Cases reported "Renal Osteodystrophy"

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1/71. Musculoskeletal manifestations of osteomalacia: report of 26 cases and literature review.

    OBJECTIVE: This study was undertaken to describe the musculoskeletal manifestations in a selected population of 26 patients with biopsy-proven osteomalacia (OM) and provide a literature update. methods: The 26 patients with biopsy-proven OM were selected from a total number of 79 patients who underwent anterior iliac crest biopsy. The diagnosis of OM was confirmed by the presence of an osteoid volume greater than 10%, osteoid width greater than 15 microm, and delayed mineralization assessed by double-tetracycline labeling. RESULTS: OM was caused by intestinal malabsorption in 13 patients, whereas six other patients presented with hypophosphatemia of different causes. Five elderly patients presented with hypovitaminosis D, and in two patients the OM was part of renal osteodystrophy. Twenty-three patients presented with bone pain and diffuse demineralization, whereas three other patients had normal or increased bone density. Characteristic pseudofractures were seen in only seven patients. Six of the 23 patients with diffuse demineralization had an "osteoporotic-like pattern" without pseudofractures. Prominent articular manifestations were seen in seven patients, including a rheumatoid arthritis-like picture in three, osteogenic synovitis in three, and ankylosing spondylitis-like in one. Two other patients were referred to us with the diagnosis of possible metastatic bone disease attributable to polyostotic areas of increased radio nuclide uptake caused by pseudofractures. Six patients also had proximal myopathy, two elderly patients were diagnosed as having polymalgia rheumatica, and two young patients were diagnosed as having fibromyalgia. One of the patients who presented with increased bone density was misdiagnosed as possible fluorosis. CONCLUSION: OM is usually neglected when compared with other metabolic bone diseases and may present with a variety of clinical and radiographic manifestations mimicking other musculoskeletal disorders.
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2/71. Calcific uremic arteriolopathy in association with low turnover uremic bone disease.

    We report seven cases (out of 100 dialysis patients) at the University of kentucky who were diagnosed with calciphylaxis syndrome between 1993 and 1998. Of note is the fact that five of these patients had bone biopsy-proven adynamic renal bone disease, rather low intact PTH, and relatively low calcium-phosphorus product. This is in contrast to the previous view that calciphylaxis is usually seen in patients with excessive parathyroid activity. The reemergence of calciphylaxis with renal bone disease is an intriguing finding and does not correspond to earlier reports associating calciphylaxis with hyperparathyroid bone disease. This report reviews the clinical, biochemical, and bone histology findings of these patients, and provides a review of the literature.
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3/71. Pentavalent technetium-99m DMSA uptake in pseudofractures of osteomalacia.

    Tc-99m MDP and Tc-99m (V) DMSA images are described from a 49-year-old woman with chronic renal insufficiency complicated by osteomalacia. Clinical, biochemical, and radiologic bone profiles were compatible with osteomalacia. osteomalacia is a condition associated with disorders in which mineralization of the organic matrix is defective. All bone lesions visualized with Tc-99m MDP also showed increased uptake of Tc-99m (V) DMSA. Tc-99m (V) DMSA accumulation has been reported in many malignant and some benign conditions. Pseudofractures in osteomalacia could be included in the spectrum of benign lesions that accumulate Tc-99m (V) DMSA.
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4/71. Macrognathia of renal osteodystrophy in a dialysis patient. Report of a case.

    A case of macrognathia secondary to renal osteodystrophy in a dialysis patient is presented. The case reviewed demonstrates a variety of radiographic and histopathologic features, some of which resemble fibrous dysplasia and others suggestive of Paget's disease of bone. This article contains diagnostic criteria for differentiating renal osteodystrophy from similar fibro-osseous diseases. There is a discussion of the underlying cause and appropriate therapeutic interventions of renal osteodystrophy.
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5/71. immobilization hypercalcaemia in patients on regular haemodialysis.

    immobilization of normal people causes reabsorption of calcium from bone, a small rise in serum ionized calcium, and, rarely, frank hypercalcaemia. The hazard is increased when patients with renal osteodystrophy are immobilized because of pathological fractures.
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6/71. Neglected bilateral femoral neck fractures in a patient with end-stage renal disease before chronic dialysis.

