Sustained loss of kidney function leads to the evolution of progressive secondary hyperparathyroidism associated with a characteristic high-turnover form of metabolic bone disease. The drivers of hyperparathyroidism include the failure of renal bioactivation of vitamin D, phosphate retention and, in some cases, hypocalcaemia. As renal impairment becomes more severe, some patients, particularly under the influence of treatment, and particularly if they have diabetes, evolve in a different direction, with the development of low-turnover adynamic bone disease associated with relative suppression of the parathyroid glands.