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CME

Hyperphosphatemia: Understanding the role of phosphate metabolism

Daniel Podd, MPAS, PA-C

July 07, 2010

PDF of CME Hyperphosphatemia 0710

Hyperphosphatemia: Understanding the role of phosphate metabolism

TREATMENT 

Efficacious treatment of hyperphosphatemia, where applicable, consists of successful treatment of the underlying pathologies. Otherwise, treatment centers on lowering phosphate intake and increasing renal excretion. Acute severe hyperphosphatemia with symptomatic hypocalcemia can be life threatening. Phosphate excretion can be increased with saline infusions; however, this may exacerbate hypocalcemia by diluting serum calcium concentration. Hemodialysis is often indicated for patients with symptomatic hypocalcemia, particularly if renal function is impaired.¹¹ 

Hyperphosphatemia related to renal failure is predominantly treated by limiting phosphate ingestion and through dialysis. Hyperphosphatemia as a result of tumor lysis responds to the use of forced saline diuresis to enhance urinary losses. Reduced ingestion may be accomplished by curtailing phosphate-containing foods, such as meat and dairy, as well as phosphate-containing supplements. Limiting phosphate ingestion to 600 mg/d is desirable, primarily for patients with mild renal insufficiency.  

As renal failure progresses, dietary restriction becomes less feasible and less effective. Phosphate-binding drugs and antacids as a second phosphate-lowering mechanism are then indicated. These drugs are taken concomitantly with meals and block GI absorption of phosphate in the intestines. Aluminum hydroxide and aluminum hydroxide sucrose gels were commonly used phosphate binders; however, calcium carbonate (calcium acetate) and calcium citrate binders have largely replaced aluminum-containing binders for patients with ESRD because of the risk of aluminum-related osteomalacia, dementia, and anemia. Although calcium carbonate is a less effective phosphate binder than aluminum, calcium carbonate has a lower toxicity profile and the added benefit of calcium supplementation.  

A phosphate-binding resin without calcium (sevelamer), is available in doses of 800 to 2,400 mg, three times a day with meals, for patients on dialysis. A second PO₄ binder without calcium is lanthanum carbonate, which can also be given to dialysis patients in doses of 500 to 1,000 mg three times a day with meals.⁴ In a comparative crossover study of calcium acetate and sevelamer conducted with patients on hemodialysis, both drugs demonstrated similar efficacy in controlling hyperphosphatemia; however, calcium acetate was far more cost-effective. A trend toward higher serum calcium concentrations and lower PTH concentrations during treatment with calcium acetate was observed.²² In addition, vascular calcification is possible in patients on dialysis who were taking calcium-containing phosphate binders; these agents should thus be avoided in patients who demonstrate coronary artery or systemic calcification.^6,7  

CONCLUSION 

The most common cause of hyperphosphatemia is compromised renal function. Other important causes include excessive phosphate intake, vitamin D intoxication, hypoparathyroidism, hyperthyroidism, malignancy, and transcellular-shifting. Evaluation of pseudohyperphosphatemia resulting from paraproteinemia, hyperlipidemia, and hemolysis should also be considered. Most patients with hyperphosphatemia are asymptomatic; however, coexisting hypocalcemia may cause neurologic manifestations. Chronic, severe hyperphosphatemia induces renal dysfunction, as well as extensive soft tissue, vascular, organ, and periarticular calcifications.  

The diagnostic assessment should include a CBC, complete metabolic panel, lipid and thyroid panels, a PTH assay, and vitamin D and urinary phosphate levels. Ancillary diagnostic studies, such as ECG, plain film radiography, and renal ultrasonography, may also be indicated. Evaluation of coronary arterial calcification by EBCT and MDCT may be useful but is reserved for patients with chronically elevated hyperphosphatemia who are on hemodialysis. Underlying causes of hyperphosphatemia should be identified and treated. Otherwise, reducing phosphate intake, blocking GI absorption, and enhancing phosphate excretion are the mainstays of treatment. JAAPA 

Daniel Podd is an assistant professor at the Saint John's University PA program in Queens, New York, and practices in primary care and pain management in Howard Beach, New York. He has indicated no relationships to disclose relating to the content of this article. 

DRUGS MENTIONED 

Amphotericin B (Ambisome)
Calcium acetate (Eliphos, PhosLo)
Cytarabine (Cytosar-U, DepoCyt, generics)
Doxorubicin (Doxil, generics)
Etidronate (Didronel) 
Furosemide (Lasix, generics)
Lanthanum carbonate (Fosrenol)
Penicillin
Sevelamer (Renagel, Renvela)

IMPORTANT NOTE: JAAPA CME activities consist of 2 articles. To obtain credit, you must also read Helicobacter pylori infection: An update on diagnosis and management; the post-test will include questions related to both articles. AAPA Fellow members should complete and submit the post-test on the AAPA Web site by going to www.aapa.org and searching for keyword JAAPA post-tests. All others may complete and submit the post-test online at no charge at www.mycme.com. To obtain 1 hour of AAPA Category I CME credit, PAs must receive a score of 70% or better on each test taken.

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