<unk>  has been classically described to be 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 hypocalcaemia. High levels of fibroblast growth factor 23 seem now 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. However, in other situations, the initial increase in parathyroid hormone and bone remodeling may be slowed excessively by a multitude of factors, including age, ethnic origin, sex, and treatments such as vitamin D, calcium salts, calcimimetics, steroids, and so forth, leading to low bone turnover or adynamic bone disease. Both high and low bone turnover diseases are currently observed equally in CKD patients treated by dialysis, and all types of<unk>  are associated with an increased risk of skeletal fractures, reduced quality of life, and poor clinical outcomes.
Renal osteodystrophy
Secondary hyperparathyroidism
Primary hyperparathyroidism
AA amyloidosis
Oncogenic osteomalacia
Phosphate nephropathy
Tertiary hyperparathyroidism
Osteolathyrism