Low bone turnover in patients with renal failure

Renal failure inevitably leads to metabolic bone disease. Low turnover dise ase or adynamic bone disease (ABD) is characterized by a low number of oste oblasts with normal or reduced numbers of osteoclasts. Mineralization proce eds at a normal rate, resulting in normal or decreased osteoid thickness. R ecently, it became clear that the relative contribution of the various type s of renal osteodystrophy (ROD) to the spectrum of the histologic picture i n renal failure patients underwent profound changes during the last 25 year s. At the moment, the exact physiopathological mechanisms behind ABD are no t yet elucidated, and thus the reason(s) for its increasing prevalence rema ins poorly understood. A number of epidemiological and experimental data su ggest a multifactorial pathophysiologic process, in which hypoparathyroidis m and suppression of the osteoblast are the main actors. Compared to adynam ic bone disease, osteomalacia has now become a much rarer disease (around 4 %), at least in Western countries. On the other hand, recent studies indica te that this particular bone disease entity might still regularly occur in less developed countries. Osteomalacia originates from a direct effect on t he mineralization process. With this type of renal bone disease, the effect s of secondary hyperparathyroidism on bone are overridden by a number of me tabolic abnormalities that finally result in a defective bone mineralizatio n, as occurs, for instance, when the lag time between osteoid deposition an d its mineralization is increased. The relationship between exogenous and e ndogenous vitamin D deficiency (mainly calcitriol) and the histologic findi ng of osteomalacia in uremic patients is well known. Recent data showed dis tinctly lowered 25-(OH) vitamin D-3 levels in the presence of unaffected ca lcitriol concentrations in patients with osteomalacic lesions, as assessed radiologically by the presence of Looser's zones. Recently, we found that b one strontium levels were increased in patients with osteomalacia as compar ed to all other types of ROD. Strontium accumulation appeared to originate mainly from the use of strontium-contaminated dialysate, which resulted fro m the addition of strontium-containing acetate-based concentrates. Evidence for a causal role of the element in the development of a mineralization de fect could be tested experimentally by adding strontium to drinking water i n a chronic renal failure rat model.