Hyperparathyroidism and long‐term bone loss after renal transplantation

Heaf, James; Tvedegaard, Erling; Kanstrup, Inge‐Lis; Fogh‐Andersen, Niels

doi:10.1034/j.1399-0012.2003.00047.x

Cited by 75 publications

(68 citation statements)

References 18 publications

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“…The mean iPTH concentration was similar among the treated and untreated patients, but the percentage of recipients with iPTH in the normal range was significantly higher in the treated group. Our findings agreed with those from Heaf et al, 9 who observed that vitamin D prescription increased 25OHD and 1.25OHD serum levels without any change in the prevalence of elevated PTH. The lack of effectiveness of vitamin D treatment may be attributed to the administered doses of vitamin D. Our patients were on treatment with low doses of vitamin D to prevent the risk of adverse effects, such as hypercalcemia and renal function deterioration, as calcitriol doses Ͻ0.25 g/d engender a low risk of both complications.…”

Section: Discussionsupporting

confidence: 93%

Secondary Hyperparathyroidism After Kidney Transplantation: A Cross-Sectional Study

Marcén

Ponte

Rodríguez-Mendiola

et al. 2009

Transplantation Proceedings

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Introduction. The purpose of the present study was to investigate the prevalence of hyperparathyroidism among a population of kidney graft recipients. Patients and Methods. We investigated biochemical bone parameters of 509 renal transplant recipients with a mean follow-up of 113 Ϯ 76 months. Among these patients, 257 patients were treated with either vitamin D or calcium supplements or both.Results. The mean estimated glomerular filtration rate (eGFR) was 47.2 Ϯ 18.4 mL/min/1.73 m 2 and the mean intact parathyroid hormone (iPTH) level was 144 Ϯ 149 pg/mL. A total of 70 patients (13.7%) had hypercalcemia defined by a corrected serum calcium Ͼ10.2 mg/dL. When the patients were classified according to iPTH concentrations following the Kidney Disease Outcome Quality Initiative (K/DOQI) clinical practice guidelines: 22.4% had iPTH Ͻ70 pg/mL; 30.8% between 70 and 110 pg/mL; 16.5% between 110 and 150 pg/mL; 24.3% between 150 and 300 pg/mL; and 6.9% Ͼ300 pg/mL. There were no differences in biochemical bone parameters between those that were or were not on calcium and vitamin D supplements, but there was a higher percentage of patients with normal iPTH among the treated group (28.0% vs 16.7%; P ϭ 0.003). In patients not receiving calcium and/or vitamin D supplements, multiple linear regression demonstrated that only time on dialysis, eGFR, and serum 25-hydroxyvitamin D (25OHD) levels were significantly predictive of iPTH concentrations (R 2 ϭ 0.21; P ϭ .000).

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Section: Discussionsupporting

confidence: 93%

Secondary Hyperparathyroidism After Kidney Transplantation: A Cross-Sectional Study

Marcén

Ponte

Rodríguez-Mendiola

et al. 2009

Transplantation Proceedings

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“…Indeed, most transplant patients have various forms of preexisting bone disease that may persist after transplantation. The prevalence of hyperparathyroidism among transplant patients is approximately 30 to 50% (23)(24)(25)(26).…”

Section: Pathogenesis Of Posttransplantation Bone Diseasementioning

confidence: 99%

Bone Disease after Renal Transplantation

Weisinger¹,

Carlini²,

Rojas³

et al. 2006

Clinical Journal of the American Society of Nephrology

125

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It has been well established that a rapid decrease in bone mineral density (BMD) occurs in the first 6 to 12 mo after a successful renal transplantation and persists, albeit at a lower rate, for many years. This rapid BMD loss significantly increases the fracture risk of these patients to levels that are even higher than those of patients who have chronic kidney disease stage 5 and are on dialysis. The presence of low BMD in renal transplant patients as a predictor of risk fracture is controversial. Indeed, as has been suggested also for patients with postmenopausal osteoporosis, there is not a compelling correlation between the decline in BMD and skeletal fractures. However, bone disease after renal transplantation probably represents a unique bone disorder that must encompass underlying renal osteodystrophy. In fact, this syndrome results from multiple factors that include pretransplantation bone status, use of glucocorticoids and other immunosuppressive drugs, hypophosphatemia, and alterations of the calcium-vitamin D axis. Recent studies have demonstrated decreased osteoblast number, reduced bone formation rate, delayed mineralization, and increased osteoblast and osteocyte apoptosis. Bisphosphonates and vitamin D metabolites may be valuable in preventing or diminishing early bone loss. However, clinicians should be careful with the use of bisphosphonates and oversuppression of bone, especially in patients with low bone turnover. New prospective, controlled trials are required to confirm the real efficacy of these drugs, particularly in long-term renal transplant patients.Clin J Am Soc Nephrol 1: 1300 -1313, 2006. doi: 10.2215/CJN.01510506 K idney, heart, lung, and liver transplantation have become fairly common and successful. As the number of transplants has grown, new challenges have arisen in the management of long-term complications of transplantation. Posttransplantation bone disease represents one such important complication, because it is observed in a substantial proportion of patients. As a consequence, bone mass loss and bone fractures are common in these patients and cause substantial morbidity.In patients with chronic kidney disease (CKD), renal osteodystrophy that begins during the early stages of the disease usually worsens during dialysis and may persist after transplantation, although in many patients, improvement in these bone lesions are observed. In addition to preexisting bone lesions, not only factors that hamper recovery but also new factors could affect bone structure after transplantation. These include the potential deleterious effects on bone of the different immunosuppressive agents, the impaired renal function that frequently is observed in renal transplant patients, and several others factors that are particular to each patient, such as postmenopausal status, presence of diabetes, gender, and time after transplantation. Changes in Bone Mineral DensityBone mineral density (BMD) as assessed by dual x-ray absorptiometry has been used as a noninvasive method to assess bone mass loss...

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“…Persistent secondary or tertiary hyperparathyroidism (HPT), reported in up to 30-50% of renal transplant patients, can lead to osteitis fibrosa cystica, a form of high turnover bone disease (Heaf et al, 2003). High bone turnover is usually associated with cortical bone loss and weakening its mechanical function (Malluche et al, 2010).…”

Section: Osteitis Fibrosa Cysticamentioning

confidence: 99%

“…About 30% of patients may still have elevated PTH levels beyond 1 year despite the presence of normal renal function and vitamin D metabolism (Heaf et al, 2003). These patients likely have tertiary HPT due to the nodular transformation from a polyclonal hyperplasia into a monoclonal adenoma.…”

Section: Hyperparathyroidism and Hypercalcemiamentioning

confidence: 99%

“…The risk factors may include higher PTH level before transplant, longer time on dialysis and older age. Persistent HPT after transplant leads to continuing bone loss (Gallego et al, 2006;Heaf et al, 2003). A recent study of 201 transplant recipients reported a biphasic pattern of serum calcium levels with hypocalcemia immediately after kidney transplant and subsequent development of hypercalcemia (Evenepoel et al, 2009).…”

Section: Hyperparathyroidism and Hypercalcemiamentioning

confidence: 99%

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