Vitamin D and hyperparathyroidism in patients with chronic kidney disease

Secondary hyperparathyroidism is a common clinical problem in patients with chronic kidney disease (CKD). It causes disturbances in bone metabolism and increased risk of bone fracture. Secondary hyperparathyroidism develops as a consequence of reduced renal phosphate excretion and thereby elevated phosphate levels, hypocalcaemia, increased fibroblast growth factor 23 levels and reduced levels of calcitriol due to decreased renal 1α-hydroxylation of vitamin D. Treatment with calcitriol or its analogs suppress the secondary hyperparathyroidism. But increasing doses of calcitriol induces elevated levels of calcium and phosphate. Elevated calcium and phosphate levels are associated with extra-vascular calcification, cardiovascular disease and increased mortality. Active vitamin D analogs have been developed in order to increase the therapeutic window for parathyroid hormone suppression, without increasing phosphate and calcium levels. Observational studies have demonstrated an improved survival in patients with CKD treated with calcitriol or active vitamin D analogs. Both observational and animal studies suggest an effect of vitamin D and vitamin D analogs through mechanisms that are independent of the mineral metabolism.