The management of hyperphosphatemia by lanthanum carbonate in chronic kidney disease patients

Abstract

Takashi Shigematsu, Yuri Nakashima, Masaki Ohya, Koichi Tatsuta, Daisuke Koreeda, Wataru Yoshimoto, Shintaro Yamanaka, Toshifumi Sakaguchi, Yoshiyuki Hanba, Toru Mima, Shigeo NegiDivision of Nephrology, Department of Internal Medicine, Wakayama Medical University, Wakayama City, Wakayama, JapanAbstract: Hyperphosphatemia has been shown to be involved not only in the onset and progression of secondary hyperparathyroidism but also in vascular calcification. In addition, it influences the clinical course of patients with chronic kidney disease. Phosphate (Pi) binder is required in the management of hyperphosphatemia, because dietary Pi restriction and Pi removal by hemodialysis alone are insufficient. Lanthanum carbonate, a powerful Pi binder, has a similar effect to aluminum hydroxide in reducing serum Pi levels. As it is excreted via the liver, lanthanum carbonate has an advantage in patients with renal failure. The effect of lanthanum carbonate on serum Pi levels is almost two times higher than that of calcium (Ca) carbonate, which is commonly used. Lanthanum carbonate and Ca carbonate have an additive effect. Worldwide, there is 6 years worth of clinical treatment data on lanthanum carbonate; however, we have 3 years of clinical use in Japanese patients with hyperphosphatemia. No serious side effects have been reported. However, the most important concern is bone toxicity, which has been observed with use of aluminum hydroxide. For this study, clinical research involved analysis of bone biopsies. Although osteomalacia is the most noticeable side effect, this was not observed. Both the high- and the low-turnover bone disease concentrated into a normal bone turnover state. However, as the authors have less than 10 years' clinical experience with lanthanum carbonate, patients should be monitored carefully. In addition, it is necessary to demonstrate whether potent treatment effects on hyperphosphatemia improve the long-term outcome.Keywords: phosphate binder, end-stage renal disease (ESRD), fibroblast growth factor 23 (FGF23), vascular calcification