Optimal management of bone mineral disorders in chronic kidney disease and end stage renal disease

Abstract

Purpose of review This review summarizes recent studies on chronic kidney disease-mineral bone disorders, with a focus on new developments in disease management. Recent findings The term chronic kidney disease-mineral bone disorder has come to describe an increasingly complex network of alterations in minerals and skeletal disorders that contribute to the significant cardiovascular morbidity and mortality seen in patients with chronic kidney disease and ESRD. Clinical studies continue to suggest associations with clinical outcomes, yet current clinical trials have failed to support causality. Variability in practice exists as current guidelines for management of bone-mineral disorders are often based on weak evidence. Recent studies implicate novel pathways for therapeutic intervention in clinical trials. Summary Mineral-bone disorders in chronic kidney disease arise from alterations in a number of molecules in an increasingly complex physiological network interconnecting bone and the cardiovascular system. Despite extensive associations with improved outcomes in a number of molecules, clinical trials have yet to prove causality and there is an absence of new therapies available to improve patient outcomes. Additional clinical trials that can incorporate the complexity of mineral bone disorders and with the ability to intervene on more than one pathway are needed to advance patient care.

Role of vascular calcification inhibitors in preventing vascular dysfunction and mortality in hemodialysis patients

“…Decreased GFR results in diminished renal phosphorus excretion which, in combination with the reduced levels of vitamin D, eventually lead to hypocalcemia, hyperphosphatemia, and hyperparathyroidism; detrimental effects follow, especially on bone and the vascular system . The secondary and tertiary hyperparathyroidism observed in CKD patients is associated with an increased risk of high‐turnover bone disease, adynamic bone disease, vascular and valvular calcification, calciphylaxis, metastatic calcification, and mortality, depending on the nature of the hyperparathyroidism …”

Biochemical comparison of 8 h haemodialysis and 4 h haemodiafiltration, and two dialysis membranes, in a randomized cross‐over trial

“…Dialysis clearance of fetuin appears to be low (<15%), and similar with NHD and HDF. Retinol binding protein (21 kDa) is associated with insulin resistance and FGF23 (30 kDa) is thought to be a marker of chronic kidney disease and phosphate excess . High levels of these two markers may contribute to vascular disease and cardiac mortality .…”

“…Retinol binding protein (21 kDa) is associated with insulin resistance 23 and FGF23 (30 kDa) is thought to be a marker of chronic kidney disease and phosphate excess. 24 High levels of these two markers may contribute to vascular disease and cardiac mortality. 23,24 Our study showed there was no significant difference in clearances of retinol binding protein with both modalities.…”

“…24 High levels of these two markers may contribute to vascular disease and cardiac mortality. 23,24 Our study showed there was no significant difference in clearances of retinol binding protein with both modalities. However, clearance of FGF23 was enhanced by the convective technique, a finding which has been noted in several other studies.…”

Low Continuity Rate of Sucroferric Oxyhydroxide among Japanese Hemodialysis Patients with High Phosphate Binder Pill Burden

“…1) As a result, CKD mineral and bone disorder (CKD-MBD) is a common metabolic complication, 2) and contributes to the high cardiovascular morbidity and mortality seen in CKD patients. 3) Phosphate binders (PBs) are frequently prescribed to hemodialysis (HD) patients to prevent development of CKD-MBD. However, this often causes a higher pill burden.…”