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Management of ESRD is complicated by hyperphosphatemia (the accumulation of phosphates in the body due to the inability of dialysis patients to excrete phosphate). This increases the risk of abnormal mineral and bone metabolism (MBD) and the risk of (sudden) death from cardiovascular disease. â€‹

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Management of hyperphosphatemia depends on three approaches:

  1. Use of phosphate binders (the cornerstone);

  2. Dietary phosphate restriction (a significant hurdle for patients with Western diets); and

  3. Removal of phosphates during dialysis.

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Adherence to each of these approaches presents challenges to CKD patients. Those with co-morbidities (such as diabetes, hypertension, etc.) already endure medication-related “pill burden”. Patient-specific factors such as age, gender, genetic background, culture, and cost of treatments add more problems.

Calcium salts are effective, inexpensive, and widely used phosphate binders. A recent review suggests calcium acetate is the most cost-effective phosphate-binding therapy for first-line use in dialysis patients. However, in acidic environments, calcium acetate is converted to acetic acid, a volatile organic acid with an irritating odor and repugnant taste. In contrast, calcium succinate binds phosphate equally well in vitro and is converted to succinic acid, a nonvolatile, tasteless organic acid in the citric acid cycle.

Present Day

Since 2004, European nephrologists have recognized that multi-year treatment of hyperphosphatemia with an oral tablet made up of a combination of 110 mg calcium (as calcium acetate) and 60 mg of magnesium (as magnesium carbonate) (“Ca/Mg”) rapidly and significantly low­ered serum phosphate without increasing serum calcium or raising serum magnesium levels beyond the normal range. Of note, investigators concluded that Ca/Mg is not inferior to sevelamer, a preferred current standard of care for hyper­phosphatemia in many dialysis centers.

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See Outcomes of the CALMAG trial from five European countries

Ca/Mg vs. Sevelamer

GI absorption of diet-derived phosphate may be lowered and controlled by cations such as calcium and magnesium. Since both cations bind phosphate, addition of magnesium may provide physiological benefits not seen with calcium alone.

Changing The Picture

On Target 
For Phosphate Binding

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Management of ESRD is
Complicated by Hyperphosphatemia
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