Abstract
At first, bone and mineral metabolism anomalies were thought to be a specific bone disease related to parathyroid dys-function, abnormal levels of parathyroid hormone (PTH), and osteitis fibrosa cystica, then called renal osteodystrophy. Recently, however, new bone tissue func-tions have been described in addition to the known role in locomotion, mineral metabolism regulation, and protection of internal organs. Osteoclasts actively participate in fat metabolism, energy homeostasis, and insulin secretion, all essential functions for the cardiovascular system.
Highlights
In the last decade it has become widely accepted that bone mineral metabolism anomalies in patients with CKD reach far beyond bone tissue, which led to the introduction of a new concept: chronic kidney disease-mineral and bone disorder (CKD-MBD).[6,7]
Guideline documents have stressed the need to improve CKD patient survival and quality of life, set target ranges for serum phosphorus, calcium and PTH based on survival data of patients on dialysis, in addition to suggesting an order for the events related to patient management, as follows: management of serum phosphorus levels, serum calcium levels, and parathyroid gland function
In this issue of the Brazilian Journal of Nephrology the Committee for Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) of the Brazilian Society of Nephrology is publishing an update for the Clinical Protocols and Guidelines for the Treatment of Hyperparathyroidism Associated with CKD based on publications and evidence emerged within the last five years, to propose new treatment policies and significant changes in relation to the 2008 Brazilian Guidelines.[12]
Summary
In the last decade it has become widely accepted that bone mineral metabolism anomalies in patients with CKD reach far beyond bone tissue, which led to the introduction of a new concept: chronic kidney disease-mineral and bone disorder (CKD-MBD).[6,7] CKD-MBD is a systemic condition that manifests in the form of PTH, calcium, phosphorus, fibroblast growth factor (FGF-23), and vitamin D alterations, in addition to bone anomalies and extraskeletal calcification.[1,7].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
