Renal osteodystrophy in nondialysed adolescents. Long-term treatment with 1alpha-hydroxycholecalciferol.

Kanis, J. A.; Henderson, R. G.; Heynen, G; Ledingham, J. G. G.; Russell, R. G. G.; Smith, Roger; Walton, R. J.

doi:10.1136/adc.52.6.473

Cited by 29 publications

(6 citation statements)

References 24 publications

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“…In patients with chronic renal failure, the skeletal lesions are mostly due to hyperparathyroidism secondary to hyperphosphataemia, but are also due to decreased p r o d u c t i o n of 1-a-25-dihydroxyvitamin D3 because of impaired renal activation of 25-hydroxyvitamin D3, and to decreased intestinal absorption of calcium [5,14,19].…”

Section: Introductionmentioning

confidence: 99%

Parathyroid hormone and calcitonin secretion in uraemic infants

1978

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In six infants aged between 4 and 8 months with chronic renal failure, we have studied blood levels of calcium (Ca), phosphorus (P), alkaline phosphatase, immunoreactive parathyroid hormone (PTH), and calcitonin (CT), as well as urinary excretion of Ca, P, hydroxyproline and cyclic AMP under basal conditions and during an infusion of 20 mg/kg of 10% Ca gluconate in normal saline over 4 h. Under basal conditions four infants had normal serum Ca and P values, alkaline phosphatase levels at the upper limit of normal, and very high PTH (range: 1450--2550 pg Eq/ml) and CT (range: 700--1900 pg/ml) levels. The urinary Ca excretion was low, whereas the urinary excretion of P, hydroxyproline and cyclic AMP was high. During Ca infusion, the total serum Ca and CT levels increased, PTH fell without however reaching the normal upper limit, and urinary P and cyclic AMP excretion decreased. In two infants with osteodystrophy and the highest levels of PTH (2900 and 3500 pg Eq/ml respectively) there was no suppression of PTH during Ca infusion.

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Section: Introductionmentioning

confidence: 99%

Parathyroid hormone and calcitonin secretion in uraemic infants

1978

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“…The rapid deterioration of deformity at puberty in high turnover bone disease is well recognized, for example, in renal osteodystrophy. (22) After 3 years of intensive treatment, the patient (who had by this time reached adult bone age) was still mobile, and with the exception of some worsening of the upper thoracic kyphosis, her deformities had not progressed. Bone turnover was suppressed, and there were also substantial positive changes in audiometry, radiographic appearances, and densitometry.…”

Section: Discussionmentioning

confidence: 97%

Treatment of Idiopathic Hyperphosphatasia With Intensive Bisphosphonate Therapy

Cundy

Wheadon

King

2004

Journal of Bone and Mineral Research

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In a family with IH, a rare high turnover bone disease, two older siblings were wheelchairbound with severe skeletal deformity by age 15. Their youngest affected sibling was treated intensively with intravenous bisphosphonates for 3 years. The treatment was well tolerated and prevented the development of deformity and disability.Introduction: Idiopathic hyperphosphatasia (IH, also known as juvenile Paget's disease) is a rare genetic bone disease characterized by very high bone turnover and progressive bony deformity. Inhibitors of bone resorption have been used to suppress bone turnover in the short term, but there is no published data on long-term efficacy. Materials and Methods: An 11-year-old girl with IH, who had two severely affected older siblings, presented with progressive deformity and deafness and long bone fractures. Conventional pediatric doses of pamidronate had failed to prevent clinical deterioration or suppress bone turnover completely. Intensive bisphosphonate therapy (frequent 5-mg ibandronate infusions) was given to try and arrest progression of the skeletal disease. Growth and development, pure tone audiometry, biochemistry, radiology, densitometry (DXA), and bone histology were monitored. Results: A total of 45 mg ibandronate was given over 3 years until skeletal maturity was reached (20, 15, and 10 mg for years 1-3, respectively). Ibandronate treatment was well tolerated, and biochemical markers of bone turnover suppressed to within the age-appropriate normal range There was some progression of her thoracic kyphosis, but she had no further fractures and remained mobile and active at an age when her siblings had become wheelchair-bound. A significant recovery of hearing (p Ͻ 0.01) was documented, particularly at low frequencies. Radiographs showed improvement in spinal osteoporosis and cortical bone dimensions and arrest of progressive acetabular protrusion. Areal bone density increased substantially (lumbar spine z-score from Ϫ2.2 to ϩ 1.8). Tetracycline-labeled bone biopsy specimens were taken before and after 18 months of intensive treatment. The second biopsy showed suppression of bone turnover and a doubling of trabecular thickness, with no mineralization defect, and no osteopetrosis. Conclusions: Intensive bisphosphonate treatment prevented the development of deformity and disability and improved hearing in this child with IH. The dose of bisphosphonate, which is substantially greater than is usually used in pediatric bone disease, had no adverse effects, in particular on bone mineralization.

