PATHOPHYSIOLOGY, CLINICAL SYMPTOMS AND THERAPY OF SECONDARY HYPERPARATHYROIDISM

Background: Although in the last decades great progress has been made concerning renal replacement therapy, secondary hyper parathyroidism ( sHPT) is still of major clinical importance in patients with chronic r enal failure. sHPT demineralizes bone via enhanced osteoclastic activi ty and leads to osteofibrosis. On the other hand, defective kidneys ar e not able to synthesize enough active metabolites of vitamin Dg, lead ing to osteoidosis and osteomalacia. Recently, there is a change in th e spectrum of renal osteodystrophy in favor of low turnover lesions. H owever, changes of parathyroid gland function can be observed in sHPT and adynamic bone disease, emphasizing its central role.