Expert opinion on investigational drugs · 2014
Is there a need for new phosphate binders to treat phosphate imbalance associated with chronic kidney disease?
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Wu-Wong Jinshyun Ruth, Mizobuchi Masahide
Аннотация
INTRODUCTION: Mineral and bone disorder (MBD) begins early in the course of chronic kidney disease (CKD). Phosphate imbalance in CKD-MBD can lead to various pathologies of clinical importance such as further deterioration of kidney function, cardiovascular complications, renal osteodystrophy and increased mortality.
AREAS COVERED: The authors conducted a systematic review of the biomedical literature to evaluate currently available drugs and new phosphate binder therapeutics in development.
EXPERT OPINION: There is a need to continue searching for novel phosphate binders that better match an 'ideal' product profile. This profile should have: i) a product that is highly efficient in binding phosphate; ii) low patient compliance issues; iii) minimal interaction with other drugs; and iv) reduced side effects and safety concerns. Targeting alternative mechanisms, such as developing inhibitors for intestinal type II sodium-dependent phosphate co-transporter, may also improve the limitations of phosphate binder therapeutics. Current medical practice focuses on using serum phosphorus levels as the only marker for detecting, monitoring and treating phosphate imbalance in CKD. However, the consequences of phosphate imbalance are evident in non-dialysis patients before serum phosphate levels rise above the normal range. There is a need to search for other markers to guide detection and treatment of clinically significant alterations in phosphate metabolism of non-dialysis CKD.
AREAS COVERED: The authors conducted a systematic review of the biomedical literature to evaluate currently available drugs and new phosphate binder therapeutics in development.
EXPERT OPINION: There is a need to continue searching for novel phosphate binders that better match an 'ideal' product profile. This profile should have: i) a product that is highly efficient in binding phosphate; ii) low patient compliance issues; iii) minimal interaction with other drugs; and iv) reduced side effects and safety concerns. Targeting alternative mechanisms, such as developing inhibitors for intestinal type II sodium-dependent phosphate co-transporter, may also improve the limitations of phosphate binder therapeutics. Current medical practice focuses on using serum phosphorus levels as the only marker for detecting, monitoring and treating phosphate imbalance in CKD. However, the consequences of phosphate imbalance are evident in non-dialysis patients before serum phosphate levels rise above the normal range. There is a need to search for other markers to guide detection and treatment of clinically significant alterations in phosphate metabolism of non-dialysis CKD.