MINERALIZED BONE LOSS AT DIFFERENT SITES IN DIALYSIS PATIENTS - IMPLICATIONS FOR PREVENTION

To characterize the magnitude and location of mineralized bone loss, 4 0 patients (20 men, 20 women, 29 white, 11 black) with clinically sign ificant renal osteodystrophy who could be unambiguously classified bas ed on histologic criteria as having osteitis fibrosa (OF; 20 cases) or osteomalacia (OM; 20 cases) were studied; they had been on maintenanc e hemodialysis for 4.6 +/- 3.0 yr. One hundred forty-two healthy women of similar age and ethnic composition served as control subjects. In ah subjects, the proportions of mineralized bone, osteoid, and porosit y (nonbone soft tissue) were measured separately in cortical and cance llous bone tissue, from intact full-thickness biopsies of the ilium, r epresentative of the axial skeleton. The results were related to the v olumes of cortical and cancellous bone tissue separately and to the vo lume of the entire biopsy core. Approximately three-quarters of the pa tients had measurements in the appendicular skeleton by single photon; absorptiometry of the radius and morphometry of the metacarpal. Disea se effects did not differ significantly between ethnic groups. Mineral ized cortical bone volume (per unit of core volume) was reduced by app roximately 45% in both patient groups. Mineralized cancellous bone vol ume was significantly increased by 36% in the patients with OF and non significantly reduced by 9% in the patients with OM; however, the redu ction in the latter patients was significant in relation to tissue vol ume. The combined total deficit for both types of iliac bone was appro ximately 20% in the patients with OF and approximately 40% in the pati ents with OM. Significant reductions in appendicular cortical bone wer e demonstrated in both patient groups at both measurement sites. Regar dless of the current histologic classification, the major structural a bnormality in the skeleton is generalized thinning of cortical bone du e to increased net endocortical resorption, the most characteristic ef fect on bone of hyperparathyroidism. Protection of the skeleton from t he adverse consequences of renal failure will require therapeutic inte rvention in patients with no symptoms of either renal or bone disease.