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Renal bone disease or renal osteodystrophy is the term used to describe the spectrum of histologic abnormalities encountered in patients with chronic kidney disease (CKD). The patterns of bone histology encountered in the setting of CKD range from states of high bone turnover, such as osteitis fibrosa, the result of hyperparathyroidism, to states of abnormally low bone turnover, such as adynamic bone.1 The major factors involved in the pathogenesis of secondary hyperparathyroidism include phosphate retention as glomerular filtration rate decreases and low levels of calcitriol as renal mass is reduced. Both of these factors may lower serum calcium and therefore stimulate parathyroid hormone (PTH) secretion. In addition to these indirect effects, low levels of calcitriol and high serum phosphorus have been shown to have direct effects on the parathyroid gland to increase PTH secretion. The pathogenetic factors involved in the development of adynamic bone disease are less well understood, but it appears that oversuppression of PTH and the use of vitamin D compounds may play a role. Thus, in the management of renal osteodystrophy, it is important to be able to monitor and treat hyperparathyroidism effectively while at the same time avoiding oversuppression of PTH. In this regard, accurate measurements of circulating PTH levels are an essential guide in the management of renal bone disease. It is well accepted that PTH is present in the circulation in the form of both the intact 84-amino acid peptide and a variety of truncated fragments.2–4 Although the role of the intact PTH molecule as a major regulator of mineral ion homeostasis is well established, the actions of PTH fragments have remained poorly understood. In this review, we discuss the generation of PTH metabolites and the evidence supporting their biologic activity and their potential role in renal bone disease.