ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: PO0328

Magnesium's Roles in the Treatment of Hyperphosphatemia of CKD

Session Information

Category: Bone and Mineral Metabolism

  • 401 Bone and Mineral Metabolism: Basic

Author

  • Nelson, Deanna J., BioLink Life Sciences, Inc., Cary, North Carolina, United States
Background

Hyperphosphatemia is causally related to atherosclerotic cardiovascular disease, the most important cause of death in all stages of renal failure and the single greatest threat to survival among ESRD patients undergoing dialysis. To meet the current K/DOQI guideline, patients use cationic binders to bind phosphate (Pi) in the gastrointestinal tract and prevent its uptake. FDA-approved phosphate binders include calcium salts, lanthanum salts, sevelamer, and ferric citrate. Combinations of calcium and magnesium salts have the potential both for phosphate binding with reduced calcium load and for reduction in oxidative stress, vascular calcification, and bone dysfunction.

Methods

Recent literature describing treatment of hyperphosphatemia with phosphate binders composed of calcium acetate/magnesium carbonate and calcium citrate/magnesium carbonate was analyzed. The results highlight aspects of magnesium’s roles in the treatment of hyperphosphatemia of Stage 4-5 CKD and illustrate the potential benefits of these combination therapies in treatment of hyperphosphatemia.

Results

Recent clinical data strongly suggest that combinations of calcium and magnesium salts exhibit pleiotropic benefits for hyperphosphatemic Stage 4-5 CKD patients. In addition to reducing the calcium load, magnesium appears to act in the following ways. (1) Treatment lowered serum phosphorus into the K/DOQI target range in about 24 weeks. (2) Although treatment increased serum magnesium concentrations, [Mg2+] was in the high normal range and comparable to the intracellular magnesium concentration. (3) Short-term treatment raised the T50 value. Since lower values are associated with accelerated conversion of soluble calciprotein particles composed of amorphous calcium phosphate to secondary (insoluble) calciprotein particles containing needle-like calcium phosphate particles, higher magnesium appeared to beneficially slow the rate of conversion. (4) Analyses of bone turnover parameters suggested that higher magnesium may have supported more normal bone remodeling.

Conclusion

Clinical data from several sources suggest that combinations of calcium and magnesium have unique potential for providing pleiotropic benefits to Stage 4-5 CKD patients of all ages. Additional preclinical studies are underway to confirm that calcium magnesium citrates and propionates can be effectively and safely administered to hyperphosphatemic ESRD patients.

Funding

  • Commercial Support