of Nephrology for asn council position; Received salary from University of Louisville for employment; Received salary from University of Louisville Physicians for employment; Received contract payment from American Physician Institute for Advanced Professional Studies, LLC for independent contractor; Received contract payment from Healthcare Quality Strategies, Inc for independent cont.

Coauthor(s)

Rosemary Ouseph, MD Professor of Medicine, Director of Kidney Transplant, University of Louisville School of Medicine

Rosemary Ouseph, MD is a member of the following medical societies: American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplant Surgeons

Disclosure: Nothing to disclose.

Vibha Nayak, MD Assistant Professor of Nephrology, Director of Home Dialysis, Kidney Disease Program, University of Louisville School of Medicine

Vibha Nayak, MD is a member of the following medical societies: American Society of 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.

Acknowledgements

Jeffrey L Arnold, MD, FACEP Chairman, Department of Emergency Medicine, Santa Clara Valley Medical Center

Jeffrey L Arnold, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Physicians

Disclosure: Nothing to disclose. Andrew J Dailey, MD Fellow, Department of Medicine, Division of Nephrology, University of Louisville School of Medicine

Disclosure: Nothing to disclose.

Stephanie Dianne Hill Dailey, MD Fellow, Department of Medicine, Division of Nephrology, University of Louisville School of Medicine

Disclosure: Nothing to disclose.

Peter MC DeBlieux, MD Professor of Clinical Medicine and Pediatrics, Section of Pulmonary and Critical Care Medicine, Program Director, Department of Emergency Medicine, Louisiana State University School of Medicine in New Orleans

Peter MC DeBlieux, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Radiological Society of North America, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Robin R Hemphill, MD, MPH Associate Professor, Director, Quality and Safety, Department of Emergency Medicine, Emory University School of Medicine

Robin R Hemphill, MD, MPH is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Leigh A Patterson, MD Assistant Professor, Residency Director, Department of Emergency Medicine, Brody School of Medicine at East Carolina University

Leigh A Patterson, MD is a member of the following medical societies: American College of Emergency Physicians, American Institute of Ultrasound in Medicine, American Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

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

Christie P Thomas, MBBS, FRCP, FASN, FAHA Professor, Department of Internal Medicine, Division of Nephrology, Departments of Pediatrics and Obstetrics and Gynecology, Medical Director, Kidney and Kidney/Pancreas Transplant Program, University of Iowa Hospitals and Clinics

Christie P Thomas, MBBS, FRCP, FASN, FAHA is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, and Royal College of Physicians

Disclosure: Nothing to disclose.

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Approximately 60-70% of dietary phosphate, 1000-1500 mg/day, is absorbed in the small intestine. Although vitamin D can enhance the absorption, especially under conditions of dietary phosphate depletion, intestinal phosphate absorption does not require the presence of active vitamin D. Specifically, high serum phosphate and high dietary phosphate intake do not significantly impair intestinal uptake. The movement of phosphate in and out of bone, the reservoir containing most of the total body phosphate, is generally balanced. Renal excretion of excess dietary phosphate intake ensures maintenance of phosphate homeostasis, maintaining serum phosphate at a level of approximately 3-4 mg/dL in the serum.
The vast majority of filtered phosphate is reabsorbed by type 2a sodium phosphate cotransporters located on the apical membrane of the renal proximal tubule. The expression of these cotransporters is increased by low dietary phosphate intake and several growth factors to enhance phosphate absorption. The expression is decreased by high dietary phosphate intake, parathyroid hormone (PTH), FGF23, and dopamine. Phosphate absorption in the remainder of the nephron is generally mediated by type 3 sodium phosphate cotransporters. No direct evidence has been found related to the regulation of these transporters in renal cells under physiologic conditions. The absorption in the proximal tubule is regulated such that the final excretion matches the dietary excess in order to maintain homeostasis.
Hyperphosphatemia inhibits 1-alpha hydroxylase in the proximal tubule directly and indirectly through stimulation of FGF23, thus inhibiting the conversion of 25-hydroxy vitamin D3 to the active metabolite, 1,25 dihydroxyvitamin D3. FGF23 additionally increases the expression of 24-hydroxylase, leading to inactivation of active 1,25 dihydroxyvitamin D3. The decrease in active vitamin D production with high phosphate is somewhat offset by the ability of hyperphosphatemia to stimulate the secretion of parathyroid hormone (PTH), which will increase the activity of 1-alpha hydroxylase. The result is generally a neutral effect on intestinal phosphate absorption. Hyperphosphatemia-stimulated PTH secretion is mediated through an as yet unidentified pathway. With normal renal function, the transient increase in PTH and decrease in vitamin D serve to inhibit renal and intestinal absorption of phosphate, resulting in resolution of the hyperphosphatemia. In contrast, under conditions of renal failure, sustained hyperphosphatemia results in sustained hyperparathyroidism. The hyperparathyroidism enhances renal phosphate excretion but also enhances bone resorption, releasing more phosphate into the serum. As renal failure progresses and the ability of the kidney to excrete phosphate continues to diminish, the action of PTH on the bone can exacerbate the already present hyperphosphatemia.
 
 
 
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