Cases reported "Renal Osteodystrophy"

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1/9. renal osteodystrophy presenting with multiple calcified periarticular swellings.

    renal osteodystrophy denotes skeletal abnormality in patients with renal disease. Although radiological and histological evidences of osseous abnormality are commonly seen in advanced renal failure, clinical symptoms of bone disease are uncommon. In this article a case of chronic renal failure presented with multiple calcified periarticular swellings measuring up to 5 cm in diameter is described. The patient also had severe osteopenia, subperiosteal erosions, bilateral shrunken echogenic kidneys as well as clinical and biochemical evidences of chronic renal failure. renal osteodystrophy is discussed and related literature is reviewed.
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2/9. Avulsion of the long head of the triceps in kidney transplant.

    The authors describe a case of avulsion of the long head of the triceps in a patient with kidney transplant. An analysis of the case and a review of the literature suggest weakening of the osteotendinous junction due to the associated action of renal osteodystrophy and cortisone therapy.
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3/9. Management of pediatric patients with chronic kidney disease.

    Chronic kidney disease in children is associated with complications that require nursing interventions in both the inpatient and outpatient settings. Given the progressive nature of the disease and the complexity of the treatment regimen, it is important that nurses be comfortable implementing acute and preventive care strategies and facilitating the coordination of care. In addition, the need for multiple therapies can be distressing for patients and theirfamilies, further supporting the role of the nurse in patient and family education and decision making regarding the plan of care. In this review, we discuss the pertinent issues of pediatric chronic kidney disease in the context of a case study to promote better understanding of real-world nursing practice.
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ranking = 1029.7871241551
keywords = kidney disease, kidney
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4/9. Primary bone oxalosis: the roles of oxalate deposits and renal osteodystrophy.

    Primary oxalosis is a rare congenital disorder. The excessive oxalate biosynthesis induces deposits in many organs, particularly in kidney and bone. The late onset of primary oxalosis is reported in a 50-year-old man. His chronic renal failure was treated by maintenance hemodialysis for 3 years. He then developed a diffuse bone disease with osteosclerosis and roentgenographic features of hyperparathyroidism. A parathyroidectomy was performed, with debatable improvement of bone lesions. Laboratory results and histologic and histomorphometric studies before and after parathyroidectomy suggest a double histopathogenetic mechanism for this bone disease: renal osteodystrophy and massive bone oxalate deposits. Such deposits may induce both a heterogeneous osteosclerosis with dense metaphyseal bands and histologic bone lesions similar to those of hyperparathyroidism. The crystalline deposits induce in the bone tissue a granulomatous macrophagic reaction. These macrophages are unable to phagocytize the crystals and may be involved in active bone resorption. Bone lesions of oxalosis occur in patients with chronic renal failure, and hyperparathyroidism has a worsening role.
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5/9. Total parathyroidectomy and autotransplantation for tertiary hyperparathyroidism in children with chronic renal failure.

    An association between chronic renal failure and skeletal deformities in the adolescent patient was first documented by Lucas in 1883. Since then it has been established that the kidneys play a major role in the regulation of calcium, phosphate, and parathyroid hormone, and that chronic renal failure is characterized by profound alterations in the normal metabolic homeostasis of the human body. With the hyperphosphatemia of uremia, compensatory hyperparathyroidism is also a well known complication. Due to these factors, loss of normal renal function ultimately leads to derangement in mineral and bone metabolism resulting in severe skeletal deformities. Reports in the English literature suggest that the changes of renal osteodystrophy are much more pronounced in the pediatric patient, as compared to those in the adult. In the last two decades, renal transplantation has come to be recognized as a satisfactory modality for controlling renal failure and its complications. This procedure is often not available as an option, however, in small patients, especially those under three years of age. The pediatric nephrologist is often forced to manage these patients for long periods with conservative therapy, in an attempt to control the ravages of renal osteodystrophy. The problem becomes unmanageable when the compensatory hyperparathyroidism proceeds to autonomy. When this occurs, despite maintenance of normal serum calcium levels, the renal osteodystrophy progresses rapidly, producing pain, deformities and growth retardation. At this point, the condition is often refractory to medical management and resection of parathyroid tissue remains the only satisfactory modality for control.(ABSTRACT TRUNCATED AT 250 WORDS)
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6/9. Southwestern internal medicine Conference: bone disease in kidney failure: diagnosis and management.

