Secondary hyperparathyroidism, and not beta 2-microglobulin amyloid, as a cause of spontaneous tendon rupture in patients on chronic hemodialysis
- PMID: 7985675
- DOI: 10.1016/s0272-6386(12)81067-5
Secondary hyperparathyroidism, and not beta 2-microglobulin amyloid, as a cause of spontaneous tendon rupture in patients on chronic hemodialysis
Abstract
Spontaneous bilateral rupture of the extensor mechanisms of the knees, without significant history of trauma, has been reported rarely, generally in association with chronic metabolic disorders, such as chronic renal failure and secondary hyperparathyroidism. We report spontaneous tendon rupture in two patients on chronic hemodialysis for 4 and 11 years, with documented severe secondary hyperparathyroidism. One patient had spontaneous bilateral rupture of his quadriceps and partial avulsion of the left triceps tendons. The other patient had spontaneous rupture of his right quadriceps tendon. Both patients had markedly elevated serum intact parathyroid hormone and moderately elevated serum beta 2-microglobulin levels. Pathologic examination revealed diffuse immunohistochemical staining for beta 2-microglobulin but negative Congo-red staining of the ruptured tendon specimens. These cases and the previous reports in the literature suggest that secondary hyperparathyroidism may play a role in the pathogenesis of this clinical entity.
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