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“…Vitamin D sterols may also suppress PTH indirectly, through increasing osteocytic FGF23 production [43] which, in turn, suppresses parathyroid gland PTH expression[44-45]. Calcitriol and alfacalcidol have been effective in decreasing PTH levels and preventing osteitis fibrosis cystica for decades [46-47]. Beneficial effects of calcitriol, including improved survival in hemodialysis patients [48-50], amelioration of cardiac hypertrophy in animals[51], improved cardiac systolic function in hemodialysis patients[52], reductions in proteinuria, fibrosis, and podocyte hypertrophy in sub-totally nephrectomized rats [53] and decreased proteinuria in patients with pre-dialysis CKD patients [54] have been demonstrated.…”

Section: Vitamin D Therapymentioning

confidence: 99%

Phosphate binders, vitamin D and calcimimetics in the management of chronic kidney disease–mineral bone disorders (CKD-MBD) in children

Wesseling‐Perry

Salusky

2013

Pediatr Nephrol

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In order to minimize complications on the skeleton and to prevent extraskeletal calcifications, the specific aims of the management of Chronic Kidney Disease Mineral and Bone Disorder (CKD-MBD) are to maintain blood levels of serum calcium and phosphorus as close to the normal range as possible, thereby maintaining serum PTH at levels appropriate for stage of CKD, preventing hyperplasia of the parathyroid glands, avoiding the development of extra-skeletal calcifications, and preventing or reversing the accumulation of toxic substances such as aluminum and β2-microglobulin. In order to limit cardiovascular calcification, daily intake of elemental calcium, including from dietary sources and from phosphate binders, should not exceed twice the daily recommended intake for age and should not exceed 2.5 g/day. Calcium-free phosphate binders such as sevelamer hydrochloride and sevelamer carbonate are safe and effective alternatives to calcium-based binders and their use widens the margin of safety for active vitamin D sterol therapy. Vitamin D deficiency is highly prevalent across the spectrum of CKD and replacement therapy is recommended in vitamin D deficient and insufficient individuals. Therapy with active vitamin D sterols is recommended after correction of vitamin D deficiency state and should be titrated based on target PTH levels across the spectrum of CKD. Although the use of calcimimetics drugs have proven to effectively control the biochemical features of secondary hyperparathyroidism, there is very limited experience with the use of such agent in pediatric patients and mainly during the first years of life. Studies are needed to further define the role of such agents in the treatment of pediatric CKDMBD.

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Renal osteodystrophy in nondialysed adolescents. Long-term treatment with 1alpha-hydroxycholecalciferol.

Cited by 29 publications

References 24 publications

Parathyroid hormone and calcitonin secretion in uraemic infants

Parathyroid hormone and calcitonin secretion in uraemic infants

Treatment of Idiopathic Hyperphosphatasia With Intensive Bisphosphonate Therapy

Phosphate binders, vitamin D and calcimimetics in the management of chronic kidney disease–mineral bone disorders (CKD-MBD) in children

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