Hyperparathyroidism in chronic kidney disease patients: an update on current pharmacotherapy

Secondary hyperparathyroidism is the most common abnormalities of mineral metabolism in chronic kidney disease (CKD), which causes bone disease and vascular calcification, leading to increased risk of mortality.

The aim of this review is to provide an overview of pharmacological therapies for secondary hyperparathyroidism, based on current understanding of the disease.

The initial event in the pathogenesis of secondary hyperparathyroidism is the phosphorus overload per nephron that lead to the secretion of a new phosphaturic hormone, fibroblast growth factor 23 from the bone. Such an abnormality develops very early in CKD, even without hyperphosphatemia. When hyperphosphatemia develops, phosphate binders are prescribed in many CKD patients. Non-calcium containing binders are gaining popularity because of less risk of excess calcium load; however, no specific superiority in patient-level outcomes has been fully established yet. For the direct control of parathyroid hormone secretion, cinacalcet hydrochloride has become widespread in addition to vitamin D receptor activators. As adverse events related to these therapeutic agents occur occasionally, however, and better adherence is one of the most important determinants of the benefits of the drugs, fewer adverse events as well as more potent therapeutic effects should be aimed in the development of new agents in future.