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 |