The consequences of uncontrolled secondary hyperparathyroidism and its treatment in chronic kidney disease.
Secondary hyperparathyroidism (HPT) is a common complication of chronic kidney disease (CKD) and a frequent cause of clinically significant bone disease. Soft-tissue and vascular calcification, cardiovascular disease, and calcific uremic arteriolopathy (CUA) are additional serious consequences of the disorder that may contribute directly to cardiovascular morbidity and mortality in patients with CKD. Less widely appreciated manifestations include neurological disturbances, hematological abnormalities, and endocrine dysfunction. Secondary HPT arises from alterations in calcium, phosphorus, and vitamin D metabolism that develop early in the course of CKD and become more pronounced as kidney function declines. Treatment is often delayed, however, until the disease is well established. Current therapeutic strategies rely largely on the use of vitamin D sterols to diminish excess parathyroid hormone (PTH) synthesis and to lower serum or plasma PTH levels, but their use is often confounded by increases in serum calcium and phosphorus concentrations, changes that can aggravate soft-tissue and vascular calcification. As such, there is a need for new therapeutic interventions that can effectively lower serum or plasma PTH levels without producing untoward side effects. The current review summarizes the diverse manifestations of secondary HPT in patients with CKD. The consequences of inadequately controlled secondary HPT and the adverse effects of selected therapeutic interventions for the disorder on vascular calcification and cardiovascular disease in those with CKD are discussed.
Goodman
William G
WG
Division of Nephrology, UCLA School of Medicine, Los Angeles, California, USA. bgoodman@mednet.ucla.edu
D002114:Calcinosis / Q000209:etiology / Q000503:physiopathology; D002117:Calcitriol / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002318:Cardiovascular Diseases / Q000209:etiology / Q000503:physiopathology; D002908:Chronic Disease; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000150:complications* / Q000209:etiology / Q000503:physiopathology / Q000628:therapy; D007333:Insulin Resistance / Q000502:physiology; D007674:Kidney Diseases / Q000150:complications*; D010006:Osteoblasts / Q000502:physiology; D010010:Osteoclasts / Q000502:physiology; D010281:Parathyroid Hormone / Q000097:blood; D010758:Phosphorus / Q000378:metabolism
D002120:Calcium Channel Agonists; D010281:Parathyroid Hormone; D010758:Phosphorus; D002117:Calcitriol; D002118:Calcium