Oral paricalcitol reduces the prevalence of posttransplant hyperparathyroidism: Results of an open label randomized trial

H. Amer, M. D. Griffin, Mark D Stegall, Fernando G Cosio, W. D. Park, Walter K Kremers, R. L. Heilman, M. J. Mazur, K. Hamawi, T. S. Larson, Rajiv Kumar

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Postkidney transplant hyperparathyroidism is a significant problem. Vitamin D receptor agonists are known to suppress parathyroid hormone (PTH) secretion. We examined the effect of oral paricalcitol on posttransplant secondary hyperparathyroidism by conducting an open label randomized trial in which 100 incident kidney transplant recipients were randomized 1:1 to receive oral paricalcitol, 2 μg per day, for the first year posttransplant or no additional therapy. Serial measurements of serum PTH, calcium and bone alkaline phosphatase, 24-h urine calcium and bone density were performed. The primary endpoint was the frequency of hyperparathyroidism 1-year posttransplant. Eighty-seven patients completed the trial. One-year posttransplant, 29% of paricalcitol-treated subjects had hyperparathyroidism compared with 63% of untreated patients (p = 0.0005). Calcium supplementation was discontinued in two control and 15 treatment patients due to mild hypercalcemia or hypercalcuria. Paricalcitol was discontinued in four patients due to hypercalcuria/ hypercalcemia and in one for preference. Two subjects required decreasing the dose of paricalcitol to 1 μg daily. Hypercalcemia was asymptomatic and reversible. Incidence of acute rejection, BK nephropathy and renal function at 1 year were similar between groups. Moderate renal allograft fibrosis was reduced in treated patients. Oral paricalcitol is effective in decreasing posttransplant hyperparathyroidism and may have beneficial effects on renal allograft histology. Paricalcitol decreases the prevalence of post-kidney transplant hyperparathyroidism and may have beneficial effects on renal allograft histology.

Original languageEnglish (US)
Pages (from-to)1576-1585
Number of pages10
JournalAmerican Journal of Transplantation
Volume13
Issue number6
DOIs
StatePublished - Jun 2013

Fingerprint

Hyperparathyroidism
Kidney
Hypercalcemia
Allografts
Calcium
Parathyroid Hormone
Histology
Transplants
Calcitriol Receptors
Secondary Hyperparathyroidism
paricalcitol
Bone Density
Alkaline Phosphatase
Fibrosis
Urine
Bone and Bones
Incidence
Therapeutics
Serum

Keywords

  • Bone disease
  • hyperparathyroidism
  • kidney transplant
  • paricalcitol
  • vitamin D receptor agonist

ASJC Scopus subject areas

  • Transplantation
  • Immunology and Allergy
  • Pharmacology (medical)

Cite this

Oral paricalcitol reduces the prevalence of posttransplant hyperparathyroidism : Results of an open label randomized trial. / Amer, H.; Griffin, M. D.; Stegall, Mark D; Cosio, Fernando G; Park, W. D.; Kremers, Walter K; Heilman, R. L.; Mazur, M. J.; Hamawi, K.; Larson, T. S.; Kumar, Rajiv.

In: American Journal of Transplantation, Vol. 13, No. 6, 06.2013, p. 1576-1585.

Research output: Contribution to journalArticle

Amer, H. ; Griffin, M. D. ; Stegall, Mark D ; Cosio, Fernando G ; Park, W. D. ; Kremers, Walter K ; Heilman, R. L. ; Mazur, M. J. ; Hamawi, K. ; Larson, T. S. ; Kumar, Rajiv. / Oral paricalcitol reduces the prevalence of posttransplant hyperparathyroidism : Results of an open label randomized trial. In: American Journal of Transplantation. 2013 ; Vol. 13, No. 6. pp. 1576-1585.
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AU - Cosio, Fernando G

AU - Park, W. D.

AU - Kremers, Walter K

AU - Heilman, R. L.

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AU - Larson, T. S.

AU - Kumar, Rajiv

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AB - Postkidney transplant hyperparathyroidism is a significant problem. Vitamin D receptor agonists are known to suppress parathyroid hormone (PTH) secretion. We examined the effect of oral paricalcitol on posttransplant secondary hyperparathyroidism by conducting an open label randomized trial in which 100 incident kidney transplant recipients were randomized 1:1 to receive oral paricalcitol, 2 μg per day, for the first year posttransplant or no additional therapy. Serial measurements of serum PTH, calcium and bone alkaline phosphatase, 24-h urine calcium and bone density were performed. The primary endpoint was the frequency of hyperparathyroidism 1-year posttransplant. Eighty-seven patients completed the trial. One-year posttransplant, 29% of paricalcitol-treated subjects had hyperparathyroidism compared with 63% of untreated patients (p = 0.0005). Calcium supplementation was discontinued in two control and 15 treatment patients due to mild hypercalcemia or hypercalcuria. Paricalcitol was discontinued in four patients due to hypercalcuria/ hypercalcemia and in one for preference. Two subjects required decreasing the dose of paricalcitol to 1 μg daily. Hypercalcemia was asymptomatic and reversible. Incidence of acute rejection, BK nephropathy and renal function at 1 year were similar between groups. Moderate renal allograft fibrosis was reduced in treated patients. Oral paricalcitol is effective in decreasing posttransplant hyperparathyroidism and may have beneficial effects on renal allograft histology. Paricalcitol decreases the prevalence of post-kidney transplant hyperparathyroidism and may have beneficial effects on renal allograft histology.

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