Overview of renal bone disease: Causes of treatment failure, clinical observations, the changing pattern of bone lesions, and future therapeutic approach: Management of comorbidities in kidney disease in the 21st century: Anemia and bone disease

Abstract

Divalent ions, metabolism abnormalities, and hyperparathyroid bone disease noted in patients with chronic kidney disease (CKD) develop early in the course of renal insufficiency. In the last two decades, therapy has focused mostly in treating the bone lesion as well as controlling the secondary hyperparathyroidism. However, recent large epidemiologic studies have highlighted the importance of both hyperphosphatemia and an increase in the calcium burden as major factors leading to the high mortality rate of end-stage renal disease (ESRD) patients [1–3]. Furthermore, a recent study strongly suggests the high mortality rate may be due to an increase in cardiac events [4]. In the present manuscript, the causes for the failure of the original therapeutic goals will be discussed first; the changing pattern in the bone lesions will be assessed second; and third, future therapeutic approaches will be explored, with special emphasis in early therapy and avoiding the cardiovascular abnormalities recently noted in CKD patients.