Osteomalacia and Aplastic Bone Disease in Aluminum-Related Osteodystrophy*
- 1 July 1987
- journal article
- research article
- Published by The Endocrine Society in Journal of Clinical Endocrinology & Metabolism
- Vol. 65 (1) , 11-16
- https://doi.org/10.1210/jcem-65-1-11
Abstract
The bone histology in patients with chronic renal failure and aluminum-related bone disease does not always show the excess accumulation of unmineralized osteoid (matrix) characteristic of osteomalacia. Frequently, bone aluminum accumulation is associated with normal or reduced amounts of unmineralized osteoid and low bone formation and is referred to as aplastic bone disease. In this study, we compared static and dynamic bone histomorphometric parameters and plasma PTH and aluminum levels in 12 patients with osteomalacia and 18 patients with aplastic bone disease who had been receiving dialysis for the same duration to determine if the difference in osteoid accumulation in these 2 lesions might be explained by differences in aluminum accumulation or PHT levels. The strainable bone surface aluminum level was significantly higher in the patients with osteomalacia compared to that in the group with aplastic bone [61 .+-. 5% (.+-. SEM) vs. 43 .+-. 4%; P < 0.02]. The rate of bone apposition and bone formation were lower in the group with osteomalacia (P < 0.01). Plasma amino-terminal PTH was not significantly different in the 2 groups. The increment in plasma aluminum levels after a single infusion of deferoxamine was higher in the osteomalacic group than in the aplastic group, suggesting that the patients with osteomalacia accumulated more total body chelatable aluminum than did those with aplastic bone disease during a comparable length of time on dialysis. We conclude that the excess unmineralized osteoid in aluminum-related osteomalacia results from the high rate of total body aluminum accumulation, which directly causes uncoupling of matrix mineralization and matrix production, independent of PTH levels. Patients with aplastic bone disease who have accumulated lesser amounts of total body aluminum fail to develop excess unmineralized osteoid because production and mineralization of matrix are more closely coupled than in the osteomalacic lesion, despite a decline in osteoblast numbers.This publication has 25 references indexed in Scilit:
- Use of the Deferoxamine Infusion Test in the Diagnosis of Aluminum-Related OsteodystrophyAnnals of Internal Medicine, 1984
- Decreased mineralization in hemodialysis patients after subtotal parathyroidectomyCalcified Tissue International, 1982
- Radioimmunoassay for the Middle Region of Human Parathyroid Hormone Using an Homologous Antiserum with a Carboxy-Terminal Fragment of Bovine Parathyroid Hormone as Radioligand*Journal of Clinical Endocrinology & Metabolism, 1982
- Bone Aluminum and Histomorphometric Features of Renal Osteodystrophy*Journal of Clinical Endocrinology & Metabolism, 1982
- Osteomalacia in Chronic Renal Failure: a Syndrome Previously Reported Only with Maintenance DialysisAmerican Journal of Nephrology, 1982
- Aluminum localization in bone from hemodialyzed patients: Relationship to matrix mineralizationKidney International, 1981
- Vitamin-D-Resistant Osteomalacia in Hemodialysis Patients Lacking Secondary HyperparathyroidismAnnals of Internal Medicine, 1981
- Do Parathyroid Hormone and 1,25-Dihydroxyvitamin D Modulate Bone Formation In UremiaÓ*Journal of Clinical Endocrinology & Metabolism, 1980
- Hemodialysis encephalopathy with osteomalacic fractures and muscle weaknessKidney International, 1980
- OSTEOMALACIC DIALYSIS OSTEODYSTROPHY: EVIDENCE FOR A WATER-BORNE ÆTIOLOGICAL AGENT, PROBABLY ALUMINIUMThe Lancet, 1978