Six out of 169 patients on maintenance haemodialysis showed spontaneous tendon rupture. In all six, bone erosion had previously been observed at the site of tendon insertion. In a further 13 patients whose tendons had never ruptured, marked bone erosions at the sites of tendon insertions were also observed. Both groups of patients, with tendon rupture and with bone erosion only, showed significantly greater blood alkaline phosphatase and parathyroid hormone levels than all the others. Moreover, osseous radiological findings of hyperparathyroidism were more marked in all these 19 patients than in the others. Bone erosion at the site of tendon insertion may be a true and specific sign of tendon disease in patients with uraemia. Our series shows that it bears a close relationship to hyperparathyroidism, and suggests that tendon disease is a specific sign of severe secondary hyperparathyroidism in patients with uraemia.
A rare complication, articular bone erosions adjacent to peri-articular calcifications, was observed in patients undergoing chronic haemodialysis. Three cases are described and the discussion describes the pathogenesis of the lesion, which, as far as is known by the authors, has not yet been reported in the literature.
To the author's knowledge, uraemic neuropathy has not been previously reported as a cause of Charcot's joint. In this paper they present three cases in which the association between clinical and radiographic patterns suggest the diagnosis of neuropathic arthropathy. The features of uraemic neuropathy are stressed and the role of secondary hyperparathyroidism in the development of this type of arthropathy is discussed. The extremely severe hyperparathyroidism reported here, may cause tendon and ligament disease, especially at the site of their bone insertion. Uraemic tendon and ligament failures weaken joints and produce further instability, which may be a precipitating factor of uraemic Charcot's joint in patients undergoing chronic haemodialysis.
Parathyroid hormone (PTH) affects the nervous system directly and indirectly. The induced pathology may present typical imaging findings in neuroradiology. The hormone controls the physiological level of blood calcium. Increased serum PTH causes pathological features in the kidneys and especially in the skeleton where most calcium is situated. Primary hyperparathyroidism is due to hyperplasia or to adenomatous or carcinomatous degeneration of glandular tissue. It causes relapsing nephrolithiasis and, more seldon, nephrocalcinosis. Bone shows increased osteoclastic activity with various aspects of diffuse demineralization. In severe cases pathological fractures and sub-periosteal, sub-chondral reabsorptions appear, especially at the tendon and capsuloligamentous insertions. In even more severe disease fibrous osseous cysts and brown tumours may be found in bone. In the central nervous system, clinical symptoms, such as mental confusion, lethargy and exceptionally coma may appear. Radiologically, bone resorption can be observed in the skull as microlacunar confluent osteolysis (salt and pepper skull). Body fractures may develop in the spine. Secondary hyperparathyroidism is due principally to renal failure. Both hypocalcaemia and hyperphosphoraemia cause the hormone secretion increase. In this case, other pathologic features are associated with the typical manifestations of primary hyperparathyroidism. The uraemic kidney is inable to synthetize active vitamin D, leading to rickets in the young and osteomalacia in adults. Hyperphosphoraemia causes ectopic periarticular calcifications. Furthermore, the lack of degradation of an endogenous protein (beta 2 microglobulin) by the kidney and its poor elimination by dialytic treatment, cause chronic retention and consequent systemic amyloidosis which induces intraosseous cystic lesions and severe destructive arthropathy. All these aspects, together, are known as renal osteodystrophy. The radiological features of secondary hyperparathyroidism are the same as those observed in the primary form. In addition, all the lesions of renal osteodystrophy may be associated, further worsening the disease. In the secondary form, mild hypocalcaemia, if present, rarely leads to the neurological manifestations of the primary disease. Frequently carpal tunnel syndrome arises due to local amyloid infarction. Chronic aluminium retention may produce neurological aspects of dementia. Finally, the decrease of PTH hormone blood levels, as in hypoparathyroidism and the consequent hypocalcaemia may determine neurologic symptoms such as paresthaesias, and in severe disease, tetanic contractions. Radiologically, typical micronodular calcifications can be observed in the brain basal ganglia.
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