Management of hyperphosphatemia in patients with end-stage renal disease: focus on lanthanum carbonate
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Published on: April 4, 2025
Veerle P Persy1, Geert J Behets, Marc E De Broe
1Laboratory of Pathophysiology, University of Antwerp, Belgium.
Insights
Managing hyperphosphatemia in chronic kidney disease (CKD) is crucial for reducing cardiovascular risk. Lanthanum carbonate offers a safe, non-calcium phosphate binder option for CKD patients.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Pharmacology
Background:
- Elevated serum phosphate (hyperphosphatemia) in chronic kidney disease (CKD) increases cardiovascular risk.
- Standard treatments like protein restriction and dialysis are often insufficient to control hyperphosphatemia.
- Existing phosphate binders (calcium-based, resin-based) can cause adverse effects like hypercalcemia and ectopic mineralization.
Purpose of the Study:
- To review clinical and experimental data on lanthanum carbonate as a novel phosphate binder.
- To assess the safety and efficacy of lanthanum carbonate in CKD patients.
- To evaluate the long-term effects of lanthanum carbonate on bone, vasculature, and brain.
Main Methods:
- Review of recent clinical studies and experimental data on lanthanum carbonate.
- Analysis of lanthanum bioavailability, metabolism, and toxicity.
- Examination of clinical trial data up to 6 years of follow-up.
Main Results:
- Lanthanum carbonate is a non-calcium, non-resin phosphate binder.
- Lanthanum exhibits extremely low bioavailability and a distinct metabolism, avoiding aluminum-like toxicity.
- Clinical studies show no toxic effects of lanthanum carbonate with up to 6 years of follow-up.
Conclusions:
- Lanthanum carbonate is a safe and effective option for managing hyperphosphatemia in advanced CKD.
- Its unique pharmacokinetic profile minimizes risks associated with traditional phosphate binders.
- Further evaluation of its long-term impact on bone, vasculature, and brain is warranted.
Abstract:
Elevated serum phosphate levels as a consequence of chronic kidney disease (CKD) contribute to the increased cardiovascular risk observed in dialysis patients. Protein restriction and dialysis fail to adequately prevent hyperphosphatemia, and in general treatment with oral phosphate binding agents is necessary in patients with advanced CKD. Phosphate plays a pivotal role in the development of vascular calcification, one of the factors contributing to increased cardiovascular risk in CKD patients. Treatment of hyperphosphatemia with standard calcium-based phosphate binders and vitamin D compounds can induce hypercalcemic episodes, increase the Ca × PO(4) product and thus add to the risk of ectopic mineralization. In this review, recent clinical as well as experimental data on lanthanum carbonate, a novel, non-calcium, non-resin phosphate binding agent are summarized. Although lanthanum is a metal cation no aluminium-like toxicity is observed since the bioavailability of lanthanum is extremely low and its metabolism differs from that of aluminium. Clinical studies now document the absence of toxic effects of lanthanum for up to 6 years of follow-up. The effects of lanthanum on bone, vasculature and brain are discussed and put in perspective with lanthanum pharmacokinetics.
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