Low‐Turnover Bone Disease in Hypercalcemic Hyperparathyroidism After Kidney Transplantation

Borchhardt, Kyra; Sulzbacher, Irene; Benesch, Thomas; Födinger, Manuela; Sunder‐Plassmann, Gere; Haas, Martin

doi:10.1111/j.1600-6143.2007.01950.x

Cited by 85 publications

(62 citation statements)

References 30 publications

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“…Fourth, in the absence of bone biopsies, it may be difficult to ascertain bone turnover in patients with renal transplants. 34 Nevertheless, taking into account that our results in the cinacalcet arm are similar to those previously reported 20 and that extended minimally invasive subtotal parathyroidectomy is a feasible approach, 35 our results could reasonably be reproduced in a big clinical trial.…”

Section: Discussionsupporting

confidence: 83%

A Randomized Study Comparing Parathyroidectomy with Cinacalcet for Treating Hypercalcemia in Kidney Allograft Recipients with Hyperparathyroidism

Cruzado

Moreno²,

Torregrosa

et al. 2015

JASN

131

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Tertiary hyperparathyroidism is a common cause of hypercalcemia after kidney transplant. We designed this 12-month, prospective, multicenter, open-label, randomized study to evaluate whether subtotal parathyroidectomy is more effective than cinacalcet for controlling hypercalcemia caused by persistent hyperparathyroidism after kidney transplant. Kidney allograft recipients with hypercalcemia and elevated intact parathyroid hormone (iPTH) concentration were eligible if they had received a transplant $6 months before the study and had an eGFR.30 ml/min per 1.73 m 2 . The primary end point was the proportion of patients with normocalcemia at 12 months. Secondary end points were serum iPTH concentration, serum phosphate concentration, bone mineral density, vascular calcification, renal function, patient and graft survival, and economic cost. In total, 30 patients were randomized to receive cinacalcet (n=15) or subtotal parathyroidectomy (n=15). At 12 months, ten of 15 patients in the cinacalcet group and 15 of 15 patients in the parathyroidectomy group (P=0.04) achieved normocalcemia. Normalization of serum phosphate concentration occurred in almost all patients. Subtotal parathyroidectomy induced greater reduction of iPTH and associated with a significant increase in femoral neck bone mineral density; vascular calcification remained unchanged in both groups. The most frequent adverse events were digestive intolerance in the cinacalcet group and hypocalcemia in the parathyroidectomy group. Surgery would be more cost effective than cinacalcet if cinacalcet duration reached 14 months. All patients were alive with a functioning graft at the end of follow-up. In conclusion, subtotal parathyroidectomy was superior to cinacalcet in controlling hypercalcemia in these patients with kidney transplants and persistent hyperparathyroidism.

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Section: Discussionsupporting

confidence: 83%

A Randomized Study Comparing Parathyroidectomy with Cinacalcet for Treating Hypercalcemia in Kidney Allograft Recipients with Hyperparathyroidism

Cruzado

Moreno²,

Torregrosa

et al. 2015

JASN

131

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“…This study reports the results of follow-up bone biopsies of kidney transplant recipients who underwent baseline bone biopsies [6] and were subsequently treated with cinacalcet for hypercalcemia [14]. In brief, kidney transplant recipients with persistent hypercalcemic hyperparathyroidism after kidney transplantation, i.e.…”

Section: Methodsmentioning

confidence: 99%

“…Of note, bone biopsies done in patients with hypercalcemic hyperparathyroidism revealed adynamic bone disease in 50%, and were not related to serum intact parathyroid hormone (iPTH) concentrations [6]. …”

Section: Introductionmentioning

confidence: 99%

Cinacalcet Decreases Bone Formation Rate in Hypercalcemic Hyperparathyroidism after Kidney Transplantation