    Recent technologic and therapeutic advances have improved the life of the patient with end-stage renal disease. High efficiency and high-flux hemodialyzer membranes have shortened the time required to dialyze, and recombinant erythropoietin has all but eliminated anemia as a major cause of morbidity, but the problem of renal osteodystrophy remains. The following discussion examines the spectrum of bone and joint disease in the patient with end-stage renal disease. The diagnostic and therapeutic strategies currently being tried in the management of these disorders are discussed.
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7/9. Increased bone marrow uptake on Tc-99m DMSA scintigraphy in a patient with renal osteodystrophy.

    A 16-year-old male patient was evaluated with Tc-99m Diethylenetriamine-pentaacetic acid (DTPA) and Tc-99m 2-3 Dimercaptosuccinic acid (DMSA) scintigraphy for renal failure secondary to renal calculi. The uptake in the renal cortex was significantly decreased both on DMSA and DTPA studies. Uptake calculation on DMSA scintigraphy in the kidneys disclosed values of less than 5%. The activity in the liver and bone was significantly increased. A bone scan performed with Tc-99m methylene diphosphonate (MDP) revealed increased bone uptake with decreased soft tissue activity. Findings on bone scan were compatible with super scan, most likely due to renal osteodystrophy. This case illustrates the altered biodistribution of Tc-99m DMSA and a shift of the radiopharmaceutical to the bone marrow which is not likely related to colloid formation due to changes in mineral balance in patients with renal failure.
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8/9. Predialysis calcitriol administration: effects on pre- and post-transplant renal osteodystrophy.

    twins with parallel loss of kidney function and moderate hyperparathyroid bone disease were participants in a double-blind study where twin A was given placebo and twin B calcitriol. After 8 months. A's bone disease had not improved, while B's bone had normalized. Thereafter, both received calcitriol until kidney transplantation 11 months later, when both had normal bone structure. Two years after transplantation, both twins had hyperparathyroid bone disease, but A had more pronounced changes. This report illustrates our findings in larger series: When started early in the course of renal failure, calcitriol can reverse pre-transplant hyperparathyroid bone disease and also influence post-transplant bone disease.
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9/9. Nonacidotic proximal tubulopathy transmitted as autosomal dominant trait.

    The family of a patient with a nonacidotic and hypercalciuric proximal tubulopathy was studied. The proband showed glycosuria, aminoaciduria, tubular proteinuria, renal hypophosphatemia, and urate tubular hyporeabsorption without bicarbonate loss. He also presented increased urine calcium excretion, plasma 1,25-dihydroxyvitamin D, and enteral calcium absorption. Clinical consequences of the tubulopathy were osteopenia and calcium kidney stones. Fifteen of the proband's relatives were studied; six of them had renal hypophosphatemia, 10 presented hypercalciuria, and three showed both hypercalciuria and hypophosphatemia. No other reabsorption defects were observed. High plasma levels of 1,25-dihydroxyvitamin D were found in 13 family members; their values correlated positively with calcium excretion and negatively with tubular phosphate reabsorption. None produced stones or had reduced mineral bone density. hypophosphatemia and hypercalciuria occurred in the two generations studied; their transmission was independent of gender, and male-to-male transmission occurred for both defects. Our findings suggest that a genetic alteration of proximal tubular function could cause multiple reabsorption defects in the proband or renal phosphate leakage in the proband's relatives. The genotypic alteration causing the proximal dysfunctions may be monogenic, with an autosomal dominant pattern of inheritance and variable expressivity. Increased calcium excretion may be due to the proximal tubular alteration; alternatively, it may be the result of a genetic background predisposing to idiopathic hypercalciuria. Phosphate and calcium loss could stimulate 1,25-dihydroxyvitamin D synthesis in proximal tubular cells.
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