Analysis of serum phosphate control and phosphate binder utilization in incident hemodialysis patients

Abstract

The purpose of this study was to conduct a retrospective analysis of serum phosphate level variability in patients new to hemodialysis (HD) and to identify patient characteristics associated with this variability. The medical records of 47,742 incident HD patients attending US outpatient dialysis centers between January 1, 2006 and March 31, 2009 were analyzed. Monthly mean serum phosphate levels determined over a 6-month evaluation period (months 4–9 after HD initiation) were assigned to one of three strata: low (<1.13 mmol/L [<3.5 mg/dL]); target (1.13–1.78 mmol/L [3.5–5.5 mg/dL]); or high (>1.78 mmol/L [>5.5 mg/dL]). Patients were classified into one of six serum phosphate variability groups based on variability among monthly mean phosphate levels over the 6-month evaluation period: consistently target; consistently high; high-to-target; high-to-low; target-to-low; or consistently low. Only 15% of patients (consistently target group) maintained monthly mean serum phosphate levels within the target range throughout the 6-month evaluation period. Age, Charlson comorbidity index, serum phosphate, and intact parathyroid hormone levels prior to HD initiation were strongly associated (P<0.001) with serum phosphate levels after HD initiation. Overall patient-reported phosphate binder usage increased from 35% at baseline to 52% at end of study. The low proportion of patients achieving target phosphate levels and low rates of phosphate binder usage observed during the study suggest that alternative strategies could be developed to control serum phosphate levels. Possible strategies that might be incorporated to help improve the management of hyperphosphatemia in incident HD patients include dietary modification, dialysis optimization, and earlier and sustained use of phosphate binders.

Keywords:

• chronic kidney disease
• end-stage renal disease
• hyperphosphatemia

Acknowledgments

Writing and editorial support was provided by Fernando Gibson and Rosalind Morley, employees of PharmaGenesis™ London, with funding from Shire Development LLC. Arthur Silverberg, an employee of Shire, provided statistical expertise.

Disclosure

Kimberly Farrand, J Brian Copley, Jamie Heise, Michael Keith, and Lynne Poole are employees of Shire. Moshe Fridman is a consultant to Shire. The results presented in this manuscript are derived from analysis of dialysis center data, obtained via a data licensing agreement. The analysis was funded by Shire Development LLC. The authors declare that the results presented in this paper have not been published previously in whole or part, except in abstract format. The authors report no other conflicts of interest in this work.