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Clinical data
Trade namesRenagel, Renvela
License data
  • AU: B3
  • US: C (Risk not ruled out)
Routes of
ATC code
Legal status
Legal status
Pharmacokinetic data
Excretionfaecal 100%
CAS Number
PubChem CID
ECHA InfoCard100.207.865 Edit this at Wikidata
Chemical and physical data
where a+b:c = 9:1
Molar massvariable
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Sevelamer (rINN) (/sɛˈvɛləmər/ or /sɛˈvɛləmɪər/) is a phosphate binding drug used to treat hyperphosphatemia in patients with chronic kidney disease. When taken with meals, it binds to dietary phosphate and prevents its absorption. Sevelamer was invented and developed by GelTex Pharmaceuticals. Sevelamer is currently marketed by Sanofi under the trade names Renagel (sevelamer hydrochloride) and Renvela (sevelamer carbonate).

Chemistry and pharmacology[edit]

Sevelamer consists of polyallylamine that is crosslinked with epichlorohydrin.[1] The marketed form sevelamer hydrochloride is a partial hydrochloride salt being present as approximately 40% amine hydrochloride and 60% sevelamer base. The amine groups of sevelamer become partially protonated in the intestine and interact with phosphate ions through ionic and hydrogen bonding.

Medical uses[edit]

Sevelamer is used in the management of hyperphosphatemia in adult patients with stage 4 and 5 chronic kidney disease on hemodialysis. Its efficacy at lowering phosphate levels is similar to that of calcium acetate, but without the accompanying risk of hypercalcemia.


Sevelamer therapy is contraindicated in hypophosphatemia or bowel obstruction. In hypophosphatemia, sevelamer could exacerbate the condition by further lowering phosphate levels in the blood, which could be fatal.

Adverse effects[edit]

Common adverse drug reactions (ADRs) associated with the use of sevelamer include: hypotension, hypertension, nausea and vomiting, dyspepsia, diarrhea, flatulence, and/or constipation.

Other effects[edit]

Sevelamer can significantly reduce serum uric acid.[2] This reduction has no known detrimental effect and several beneficial effects, including reducing hyperuricemia, uric acid nephrolithiasis, and gout.

Sevelamer is able to sequester advanced glycation end products (AGEs) in the gut, preventing their absorption into the blood. AGEs contribute to oxidative stress, which can damage cells (like beta cells, which produce insulin in the pancreas). As Vlassara and Uribarri explain in a 2014 review on AGEs, this may explain why sevelamer, but not calcium carbonate (a phosphate binder that does not sequester AGEs), has been shown to lower AGEs in the blood, as well as oxidative stress and inflammatory markers.[3]


  1. ^ (1) Rosenbaum, D. P.; Mandeville, W. H.; Pitruzzello, M.; Goldberg, D. I. Nephrology Dialysis Transplantation Effect of RenaGel A, a Non-Absorbable, Cross-Linked, Polymeric Phosphate Binder, on Urinary Phosphorus Excretion in Rats. 1997, 961–964.
  2. ^ Garg JP, Chasan-Taber S, Blair A, et al. (January 2005). "Effects of sevelamer and calcium-based phosphate binders on uric acid concentrations in patients undergoing hemodialysis: a randomized clinical trial". Arthritis and Rheumatism. 52 (1): 290–5. doi:10.1002/art.20781. PMID 15641045.
  3. ^ Vlassara H, Uribarri J. "Advanced Glycation End Products (AGE) and Diabetes: Cause, Effect, or Both?". J. Curr Diab Rep. 14 (453). doi:10.1007/s11892-013-0453-1. PMC 3903318.

External links[edit]