The prevalence of osteoporosis, fracture, and vascular calcification rises parallel to the advancement of chronic renal disease (CKD). A significant pathophysiologic mechanism is CKD-mineral bone disease (CKD-MBD), caused by hyperphosphatemia. Phosphate binders’ effects on bone turnover biomarkers and bone mineral density (BMD) in hemodialysis patients are still unknown. For a study, researchers sought to demonstrate how the phosphate binders affected various facets of CKD-MBD.
They studied the effect of 12-month monotherapy of phosphate binders using calcium-based phosphate binders (CPB) or non-calcium-based phosphate binders (NCPB), including sevelamer and lanthanum, on bone turnover biomarkers and BMD alterations in a prospective cohort of 65 hemodialysis patients. The ability of bone turnover indicators to predict low BMD was thoroughly investigated.
NCPB use was related to greater levels of bone turnover biomarkers as compared to CPB use. NCPB was also linked to decreased BMD at the lumbar and distal radius. Total procollagen type 1N-terminal propeptide (P1NP), bone-specific alkaline phosphatase (BALP), and tartrate-resistant acid phosphatase 5b (TRAP5b) performed best in detecting reduced BMD in hemodialysis patients.
Changing from CPB to NCPB may boost bone biomarkers and avoid the development of adynamic bone disease. NCPB, on the other hand, should be used with caution in hemodialysis patients who already have poor BMD. P1NP, BALP, and TRAP5b might be utilized to advise optimal care, including anti-resorptive and anabolic medicines, and predict poor BMD in phosphate binders-treated hemodialysis patients.