Hyperphosphatemia in Emergency Medicine Medication

  • Author: Leigh A Patterson, MD; Chief Editor: Erik D Schraga, MD   more...
 
Updated: Jun 7, 2010
 

Medication Summary

Oral phosphate binders are used to decrease the highly efficient GI 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 they are natriuretic. Acetazolamide is particularly efficient in promoting renal phosphate excretion.

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Oral phosphate binders

Class Summary

These agents decrease GI phosphate absorption.

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Sevelamer hydrochloride (Renagel)

 

The polymer forms ionic and hydrogen bonds with phosphates and bile acids to promote fecal excretion. Lowers serum phosphate to near normal levels in hemodialysis patients as effectively as calcium acetate without inducing hypercalcemia or increased aluminum levels. Maintains stable iPTH levels and increases alkaline phosphatase levels compared to calcium acetate.

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Calcium acetate (PhosLo)

 

Combines with dietary phosphate to form calcium acetate, which is then excreted in feces.

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Lanthanum carbonate (Fosrenol)

 

Noncalcium, nonaluminum phosphate binder indicated for reduction of high phosphorus levels in patients with end-stage renal disease. Directly binds dietary phosphorus in upper GI tract, thereby inhibiting phosphorus absorption.

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Calcium salts

Class Summary

These agents are used to treat symptomatic hypocalcemia resulting from hyperphosphatemia by replacing calcium.

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Calcium gluconate (Kalcinate)

 

IV preparation used in treatment of symptomatic hypocalcemia, particularly for treatment of tetany. In 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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Calcium chloride

 

IV preparation used in 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 does calcium gluconate. In 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.

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Diuretic carbonic anhydrase inhibitor

Class Summary

These agents increase renal excretion of phosphate.

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Acetazolamide (Diamox)

 

Increases renal excretion of phosphorus.

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Contributor Information and Disclosures
Author

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.

Coauthor(s)

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.

Specialty Editor Board

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

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.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

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.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

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

Disclosure: Nothing to disclose.

References

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Approximately 60-70% of dietary phosphate, 1000-1500 mg/d, is absorbed in the small intestine. Although vitamin D can enhance the absorption, especially under conditions of dietary phosphate depletion, intestinal phosphate absorption is generally unregulated. 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 4.5 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, and dopamine. Phosphate absorption in the remainder of the nephron is generally mediated by type 1 or 3 sodium phosphate cotransporters. No direct evidence related to regulation of these transporters in renal cells under physiologic conditions has been found. 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, thus inhibiting the conversion of 25-hydroxy vitamin D3 to the active metabolite, 1,25 dihydroxyvitamin D3. The decrease in active vitamin D production is somewhat offset by the ability of hyperphosphatemia to stimulate the secretion of parathyroid hormone (PTH), which increases 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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