Abstract
Renal bone disease is one of the most serious complications of chronic renal failure. Secondary hyperparathyreosis is decisive for its pathogenesis.
Current prevention and treatment emphasises pathogenetic and clinical interrelationships between bone tissue involvement and cardiovascular complications (CKD-MBD, bone and venous involvement associated with chronic renal disease). The treatment should first correct hyperphosphatemia and, subsequently, hyperreactivity of parathyroid glands through vitamin D receptor (VDR) and calcium receptor (CaR) modulation.
Three groups of drugs play a fundamental role here (GIT phosphate binders, calcimi-metics and vitamin D receptor activators). Certain other therapeutic approaches are used in some specific situations such as, among others, refractory hyperparathyreosis or calciphylaxis