Tertiary hyperparathyroidism after renal transplantation

Nieto, Juliana Serrano; Ruiz-Cuevas, P.; Escuder, A.; Regas, J.; Callı́s, L

doi:10.1007/s004670050233

Cited by 26 publications

(17 citation statements)

References 14 publications

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“…In addition, the absence of nephrolithiasis, the presence of a high level of serum phosphate (9.9 mg/dl) as compared with mild hypercalcemia, accelerated ectopic calcification which is common in secondary hyperparathyroidism, severe normocytic anemia with a low level of erythropoietin, and severe hyperplastic changes in all four parathyroid glands favor concluding that the patient initially had chronic renal failure which then induced severe secondary hyperparathyroidism. The presence of hypercalcemia supports the view that the patient might have developed tertiary hyperparathyroidism [10][11][12]. As mentioned above, the hyperparathyroidism observed in the present case most likely was secondary to chronic renal failure.…”

Section: Discussionsupporting

confidence: 85%

Severe Hyperparathyroidism with Hypercalcemia Associated with Chronic Renal Failure at Pre-Dialysis State.

et al. 1999

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Abstract. We report a case of a 23-year-old Japanese woman who had severe hyperparathyroidism associated with chronic renal failure before the start of dialysis treatment. Her chief complaints were swelling and pain in both shoulders. Laboratory examination revealed renal failure (BUN 134 mg/dl, serum Cr 7.3 mg/dl), severe normocytic normochromic anemia (hemoglobin 4.3 g/dl), hypercalcemia (11.8 mg/dl), and hyperphosphatemia (9.7 mg/dl). Serum PTH levels were extremely increased (intact PTH >1,000 pg/ml: normal range 10-50 pg/ml). X-ray examination of the skull and shoulders showed a salt and pepper appearance, and cauliflower-like deformity of the distal end of both clavicles, respectively. Accelerated ectopic calcification was observed in the costal cartilages, internal carotid arteries, and splenic arteries.Ultrasonographic examination revealed enlargement of the four parathyroid glands. Thallium-technetium subtraction scintigraphy of the parathyroid glands showed increased uptake into the upper two. Renal needle biopsy revealed severe impairment of the interstitium and tubules with much milder changes in glomeruli. The etiology of the renal failure could not be identified. Hemodialysis, total parathyroidectomy and auto-transplantation into the forearm were immediately performed. The pathological diagnosis was chief cell hyperplasia of the parathyroid glands. Based on the presence of chronic renal failure, remarkable hyperphosphatemia with mild hypercalcemia, an unusually high level of serum PTH, and accelerated ectopic calcification, the patient was diagnosed to have severe secondary hyperparathyroidism caused by chronic renal failure with major impairment of the renal interstitium and tubules.

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Section: Discussionsupporting

confidence: 85%

Severe Hyperparathyroidism with Hypercalcemia Associated with Chronic Renal Failure at Pre-Dialysis State.

et al. 1999

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“…In a recent report, Nieto et al [25] described three children in whom 3HPT was noted 1 month to 3 years after RT; in all children hemodialysis was of long duration (7-11 years) and two had undergone more than one transplant (one had 2 RT and the other had 3 RT). These three patients underwent subtotal parathyroidectomy and pathological examination revealed adenoma transformations in the affected glands.…”

Section: Studies In Childrenmentioning

confidence: 96%

Evolution of secondary hyperparathyroidism after renal transplantation

Nogueira

David

Cochat

2000

Pediatric Nephrology

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Renal osteodystrophy is an important problem in children with chronic renal failure, leading to skeletal deformities. The most-frequent type of renal osteodystrophy is secondary hyperparathyroidism, and the main factors contributing to the pathogenesis of this condition are completely or partially corrected after successful renal transplantation. The present paper reviews data on the evolution of secondary hyperparathyroidism after transplantation. Studies in both adults and children suggest that secondary hyperparathyroidism and increased bone remodelling activity may persist months after transplantation. The severity of secondary hyperparathyroidism prior to transplantation, the duration of dialysis, and the development of nodular and/or monoclonal hyperplasia of parathyroid glands are the most-important factors that determine the phenomenon. Important issues, which still need to be answered, are the possible roles of growth factors, cytokines, VDR gene polymorphism (B/b allele), and type of immunosuppressive regimen in the skeletal abnormalities observed.

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“…Tertiary HPT is an uncommon condition, affecting up to 8% of patients with secondary HPT after a successful renal transplant (2). High quantities of PTH secreted by the parathyroid glands in this condition results in a serum hypercalcemia (4).…”

Section: Discussionmentioning

confidence: 99%

“…Tertiary HPT can occur in a small number of patients, when the parathyroids activity turns autonomous and excessive, leading to hypercalcemia (1). Bone alterations are the main consequences of this endocrine condition, including the development of an osteolitic lesion called brown tumor (2,3). This paper reports a case of multiple brown tumours located in maxilla and mandible in a renal transplant recipient with tertiary HPT.…”

Section: Introductionmentioning

confidence: 99%