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.