THE APLASTIC FORM OF RENAL OSTEODYSTROPHY

Citation
Dj. Sherrard et al., THE APLASTIC FORM OF RENAL OSTEODYSTROPHY, Nephrology, dialysis, transplantation, 11, 1996, pp. 29-31
Citations number
12
Categorie Soggetti
Urology & Nephrology",Transplantation
ISSN journal
09310509
Volume
11
Year of publication
1996
Supplement
3
Pages
29 - 31
Database
ISI
SICI code
0931-0509(1996)11:<29:TAFORO>2.0.ZU;2-U
Abstract
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.