Lack of Evidence That Cyclosporine Treatment Impairs Calcium-Phosphorus Homeostasis and Bone Remodeling in Normocalcemic Long-Term Renal Transplant Recipients

Dumoulin, Gilles; Hory, B; Nguyen, Nhu Uyen; Henriet, M T; Bresson, Catherine; Regnard, Jacques; Saint‐Hillier, Y

doi:10.1097/00007890-199506270-00008

Cited by 24 publications

(11 citation statements)

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“…A possible increase in the risk of acute tubular necrosis following RT, hypercalcemia, hypophosphatemia, and the extension of renal osteodystrophy after RT are expected clinical consequences [28,32].…”

Section: Discussionmentioning

confidence: 99%

“…Although one study in humans has shown a rise in serum alkaline phosphatase activity in CyA-treated patients, suggesting a high-turnover osteopathy [27], two more-recent reports failed to confirm any deleterious effect of CyA on bone and Ca metabolism after RT [28,29]. The direct effect of CyA on parathyroid gland function, if any, has not been assessed to date, to the best of our knowledge.…”

Section: Effects Of Immunosuppressive Drugs On Post-transplant 2hptmentioning

confidence: 94%

“…It is well known that patients treated with these drugs develop osteopenia, mainly secondary to impaired intestinal absorption of Ca, inhibition of osteoblast function, and increased urinary Ca excretion [28]. All these actions promote a state of negative Ca balance that might contribute to indirect stimulation of parathyroid function after RT.…”

Section: Effects Of Immunosuppressive Drugs On Post-transplant 2hptmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

Section: Effects Of Immunosuppressive Drugs On Post-transplant 2hptmentioning

confidence: 94%

Section: Effects Of Immunosuppressive Drugs On Post-transplant 2hptmentioning

confidence: 99%

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Evolution of secondary hyperparathyroidism after renal transplantation

Nogueira

David

Cochat

2000

Pediatric Nephrology

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“…Cyclosporine has been suggested to work beneficially, with its steroidsparing effect, in bone remodeling through increasing serum concentrations of 1,25-(OH)2-vitamin D and a bone formation marker, osteocalcin (15,16). Another study showed no significant effect on calcium-regulating hormones and bone remodeling in normocalcemic renal transplant recipients with good renal functions (17). The effect of immunosuppressants on bone turnover seems to depend largely on other factors modifying calcium metabolism and needs further investigation.…”

Section: Discussionmentioning

confidence: 99%

Liver Transplantation-associated Hypercalcemia Followed by Acute Renal Dysfunction

Shirasawa

Nomura²,

Yoshida

et al. 2004

Intern. Med.

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A 34-year-old woman with liver insufficiency due to glycogen storage disease III underwent a living spousal liver transplantation. Soon after the successful operation, moderate hypercalcemia along with hyperbilirubinemia emerged without clarified reasons. The hypercalcemia persisted for over a month despite calcitonin treatment and the serum calcium level surged to 13.2 mg/dl with albumin correction. Renal dysfunction was indicated by an acute increase in serum creatinine ( 0.8 to 2.8 mg/ml), which was assumed to be hypercalcemia-induced and was effectively treated with bisphosphonate, pamidronate (

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“…Cyclosporine has been found to decrease bone resorption and osteoclast formation in vitro (Orcel et al 1991). Rats treated with cyclosporine have been shown to develop increased bone turnover and bone loss (Movsowitz et al 1988), but long-term renal transplant patients do not show evidence of impaired phosphocalcic homeostasis or impaired bone remodelling (Dumoulin et al 1995). While the direct eect of cyclosporine on bone has not yet been established, secondary hyperparathyroidism can be induced through cyclosporine nephrotoxicity.…”

Section: Discussionmentioning

confidence: 99%

Moderate endurance training has no effect on the parathyroid function of heart transplant patients

Charloux

Brandenberger²,

Lampert

et al. 1997

European Journal of Applied Physiology

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The benefit of retraining for heart transplant recipients (HTR) is now well established. The rehabilitation of these patients can be compromised by osteopenia and bone fractures. The resting levels of parathyroid hormone (PTH) and exercise-induced increases are higher in HTR than in healthy controls. To evaluate the effect of a moderate endurance training programme on parathyroid activity, six HTR, an average of 18 months after transplant, and seven healthy sedentary controls have been studied. None of the subjects had a history of bone disease. Two exercise tests (square wave endurance exercise tests, SWEET) with identical work rates were performed before and after training. Intact PTH, ionized calcium (Ca2+), phosphorus (Pi) and pH were measured at rest, during exercise and in the recovery periods. Training consisted of a 45-min SWEET three times a week for 6 weeks. Levels of Ca2+, Pi and PTH showed a significant increase during the exercise session in both groups. Ca2+ and Pi levels decreased rapidly after the cessation of exercise whereas PTH reached a peak at the 10th min of the recovery in both groups. This increase in PTH was significantly higher in HTR than in controls. However, despite a significant improvement of total endurance work (+ 28% in HTR, +29% in controls) this endurance training had no effect on resting levels of PTH, plasma Ca2+ or Pi, nor on their exercise-induced variations. The exercise-induced decrease in pH was less pronounced after training which is evidence of training. We conclude that a short endurance training programme does not alter the moderate hyperparathyroidism of HTR. The effect of such a training programme on bone mass and bone mineral density needs now to be evaluated.

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Lack of Evidence That Cyclosporine Treatment Impairs Calcium-Phosphorus Homeostasis and Bone Remodeling in Normocalcemic Long-Term Renal Transplant Recipients

Cited by 24 publications

References 0 publications

Evolution of secondary hyperparathyroidism after renal transplantation

Evolution of secondary hyperparathyroidism after renal transplantation

Liver Transplantation-associated Hypercalcemia Followed by Acute Renal Dysfunction

Moderate endurance training has no effect on the parathyroid function of heart transplant patients

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