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. Author manuscript; available in PMC: 2024 Mar 1.
Published in final edited form as: Adv Kidney Dis Health. 2023 Mar;30(2):177–188. doi: 10.1053/j.akdh.2022.12.011

Table 3.

Pharmacologic Interventions for the Management of Hyperphosphatemia

Class Name Mechanism Advantages Disadvantages

Calcium containing binders Calcium carbonate, calcium phosphate Calcium combines with phosphate in the bowel and excreted as insoluble complex in the feces Low cost Potential risk of hypercalcemia, adynamic bone disease, and vascular calcification
Non-calcium-containing binders Sevelamer carbonate or hydrochloride Cationic polymers that bind phosphate in the intestine through ion exchange Avoids positive calcium balance Cost, pill burden. Sevelamer hydrochloride might induce metabolic acidosis
Lanthanum carbonate Phosphate binding in the gastrointestinal tract Avoids positive calcium balance. Chewable, less pill burden Cost
Other mechanism Sucroferric oxyhydroxide, ferric citrate Phosphate binding in the gastrointestinal tract Avoids calcium, relatively less pill burden, small iron absorption Cost
Nicotinamide Decreases sodium-dependent phosphate transporter in the intestine Intolerance (flushing)
Tenapanor Inhibitor of intestinal sodium/hydrogen exchanger 3 (NHE3), reduce paracellular phosphate transport in the intestine Inhibits principal route of phosphate absorption, potentially less pill burden Diarrhea, cost
Aluminum hydroxide Phosphate binding in the gastrointestinal tract Low cost Rarely used chronically dueto riskof aluminum exposure in patients with CKD