Renal bone disease

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 to 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 especially if diabetic, evolve in a different direction with the development of low-turnover adynamic bone disease associated with relative suppression of the parathyroid glands. Uraemic patients also develop an internal milieu that favours soft tissue calcification involving peri-articular tissue, skin, and the vasculature. Arterial calcification is associated closely with arterial stiffening, left ventricular disease and increased cardiovascular morbidity and mortality. Current therapies aim to minimize disturbances to skeletal integrity by setting calcium, phosphate, vitamin D and parathyroid hormone within defined target ranges. It is hoped, but not yet established, that these measures will also result in a reduction of cardiovascular events in this vulnerable population.