S5 0896-8608/08 $3.00 + .00 Copyright © 2008 International Society for Peritoneal Dialysis Chronic Kidney Disease — Mineral Bone Disorder and Peritoneal Dialysis Peritoneal Dialysis International, Vol. 28 (2008), Supplement 2 Printed in Canada. All rights reserved. CHRONIC KIDNEY DISEASE – MINERAL BONE DISORDER Sharon M. Moe Indiana University School of Medicine and Roudebush VAMC, Indianapolis, Indiana, U.S.A. Correspondence to: S.M. Moe, Indiana University School of Medicine, 1001 W. 10th Street, OPW 526, Indianapolis, Indi- ana 46202 U.S.A. smoe@iupui.edu The definition, evaluation, and classification of the min- eral abnormalities and bone disease in chronic kidney dis- ease (CKD) should encompass all three clinical components: • Abnormalities in serum biochemistries • Vascular calcification • Bone abnormalities This principle was discussed at a Kidney Disease: Improv- ing Global Outcomes consensus conference, resulting in a recognition of the shortcomings of the current classifica- tion and a recommendation for the development of new ter- minology. The recommendation was that the term “renal osteodystrophy” be used exclusively to define the bone pa- thology associated with CKD. The many clinical, biochemi- cal, and imaging abnormalities that have heretofore been identified as correlates of renal osteodystrophy should be defined more broadly as a clinical entity or syndrome called “chronic kidney disease – mineral and bone disorder.” The hope is that this new terminology will enhance communi- cation and facilitate research worldwide. Perit Dial Int 2008; 28(S2):S5–S10 www.PDIConnect.com KEY WORDS: Mineral bone disorder; renal osteodys- trophy; calcium; phosphorus; parathyroid hormone; vascular calcification; bone. I n people with healthy kidneys, normal serum levels of phosphorus and calcium are maintained through the combined effects of two hormones: parathyroid hormone (PTH) and 1,25(OH) 2 D (calcitriol), the active metabo- lite of vitamin D. These hormones act on three target organs: kidney, bone, and intestine. The kidneys regu- late PTH-mediated calcium reabsorption and phosphate excretion, convert vitamin D to its active metabolite calcitriol, and increase phosphate excretion in response to changes in serum phosphorus, perhaps mediated by fibroblast growth factor 23 and other phosphatonins. Thus, the kidneys play a critical role in the regulation of normal serum calcium and phosphorus concentrations, with abnormal homeostasis occurring in the setting of chronic kidney disease (CKD). Serum or urine abnormali- ties, or both, are initially observed in patients with glo- merular filtration rate (GFR) levels below 60 mL/min and are nearly uniform when GFR declines below 30 mL/min (1). The progression of kidney disease is eventually as- sociated with an inability to completely compensate for the loss of GFR, ultimately resulting in multiple abnormalities. Until recently, the abnormal bone (termed “renal osteodystrophy”) that results from these derangements in mineral metabolism occurring nearly ubiquitously by the time patients reach end-stage renal disease has been the main focus of concern. Unfortunately, although bone biopsy remains a powerful diagnostic tool, it is not always clinically available. Moreover, the histologic no- menclature of CKD-related bone disease is not standard- ized internationally. In addition, during the last 10 – 15 years, disorders of mineral metabolism have also been associated with cardiovascular and all-cause morbidity and mortality, broadening the manifestations of renal osteodystrophy beyond the skeleton. In response to these concerns and in recognition of new research into INVITED REVIEWS