Calcium abnormalities of dialysis patients

Abstract

Four major organs are involved in the calcium-regulating system, i.e., bone, parathyroid, intestine, and kidney (Fig. 1). The kidneys regulate the excretion of calcium and phosphorus in response to dietary load and to various hormones, such as parathyroid hormone (PTH). In addition, the kidney is practically the only organ that produces active vitamin D, 1,25-dihydroxyvitamin D (1,25D), another key hormone in this regulating system. Accordingly, varieties of abnormalities of bone and mineral metabolism develop in almost all patients with chronic kidney disease (CKD), even from the early stage [1]. As shown in Table 1, the types of renal osteodystrophy (ROD) range from high-turnover bone disease to adynamic bone. Additional modifications by long-term uremic status and by therapeutic modalities result in very complex clinical features in increasing numbers of patients who have been on dialysis for a long time [2]. Furthermore, vascular calcification has recently been recognized as another major category of ROD that affects the survival of dialysis patients [3]. Despite the recent developments of potent therapeutic modalities such as vitamin D analogues, calcimimetics, and new phosphate binders, some major problems still remain to be solved in the management of ROD. These include advanced parathyroid hyperplasia, adynamic bone disease, vascular calcification, and amyloid bone disease. Further elucidation of the pathogenesis of these abnormalities are certainly needed for the establishment of better management strategies for ROD, which would lead to a better quality of life for chronic dialysis patients in future. References