PubMed · 4903130
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A Montandon. 1969. [Renal osteodystrophy].. https://pubmed.ncbi.nlm.nih.gov/4903130/
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Seizure induced bone fractures in patients with renal osteodystrophy are uncommon. A case is described where multiple bone fractures occurred following convulsions which appeared shortly after haemodialysis.
Recent advances in renal osteodystrophy deal with the pathogenesis of the disease, in particular in early renal failure, with the mechanisms of skeletal resistance to parathyroid hormone, with the potential role of iron, and with increased knowledge of adynamic bone disease. For the control of phosphatemia, aluminum-containing phosphate binders are more and more avoided, whereas calcium acetate or carbonate are more and more prescribed. X-linked hyphophosphatemia continue to cause great interest as well as the various iatrogenic osteomalacias.
Bisphosphonates appear to provide an attractive, novel approach in the management of patients with uremic bone disease. Only limited studies are available. Based on the understanding of the pathogenesis of renal bone disease, three major indications for the use of bisphosphonates in patients with uremic bone disease emerge: 1. Hypercalcemia related to increased release of calcium from bone. 2. Excessive elevation of bone turnover related to increased parathyroid hormone effects. 3. Extraosseous calcifications due to high calcium phosphorus product. Moreover, further studies may reveal how the combination between bisphosphonates and 1,25 vitamin D therapy might affect uremic bone. Details on doses, mode of administration (continuously vs. intermittently) and optimal duration of therapy should be tested in an animal model of uremic bone disease.