Improved Strategies for the Treatment of Renal Osteodystrophy

Abstract

Renal osteodystrophy (ROD) encompasses several distinct skeletal complications resulting from the metabolic abnormalities associated with chronic kidney disease (CKD). Other manifestations of altered calcium and phosphorus homeostasis include an increased risk of cardiovascular mortality and morbidity. Hyperphosphatemia and secondary hyperparathyroidism (HPT) are associated with these adverse events, and ultimately can lead to ROD. Dietary restriction of phosphorus, use of phosphate binding agents, and vitamin D therapy have been the mainstay of therapy for HPT. Recently, several new therapeutic agents have become available for the management of HPT. The nonelemental phosphate binder, sevelamer hydrochloride (Renagel ^® ) has provided an alternative to calcium-containing binders for the management of hyperphosphatemia. This agent also decreases calcium load and minimizes the risk of hypercalcemia and skin and soft tissue calcifications. Research in the area of vitamin D receptors has lead to the development of vitamin D analogs including paricalcitol (Zemplar ^® ) and doxercalciferol (Hectorol ^® ) as alternative agents for HPT. Potential benefits of these analogs include a lower risk of hypercalcemia and hyperphosphatemia compared with calcitriol, although further evaluation is warranted as these agents are used more in clinical practice. Calcimimetics are also in the pipeline as potential agents for management of HPT by inhibition of parathyroid hormone secretion. These new developments in the management of metabolic disorders of CKD provide pharmacotherapeutic alternatives to improve patient outcomes and prevent/manage ROD. The challenge is to determine appropriate guidelines for use of these agents at all stages of CKD.