Bone metabolism in chronic renal failure.

Quantitative bone histology was carried out on 37 haemodialysis patients. Hyperparathyroid bone disease (HPT) was diagnosed by an elevated osteoclast count, and high counts were associated with classic osteitis fibrosa. Osteomalacia (OM) was found in two distinct though frequently overlapping forms, both with increased osteoid surface. In classic OM (type 1), present in 19% of patients the osteoid seams were wide and the mineral apposition rate low, with the tetracycline bands wide and merging together. In the more common form of OM (type 2), present in 81%, the mineralising surface, as shown by tetracycline uptake, was reduced, but the mineral apposition rate was normal. Tetracycline surface was highly correlated with osteoblast surface, suggesting that osteoblasts play a role in mineralisation, and that type 2 OM is caused by a reduction in osteoblast surface. The osteoblast surface also correlated with serum parathyroid hormone, and so secondary hyperparathyroidism may obscure the diagnosis of type 2 OM, which may be almost universally present in haemodialysis patients. Type 1 OM is not obscured by secondary hyperparathyroidism. Of the 37 patients 5 had HPT, 9 OM and 22 HPT + OM. Only one had normal bone. Biochemical parameters had limited predictive value. The study also did not support the suggestion that endogenous calcitonin protects against HPT disease.