Borchhardt¹,

Diarra²,

Sulzbacher³

et al. 2010

Am J Nephrol

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Background/Aims: Cinacalcet reduces serum calcium in kidney transplant recipients with hypercalcemic hyperparathyroidism. Its effect on bone, however, has not been investigated in this population. Methods: We prospectively examined bone turnover, histomorphometry and density as well as serum bone biomarkers in 10 transplant recipients before and after treatment with cinacalcet. Results: After 18–24 months of treatment with cinacalcet, bone formation decreased in 7, increased in 2, and remained zero in 1 patient (p = 0.11). Trabecular bone volume was maintained. Trabecular number decreased (p = 0.03), but trabecular thickness was unchanged (p = 0.17). Osteoid decreased (p = 0.02) and osteoblast surface increased (p = 0.02). Bone mineral density of the femur remained stable in 1 patient, decreased in 2 patients, but increased in 7 patients (p = 0.153). Serum calcium concentration (p = 0.005), iPTH (p = 0.01) and calcitonin concentration decreased (p = 0.03), while 25(OH) vitamin D₃ increased (p = 0.02). No fractures were reported. Graft function remained stable. Conclusion: Whilecinacalcet might decrease bone formation rate, it did not change bone volume, and bone mineral density of the femur increased. Therefore, the use of cinacalcet in hypercalcemic hyperparathyroidism might be safe with regard to the bone disease present after kidney transplantation.

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“…Decreased calcium excretion suggests an additive tubular effect on hyper - and 3 and 12 mo after renal transplant, association of ↑Ca and ↓P with Ca-P deposits at 3 mo after transplant Abbreviations: C, calcium; eGFR, estimated glomerular filtration rate; FeCa, fractional excretion of calcium; FEP, fractional excretion of phosphate; iFGF23, intact fibroblast growth factor 23; iPTH, intact parathyroid hormone; 1,25(OH) 2D3, 1,25-dihydroxyvitamin D3; P, phosphorus; PTH, parathyroid hormone; TmP/eGFR, tubular maximum for phosphate corrected for estimated glomerular filtration rate; VitD, vitamin D calcemia. 37 Hypercalcemia can be severe enough to cause calciphylaxis, leading to renal failure, as has been reported, eventually requiring parathyroidectomy. High PTH concentrations stimulate renal production of calcitriol, which, in turn, increases intestinal absorption and improves the skeletal mobilization of calcium.…”

Section: Hypophosphatemiamentioning

confidence: 99%

Untitled

2016

Exp Clin Transplant

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Fibroblast growth factor 23 is likely to be the most important regulator of phosphate homeostasis, which mediates its functions through fibroblast growth factor receptors and the coreceptor Klotho. In addition to reducing expression of the sodium-phosphate cotransporters NPT2a and NPT2c in the proximal tubules, fibroblast growth factor 23 inhibits renal 1α-hydroxylase and stimulates 24-hydroxylase and appears to reduce parathyroid hormone secretion in short-term studies. Fibroblast growth factor 23 synthesis and secretion by osteocytes and osteoblasts are upregulated through 1,25-dihydroxyvitamin D3 and through an increased dietary phosphate intake. Recent studies have indicated that a low-protein diet and calcium deficiency reduce circulating fibroblast growth factor 23 levels, but magnesium deficiency increases fibroblast growth factor levels. Drugs such as phosphate binders, bisphosphonate, and estrogens have various effects on circulating fibroblast growth factor 23 levels. The high cardiovascular disease event rates and mortality associated with elevated levels of this hormone may be due to various effects on the cardiovascular system, including left ventricular hypertrophy, arterial stiffness, vascular calcifications, endothelial dysfunction, and increased levels of inflammatory markers. In addition, elevated levels of this hormone may contribute to mineral bone metabolism disorders and to patient and allograft survival after renal transplant. Here, we discuss the effects of fibroblast growth factor 23 on adverse renal, bone, and cardiovascular outcomes after kidney transplant.

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Low‐Turnover Bone Disease in Hypercalcemic Hyperparathyroidism After Kidney Transplantation

Cited by 85 publications

References 30 publications

A Randomized Study Comparing Parathyroidectomy with Cinacalcet for Treating Hypercalcemia in Kidney Allograft Recipients with Hyperparathyroidism

A Randomized Study Comparing Parathyroidectomy with Cinacalcet for Treating Hypercalcemia in Kidney Allograft Recipients with Hyperparathyroidism

Cinacalcet Decreases Bone Formation Rate in Hypercalcemic Hyperparathyroidism after Kidney Transplantation

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