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- W2893557090 abstract "The kidney plays an important role in bone and mineral homeostasis, regulating calcium, phosphate, PTH, fibroblast growth factor 23 (FGF23), and calcitriol metabolism. The pathophysiology of calcification in chronic kidney disease (CKD) patients clearly differs from that observed in the general population, although the mechanisms by which vascular calcification develop remain to be fully elucidated. CKD–mineral and bone disorder (CKD–MBD) pathogenesis involves a complex interplay among the kidney, bone, and parathyroid glands. Different factors have been implicated in the pathogenesis of this maladaptive response, but the primary trigger remains to be defined. Therapeutic approaches in CKD–MBD focus primarily on treating hyperphosphatemia and lowering elevated PTH levels. The goal of therapy is that optimization of these parameters limits the contribution of CKD–MBD to adverse CKD-associated outcomes, including fractures, CKD progression, and cardiovascular morbidity and mortality. Therefore, optimizing CKD-MBD treatment paradigms may improve clinical outcomes and life expectancy in the CKD population." @default.
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- W2893557090 date "2018-09-28" @default.
- W2893557090 modified "2023-09-27" @default.
- W2893557090 title "Pathophysiology and Treatment of Chronic Kidney Disease–Mineral and Bone Disorder" @default.
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- W2893557090 doi "https://doi.org/10.1002/9781119266594.ch90" @default.
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