Hypophosphataemic Osteomalacia After Cadaveric Renal Transplantation

Moorheàd, J. F.; Ahmed, K.Y.; Varghese, Z.; Wills, M. R.; Baillod, Rosemarie; Tatler, G. L. V.; Fairney, Angela

doi:10.1016/s0140-6736(74)92902-x

Cited by 76 publications

(24 citation statements)

References 6 publications

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“…[29,30] In our study, the hypophosphatemia levels were nearly normal after one year treatment. Also, serum PTH levels were decreased, and 25 (OH)D3 levels were increased; the results were the same with group 2.…”

Section: Discussionsupporting

confidence: 54%

The Effect of Low-Dose Cholecalciferol and Calcium Treatment on Posttransplant Bone Loss in Renal Transplant Patients: A Prospective Study

et al. 2008

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Background/Aim. Posttransplant steroid doses have been reduced with the use of new and potent immunosuppressive agents. However, posttransplant osteoporosis is still a serious problem. Our aim in this study was to investigate the effect of low-dose cholecalciferol and calcium supplementation on bone loss after transplantation in renal transplant patients. Methods. Fifty-eight renal transplantation patients were included in the study. Fourteen newly transplanted patients (group 1) and 44 renal transplantation patients with a graft age of at least six months (group 2) were involved. All patients received 400 IU/ day orally cholecalciferol (vitamin D3) and 600 mg/day orally calcium replacement starting from the second day posttransplantion. All patients baseline serum and urine biochemistry, serum 25-hydroxy vitamin D3 (25 (OH)D3), and bone mineral density (BMD) tests were performed. Also, the same measurements were performed at the 12th month in group 1. Results. After one year of treatment, BMDs were improved in group 1. Patients in group 1 had a nonsignificant increase of lumbar spine (8.12 ± 18.64% of baseline BMD) and femoral total (7.10 ± 13.48% of baseline BMD) BMD at the end of the first year. On the other hand, there was a significant increase in femoral neck (10.06 ± 15.70% of baseline BMD, p < 0.05) measurements. The baseline results of group 2 were similar to group 1. In group 1, 25 (OH)D3 levels were increased while PTH levels were decreased at the end of the year. Conclusion. In renal transplant patients who use low-dose metilprednisolon and new immunosuppressive agents together, low doses of vitamin D3 and calcium replacement for one year provides a reduction in lumbar spine, femoral neck, and femoral total bone loss and prevents bone loss in group 2. In addition, it contributed to the normalization of PTH levels.

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Section: Discussionsupporting

confidence: 54%

The Effect of Low-Dose Cholecalciferol and Calcium Treatment on Posttransplant Bone Loss in Renal Transplant Patients: A Prospective Study

et al. 2008

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“…Furthermore, posttransplantation serum phosphorus correlated negatively with the number of apoptotic osteoblasts and positively with the number of active osteoblasts, suggesting a role of hypophosphatemia in the mechanisms that lead to posttransplantation bone disease. Indeed, hypophosphatemia has been associated with severe alterations in bone turnover that include a decrease in osteoblast activity that leads to rickets and osteomalacia (38,43). Nevertheless, further studies are required to prove a direct association between hypophosphatemia and osteoblast apoptosis.…”

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

121

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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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“…PTH is a main factor of bone resorption, and long-term P depletion can also induce bone loss [43], In kidney transplant recipients, both persistent hyperparathyroid ism and P depletion likely add their effects to other fac tors to aggravate the preexisting renal osteodystrophy [41,44,45]. and contribute to the osteopenia regarded as a major complication of graft [46].…”

Section: Posttransplant Bone Diseasementioning

confidence: 99%

Acute Oral Calcium Load Decreases Parathyroid Secretion and Suppresses Tubular Phosphate Loss in Long-Term Renal Transplant Recipients

Dumoulin¹,

Hory

Nguyen³

et al. 1995

Am J Nephrol

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Persistent hyperparathyroidism and impaired tubular reabsorption of phosphate (P) are common after kidney transplantation. In order to assess the suppressibility of these abnormalities, we studied the effects of a single oral calcium (Ca) load (1 g) in 7 healthy subjects (HS) and in 14 normocalcemic long-term renal transplant recipients with good renal function (RT). In HS and RT, serum and urinary Ca were similar at baseline, and increased (p < 0.001) to the same extent after Ca ingestion. Serum parathyroid hormone (PTH) and nephrogenic cAMP (NcAMP) levels were higher at baseline in RT than HS (mean ± SEM; respectively, PTH 7.8 ± 0.8 vs. 3.5 ± 0.6 pmol/l, p < 0.001, and NcAMP 24.8 ± 2.3 vs. 13.9 ± 2.3 nmol/lGFRp < 0.01). After Ca, PTH (p < 0.001) and NcAMP (p < 0.01) decreased markedly in both RT and HS. Maximal changes in PTH and NcAMP were larger in RT than HS (PTH -3.3 ± 0.4 vs. -2.1 ± 0.03 pmol/l, p < 0.01, and NcAMP -18.2 ± 3.3 vs. -8.1 ± 2.6 nmol/l GFR, p < 0.05). Although PTH levels remained significantly higher in RT than HS from baseline to the end of the study (p < 0.001), PTH decreased to the normal range in RT after Ca load. Moreover, NcAMP reached similar values in RT and HS after Ca (16.0 ± 3.2 vs. 13.2 ± 2.8 nmol/l GFR at the end of the survey, NS). At baseline, RT had higher phosphaturia than HS (246 ± 25 vs. 127 ± 19 µmol/l, p < 0.01), and Ca ingestion lowered phosphaturia to similar values in both RT and HS (116 ± 13 vs. 95 ± 7 µmol/l GFR, NS). Renal P threshold expressed as TmP/GFR and tubular reabsorption rate of P were lower in RT than HS at baseline, and resumed normal values after Ca. To summarize, in normocalcemic long-term kidney transplant recipients, a single oral Ca intake acutely blunted the excessive PTH secretion and increased tubular reabsorption of P up to a normal range. We conclude therefore, that PTH is a main factor of tubular P loss in these patients.

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Hypophosphataemic Osteomalacia After Cadaveric Renal Transplantation

Cited by 76 publications

References 6 publications

The Effect of Low-Dose Cholecalciferol and Calcium Treatment on Posttransplant Bone Loss in Renal Transplant Patients: A Prospective Study

The Effect of Low-Dose Cholecalciferol and Calcium Treatment on Posttransplant Bone Loss in Renal Transplant Patients: A Prospective Study

Bone Disease after Renal Transplantation

Acute Oral Calcium Load Decreases Parathyroid Secretion and Suppresses Tubular Phosphate Loss in Long-Term Renal Transplant Recipients

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