Treatment of Hyperphosphatemia with Calcium Acetate
Calcium acetate is an effective phosphate binder for treating hyperphosphatemia in CKD patients, but its use should be restricted in patients with hypercalcemia, arterial calcification, adynamic bone disease, or persistently low PTH levels. 1
Mechanism and Efficacy
Calcium acetate works by binding dietary phosphate in the gastrointestinal tract to form an insoluble calcium phosphate complex that is excreted in feces, resulting in decreased serum phosphorus concentration 2. Clinical studies demonstrate that:
- Calcium acetate effectively reduces serum phosphorus by approximately 30% over a 12-week treatment period 2
- It is more effective at binding phosphorus than calcium carbonate, requiring less elemental calcium per phosphate bound 3, 4
- In a double-blind, placebo-controlled study, calcium acetate decreased serum phosphorus by a mean of 19% over 2 weeks 2
Dosing and Administration
- Initial dosing: 2 tablets (667 mg each) per meal for 3 meals daily 2
- Adjust dose based on serum phosphorus levels, targeting normal range 1, 5
- Average effective dose: 3-4 tablets per meal 2
- Must be taken with meals to effectively bind dietary phosphate 1, 2
- For medications where reduced bioavailability would have significant effects, advise taking them 1 hour before or 3 hours after calcium acetate 2
Treatment Algorithm for Hyperphosphatemia
First step: Implement dietary phosphate restriction (800-1,000 mg/day) 5
Second step: If serum phosphorus remains persistently elevated, initiate phosphate binder therapy 1
Choice of phosphate binder:
Monitoring:
Contraindications and Cautions
Restrict calcium acetate use in patients with:
- Hypercalcemia 1, 5
- Evidence of arterial calcification 1
- Adynamic bone disease 1
- Persistently low PTH levels 1
In these cases, consider non-calcium-based phosphate binders such as sevelamer 1, 5.
Special Considerations
- In CKD patients not on dialysis, calcium acetate has been shown to effectively reduce serum phosphorus and iPTH over a 12-week period 6
- For patients on dialysis, maintain dialysate calcium concentration between 1.25-1.50 mmol/L (2.5-3.0 mEq/L) 1
- Consider combination therapy with calcium-based and non-calcium-based binders for patients who remain hyperphosphatemic despite single-agent therapy 5
- For patients with persistent hypercalcemia during calcium acetate therapy, switching to a non-calcium-based binder is recommended 7
Common Pitfalls to Avoid
- Excessive calcium loading: Total calcium intake from diet and phosphate binders should not exceed 2,000 mg/day to avoid vascular calcification 1
- Treating normophosphatemic patients: Phosphate binders should only be initiated for persistently elevated phosphorus levels, not preventively in patients with normal levels 1
- Ignoring calcium levels: Regular monitoring of serum calcium is essential, as calcium acetate can increase serum calcium by approximately 7-9% 2
- Poor patient adherence: Calcium acetate may have lower compliance rates than calcium carbonate due to tablet formulation and potential gastrointestinal effects 3
- Failure to adjust vitamin D therapy: When using calcium-based binders, vitamin D analogs may need dose adjustment to prevent hypercalcemia 1
By following these guidelines, calcium acetate can be effectively and safely used to manage hyperphosphatemia in patients with chronic kidney disease.