The Pathophysiology of Secondary Hyperparathyroidism and the Consequences of Uncontrolled Mineral Metabolism in Chronic Kidney Disease: The Role of COSMOS

The development of secondary hyperparathyroidism (SHPT) is a common complication of chronic kidney disease. SHPT develops as a consequence of mineral metabolism disturbances and is characterized by elevated serum parathyroid hormone (PTH) and parathyroid hyperplasia. Evidence suggests that SHPT contributes to the development of vascular calcification and cardiovascular disease, as well as to the development of renal osteodystrophy. The elevated serum calcium, phosphorus, calcium–phosphorus product and PTH that accompany SHPT have been independently associated with an increased relative risk of mortality. Despite the danger that these risks represent, achieving control of mineral metabolism in SHPT is difficult. Recent evidence from the Current Management of Secondary Hyperparathyroidism: Multicentre Observational Study has shown that fewer than 1 in 10 haemodialysis patients simultaneously meet their National Kidney Foundation Kidney Disease Outcomes Quality Initiative targets for serum calcium, phosphorus, calcium–phosphorus product and PTH with standard treatments. There is therefore an urgent need for new strategies and novel pharmacologic therapies that improve control of mineral metabolism and PTH secretion in SHPT and thus reduce the mortality associated with this condition.