Bone disease is one of the most challenging complications in patients with chronic kidney disease. Today, it is considered to be part of a complex systemic disorder manifested by disturbances of mineral metabolism and vascular calcifications called chronic kidney disease – mineral bone disorder (CKD-MBD). The term renal osteodystrophy is reserved to define the specific bone lesion in CKD-MBD, whose spectrum ranges from high turnover to low turnover disease. Phosphate retention, decreased serum calcium, and 1,25-dihydroxy vitamin D synthesis are involved in the pathogenesis of high bone turnover. However, the various therapeutic approaches (calcium supplements, phosphate binders, and vitamin D metabolites, among others), the renal replacement modality (hemodialysis or continuous ambulatory peritoneal dialysis), and the types of patients to whom dialysis is offered (more patients who are diabetic or older, or both) may influence the evolution of the bone disorder. As a result, recent studies have reported a greater prevalence of adynamic forms of renal osteodystrophy, especially in diabetic and peritoneal dialysis patients. The present article reviews, for patients treated with peritoneal dialysis, the pathophysiologic mechanisms involved in the evolution and perpetuation of this bone disease and the therapeutic modalities for treating and preventing adynamic bone.
Chronic Kidney Disease: Treatment of Comorbidities I (Nutrition, Growth, Neurocognitive Function, and Mineral Bone Disease)
