That bone disease accompanies renal failure has been known for over 10
0 years. This bone disease (renal osteodystrophy) has been variously a
ttributed to hyperparathyroidism, vitamin D deficiency, aluminium toxi
city, iron toxicity, uraemia, and a host of other aetiologies. In addi
tion, the form the bone disease takes has been variously described as
osteitis fibrosa, osteomalacia, mixed uraemic osteodystrophy and the a
plastic (adynamic) lesion. In this manuscript we will focus on the aet
iology, consequences, diagnosis and possible management of the aplasti
c form of the disease. The renal osteodystrophy study was a prospectiv
e, cross-sectional study of renal bone disease in a largely unselected
population of patients receiving dialysis in three hospitals in Toron
to. A variety of non-invasive data (parathyroid hormone (PTH), alumini
um, etc.) and bone histology were obtained and analysed to assess path
ogenesis, diagnostic criteria and management. We have defined the apla
stic lesion as having low bone formation without a marked increase in
unmineralized osteoid (i.e. excluding osteomalacia). We have noted tha
t it may be associated with increased aluminium or little to no alumin
ium. With increased aluminium the patients have a poorer prognosis bot
h with regards to bone disease and mortality, and they should be manag
ed appropriately to alleviate aluminium toxicity. With lesser amounts
of aluminium, morbidity and mortality are less severely impacted, but
not normal. We have shown that the low bone formation, of the aplastic
lesion without aluminium may be 'normalized' by increasing PTH levels
. It is concluded that aplastic bone disease carries adverse consequen
ces both in terms of bone problems and survival. In the absence of alu
minium toxicity the stimulation of PTH effectively corrects the bone f
ormation abnormality. Whether this will alleviate the adverse conseque
nces will be difficult to study. Avoiding the problem by not over-supp
ressing PTH seems a reasonable approach at this point.