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Management of hyperphosphatemia in patients with end-stage renal disease: focus on lanthanum carbonate.

Persy VP, Behets GJ, De Broe ME, D'Haese PC - Int J Nephrol Renovasc Dis (2009)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Pathophysiology, University of Antwerp, Belgium.

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.

No MeSH data available.


Related in: MedlinePlus

Comparison of the pharmacokinetics of aluminium and lanthanum. In contrast to aluminium, there is no increased deposition of lanthanum in CKD compared to patients with normal renal function, as the fraction of lanthanum absorbed in the gut is much lower, and lanthanum elimination is independent of renal function as it is mainly eliminated via the bile. Adapted with permission from Persy VP et al. Semin Dial. 2006;19(3):195–199.59 Copyright © 2006 Blackwell Publishing.Abbreviations: ESRF, end stage renal failure.
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f1-ijnrd-2-001: Comparison of the pharmacokinetics of aluminium and lanthanum. In contrast to aluminium, there is no increased deposition of lanthanum in CKD compared to patients with normal renal function, as the fraction of lanthanum absorbed in the gut is much lower, and lanthanum elimination is independent of renal function as it is mainly eliminated via the bile. Adapted with permission from Persy VP et al. Semin Dial. 2006;19(3):195–199.59 Copyright © 2006 Blackwell Publishing.Abbreviations: ESRF, end stage renal failure.

Mentions: The introduction of yet another metal as a phosphate binder agent prompted concern for the potential aluminium-like toxic effects of lanthanum carbonate on bone and brain. However, lanthanum pharmacokinetics differ substantially from the pharmacokinetic profile of aluminium, as illustrated in Figure 1. In contrast with aluminium, accumulation of lanthanum in the context of impaired renal function is low because firstly, the absorption and bioavailibility of lanthanum are extremely low, and secondly, the very small absorbed fraction is mainly cleared via biliary excretion, with renal clearance of lanthanum being almost negligible.31


Management of hyperphosphatemia in patients with end-stage renal disease: focus on lanthanum carbonate.

Persy VP, Behets GJ, De Broe ME, D'Haese PC - Int J Nephrol Renovasc Dis (2009)

Comparison of the pharmacokinetics of aluminium and lanthanum. In contrast to aluminium, there is no increased deposition of lanthanum in CKD compared to patients with normal renal function, as the fraction of lanthanum absorbed in the gut is much lower, and lanthanum elimination is independent of renal function as it is mainly eliminated via the bile. Adapted with permission from Persy VP et al. Semin Dial. 2006;19(3):195–199.59 Copyright © 2006 Blackwell Publishing.Abbreviations: ESRF, end stage renal failure.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3108761&req=5

f1-ijnrd-2-001: Comparison of the pharmacokinetics of aluminium and lanthanum. In contrast to aluminium, there is no increased deposition of lanthanum in CKD compared to patients with normal renal function, as the fraction of lanthanum absorbed in the gut is much lower, and lanthanum elimination is independent of renal function as it is mainly eliminated via the bile. Adapted with permission from Persy VP et al. Semin Dial. 2006;19(3):195–199.59 Copyright © 2006 Blackwell Publishing.Abbreviations: ESRF, end stage renal failure.
Mentions: The introduction of yet another metal as a phosphate binder agent prompted concern for the potential aluminium-like toxic effects of lanthanum carbonate on bone and brain. However, lanthanum pharmacokinetics differ substantially from the pharmacokinetic profile of aluminium, as illustrated in Figure 1. In contrast with aluminium, accumulation of lanthanum in the context of impaired renal function is low because firstly, the absorption and bioavailibility of lanthanum are extremely low, and secondly, the very small absorbed fraction is mainly cleared via biliary excretion, with renal clearance of lanthanum being almost negligible.31

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Pathophysiology, University of Antwerp, Belgium.

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.

No MeSH data available.


Related in: MedlinePlus