%0 Journal Article
%T Preparation and Characterization of Lanthanum Carbonate Octahydrate for the Treatment of Hyperphosphatemia
%A Anqi He
%A Fengshan Zhou
%A Fang Ye
%A Ying Zhang
%A Xiren He
%A Xin Zhang
%A Ran Guo
%A Xing Zhao
%A Yan Sun
%A Ming Huang
%A Qin Li
%A Zhanlan Yang
%A Yizhuang Xu
%A Jinguang Wu
%J Journal of Spectroscopy
%D 2013
%R 10.1155/2013/593636
%X We proposed a new approach to prepare lanthanum carbonate via reactions between lanthanum chloride and NaHCO3. In the reaction, small amount of NaHCO3 solution was firstly added to the acidic lanthanum chloride solution to generate lanthanum carbonate nuclei and then NaHCO3 is added to the lanthanum chloride at a constant speed. This approach makes both precipitation reaction and neutralization reaction take place simultaneously. Consequently, lanthanum carbonate is produced at low pH environment (pH below 4.0) so that the risk of generating lanthanum carbonate hydroxide is reduced. The product of the above reaction is validated by EDTA titration, elemental analysis, and XRD characterization. In addition, we established a FTIR spectroscopic method to identify La(OH)CO3 from La2(CO3)2¡¤8H2O. Lanthanum carbonate exhibits considerable ability to bind phosphate. 1. Introduction Hyperphosphatemia is a complication of end stage renal failure. In healthy adults, the average daily intake of phosphate is around 1000¨C1500£¿mg, which is balanced by faecal and urinary outputs [1]. For patients with renal failure, however, the phosphate excretion ability of kidneys is reduced significantly. Consequently, the concentration of phosphate in the blood increases, leading to hyperphosphatemia [2]. Hyperphosphatemia causes secondary hyperparathyroidism, renal osteodystrophy, and other diseases. Moreover, high concentration of phosphate in serum results in the formation of calcium phosphate precipitates. Large amount of calcium phosphate precipitates deposited in blood vessels may lead to fetal cardiovascular and cerebrovascular problems in end stage renal failure patients [3]. Current treatment of hyperphosphatemia involves dietary phosphate restrictions, dialysis, and taking phosphate binder and vitamin D [3]. Most dietary phosphate is derived from protein, and the phosphate content has an almost linear correlation with protein intake. Dialysis patients have a higher dietary protein requirement than healthy persons [4]. It is difficult to rely on dietary restrictions to achieve control of phosphate. Moreover, dialysis provides inadequate removal of phosphate in serum. Therefore, renal failure patients have to take phosphate binders [5]. The use of phosphate binder began in the early 1970s [5] and the earliest phosphate binders are aluminum-based compounds. The drug is highly effective and cheap [1]. However, aluminum may accumulate in bone, brain, heart, and liver, causing aluminum toxicity in long-term use [6, 7]. Later, a calcium-based phosphate binder was developed.
%U http://www.hindawi.com/journals/jspec/2013/593636/