Adynamic bone disease-bone and beyond.

Abstract

Disturbances of bone and mineral metabolism are a hallmark of chronic kidney disease (CKD). Renal osteodystrophy (ROD) is the traditional term for bone lesions in conjunction with CKD and is now considered a part of the ‘chronic kidney disease—mineral and bone disorder’ (CKD-MBD) [1]. ROD comprises various subtypes with substantial differences in aetiology and fundamental differences in treatment strategies. In long-term dialysis patients the prevalence of some types of ROD is virtually 100% [2]. A simple, easy to apply but still sophisticated and comprehensive descriptive system of ROD is the TMV system [1]. The TMV system comprises bone turnover (T), bone mineralization (M) as well as bone volume (V). Bone turnover and bone volume may both be classified as high, normal or low. Bone mineralization may be categorized as normal or abnormal. As an alternative to volume, the bone balance may be considered [3,4]. Based on the above system, the NKF/KDOQI guidelines distinguish six types of bone pathology in CKD-MBD (Table 1) (Figures 1 and 2). The focus on cancellous bone parameters in this classification system has been questioned regarding the importance of cortical bone quality for structural integrity [5]. Moreover, bone histomorphometric parameters comprise a continuum, and categorization may be an oversimplified approach [5]. Nevertheless, categorical CKD-MBD classification is helpful for clinical practice and widely used as the basis for therapeutic decision making. In this review we will focus particularly on adynamic bone disease (ABD), which is increasing in prevalence and, in