Renal osteodystrophy.

Abstract

Patients with chronic renal failure suffer from four different kinds of typical bone lesions which are summarized as renal osteodystrophy (ROD). These changes can occur early during renal disease and are dependent on several factors, such as the calcium-phosphorus homeostasis, the type of renal disease or the frequency and dose of potentially harmful drugs administered. ROD usually gets worse as renal failure progresses, and during hemodialysis, and culminates, in the case of kidney transplantation, in the early post-transplant phase. Although the decrease of parathyroid hormone (PTH) and the dose of immunosuppression administered subsequently permit a certain restitution of bone stability, ROD persists lifelong in the majority of cases and is associated with a high rate of bone fractures. However, the abnormalities of mineral metabolism that lead to ROD are not only confined to bone morphology but also predispose to vascular or soft tissue calcification. This might lead to severe tissue or coronary artery calcification. It is therefore not surprising that life expectancy on hemodialysis is correlated to the expression and form of ROD. The awareness and early diagnosis of renal osteodystrophy are therefore of great importance, in particular since a number of new treatment options have recently evolved. Previously-used phosphate binders, which contain either aluminium or calcium, might be replaced by non-absorbable drugs which bind phosphate through ion exchange. In addition, PTH production can be reduced efficiently by administration of recently developed calcimimetic agents that increase the sensitivity of calcium-sensing receptors in the parathyroid gland. In patients with high-turnover bone disease or after transplantation, bisphosphonates might prevent or restore bone loss.