Renal failure inevitably leads to metabolic bone disease. Low turnover disease or adynamic bone disease (ABD) is characterized by a low number of osteoblasts with normal or reduced numbers of osteoclasts. Mineralization proceeds at a normal rate, resulting in normal or decreased osteoid thickness. Recently, it became clear that the relative contribution of the various types of renal osteodystrophy (ROD) to the spectrum of the histologic picture in renal failure patients underwent profound changes during the last 25 years. At the moment, the exact physiopathological mechanisms behind ABD are not yet elucidated, and thus the reason(s) for its increasing prevalence remains poorly understood. A number of epidemiological and experimental data suggest a multifactorial pathophysiologic process, in which hypoparathyroidism and suppression of the osteoblast are the main actors. Compared to adynamic bone disease, osteomalacia has now become a much rarer disease (around 4%), at least in Western countries. On the other hand, recent studies indicate that this particular bone disease entity might still regularly occur in less developed countries. Osteomalacia originates from a direct effect on the mineralization process. With this type of renal bone disease, the effects of secondary hyperparathyroidism on bone are overridden by a number of metabolic abnormalities that finally result in a defective bone mineralization, as occurs, for instance, when the lag time between osteoid deposition and its mineralization is increased. The relationship between exogenous and endogenous vitamin D deficiency (mainly calcitriol) and the histologic finding of osteomalacia in uremic patients is well known. Recent data showed distinctly lowered 25-(OH) vitamin D3 levels in the presence of unaffected calcitriol concentrations in patients with osteomalacic lesions, as assessed radiologically by the presence of Looser's zones. Recently, we found that bone strontium levels were increased in patients with osteomalacia as compared to all other types of ROD. Strontium accumulation appeared to originate mainly from the use of strontium-contaminated dialysate, which resulted from the addition of strontium-containing acetate-based concentrates. Evidence for a causal role of the element in the development of a mineralization defect could be tested experimentally by adding strontium to drinking water in a chronic renal failure rat model.