    Bilateral femoral neck fractures are rarely reported in patients with end-stage renal disease before chronic dialysis. We report on a 39-year-old woman with neglected bilateral femoral neck fractures, who presented with severe uremic complications prior to chronic dialysis. Three years before admission, she had injured herself in a trivial slip with subsequent bilateral hip pain. She had progressively waddled since then. Pelvic X-ray taken after admission revealed bilateral femoral neck fractures. Bilateral hip hemiarthroplasties were subsequently performed. Displaced femoral neck fractures were found intraoperatively. Pathologic findings and results of examinations supported the coexistence of osteoporosis and high turnover renal osteodystrophy, rendering this woman at high risk of bilateral femoral neck fractures. Therefore, preventing a simple fall or trivial accident and treating renal osteodystrophy and osteoporosis are paramount in patients with chronic renal failure even before the start of dialysis therapy. We also emphasize the need to seek any possible underlying metabolic bone disease once a patient presents with unusual fractures.
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7/71. The pathophysiology and management of renal bone disease in dialysis patients.

    As renal function declines, changes in mineral metabolism occur including phosphate retention, calcitriol deficiency, and the development of secondary hyperparathyroidism. Renal bone disease related to disordered mineral metabolism may result in increased patient morbidity and mortality. Uncontrolled parathyroid hormone (PTH) secretion will result in osteitis fibrosa, a high turnover bone disease. The use of calcium and aluminum-based phosphate binders and vitamin d sterols may contribute to the development of low turnover bone diseases such as osteomalacia and aplastic bone disease. Prevention and control of renal bone disease is an important goal for the interdisciplinary health care team. This paper discusses disordered mineral metabolism and its relationship to renal bone disease. Case studies illustrate the development and treatment of renal bone disease related to secondary hyperparathyroidism and aluminum intoxication.
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8/71. Sacro-iliac joint in renal osteodystrophy: roentgenographic-Pathologic correlation.

    A detailed roentgenographic and pathologic study of the sacro-iliac joint in a cadaver with renal osteodystrophy revealed subchondral abnormalities, particularly in the ilium, which consisted of resorption of bone, substitutive fibrosis, and thickening of remaining trabeculae. Overlying articular cartilage degeneration was also apparent. The "pseudo-widening" of the joint space noted in ante and post-mortem radiographs in this patient simulated the findings in early ankylosing spondylitis.
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9/71. Discrepancy in results between spine and hip scans of a woman with end stage renal disease.

    Conditions and artifacts such as aortic calcifications, osteophytes, hip prostheses, and metallic objects can affect the results of dual X-ray absorptiometry scans of the spine and hip. Abdominal surgery often entails the use of metal sutures causing subtle artifacts near or over the lumbar spine resulting in inaccurate bone mineral density (BMD) measurements. We herein report a case of a woman whose spine BMD appeared normal while her hip BMD was > -3.5 SDs. Although the abdominal artifacts create some uncertainty in the diagnosis, renal osteodystrophy is suspect owing to the patient's renal history. This case demonstrates the importance of acquiring scans at two or more sites, closely evaluating scans for artifacts, and obtaining the patient's medical history.
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10/71. Osteoclast dysfunction in the osteosclerotic variant of renal osteodystrophy.

    Six iliac crest bone biopsies were obtained from five patients with renal osteodystrophy and osteosclerotic lesions to investigate the mechanism of osteosclerosis in renal osteodystrophy. Each specimen was prepared in an undecalcified fashion and measured under light microscopy for routine analysis and histomorphometry. Osteoclast resorptive lacunae were estimated by measuring the lacunar length and depth. Histomorphometric studies revealed an increase in all parameters with a mean trabecular bone volume of 66% (normal: 19%-26%), mean trabecular osteoid surface of 71% (normal: 16%-22%), and a mean trabecular osteoid volume of 15% (normal: 1%-2%). In one patient, there was a ten-fold increase over the norm of osteoclasts/mm2 (0.3; normal: 0.02-0.04), whereas the mean width of trabecular bone was twice the norm. In all biopsies, the calculated lacunar area was markedly diminished compared to published controls. These results support the hypothesis that osteoclast function is impaired in patients with renal osteodystrophy.
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