Renal osteodystrophy has been classically described as the result of
hyperparathyroidism secondary to
hyperphosphatemia combined with
hypocalcemia, both of which are due to decreased excretion of phosphate by the damaged kidney. Low activated
vitamin D3 levels are a result of the damaged kidneys' inability to convert vitamin D3 into its active form,
calcitriol, and result in further
hypocalcemia. High levels of
fibroblast growth factor 23 seem to be the most important cause of decreased calcitriol levels in CKD patients. In CKD, the excessive production of
parathyroid hormone increases the bone resorption rate and leads to histologic bone signs of secondary hyperparathyroidism. Both high and low bone turnover diseases are observed equally in CKD patients treated by dialysis, and all types of renal osteodystrophy are associated with an increased risk of skeletal fractures, reduced quality of life, and poor clinical outcomes. ==Diagnosis==