Abstract
Associations between renal insufficiency and bone disease have been known for at least a century. It has been well established for a long time that disturbances of the metabolism of calcium, phosphorus, vitamin D, and parathyroid hormone occur in renal failure and contribute to the development of renal osteodystrophy which is mainly characterized by secondary hyperparathyroidism, defective mineralization, and mixed features of both of these disorders. Pathophysiology and clinical course of renal osteodystrophy have been studied extensively and fundamental principles of prevention and treatment have been achieved worldwide. However, the pathophysiological and clinical spectrum of bone disease in patients with chronic renal failure and on regular dialysis treatment have changed within the last decade: in patients on long-term hemodialysis clinically severe, fracturing osteomalacia which is refractory to therapy with various analogues of vitamin D may develop. Dialysis osteomalacia has been associated with aluminium loading of the organism and during the last years abundant evidence has been presented that aluminium accumulation in bone plays the primary role in the occurrence of vitamin D resistant osteomalacia. Aluminium has been shown to be localized at the mineralization front in bone, suggesting it may be a cause of this disorder.
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Henning, H.V. (1987). Dialysis-Osteomalacia and Renal Osteodystrophy: Pathogenesis, Diagnostic and Clinical Problems. In: Kuhlencordt, F., Dietsch, P., Keck, E., Kruse, HP. (eds) Generalized Bone Diseases. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-73346-8_12
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