Strontium overload and toxicity: impact on renal osteodystrophy.

Although the prevalence of aluminium-related bone diseases has declined, osteomalacia still persists at a low prevalence. The redistribution of bone disease prevalence corresponds to evolving regimens in the treatment of renal disease. Studies have demonstrated an association between the accumulation of strontium in bone and the presence of osteomalacia. The uptake of strontium has been shown to be dose-dependent, with distribution mainly in newly formed compact and cancellous bone. Animal studies demonstrated that high doses of strontium induced alterations of mineralization and, in a rat model of chronic renal failure, high strontium doses induced mineralization defects, with a corresponding 160-fold accumulation of strontium in bone. Studies indicated that the accumulation of metals in bone might be synergistic. Aluminium bone content was shown to be higher when both aluminium and strontium were administered compared with when only strontium was given. Studies in dialysis patients demonstrated that strontium levels and strontium/calcium ratios were elevated in the bone of osteomalacia patients compared with other types of renal osteodystrophy. In certain dialysis centres of developing countries, high strontium levels present in dialysis fluids correlated with strontium serum content. At these centres, the use of acetate-based concentrates may have been the source of strontium-contaminated dialysis fluids. In a recent study of bone biopsies taken from patients of French dialysis centres, strontium content was increased in bone of osteomalacic patients compared with other bone diseases and with controls. Several other trace elements have been found to accumulate in the bone of uraemic patients, with significant concern regarding associated pathology. Environmental and medical exposure to such trace metals should be evaluated to establish toxic thresholds and to eliminate the possibility of associated renal osteopathies.