Although
hyperparathyroidism is a common feature in renal transplant recipients, the long-term course of
parathyroid hormone (PTH) secretion in these patients is not well established, and the actual contribution of PTH to posttransplant
bone disease remains incompletely understood. Therefore, we studied
calcium-regulating hormones and serum
osteocalcin, as a marker of bone remodeling, in 82 normocalcemic renal transplant recipients with good renal function who had received a graft 6 to 73 months previously and in 82 healthy subjects matched for age and sex. In all subjects, fasting serum and 24-hour urinary samples were collected. The transplant recipients had excessive PTH secretion (serum PTH, 6.9 +/- 0.5 pmol/L in recipients v 3.0 +/- 0.1 pmol/L in healthy subjects; P < 0.001) and high bone turnover (
osteocalcin, 16.6 +/- 0.8 microg/L v 8.0 +/- 0.3 microg/L; P < 0.001). (Values are mean +/- SEM.) In addition, transplant recipients had a slightly higher ionized
calcium than the healthy subjects, providing definite evidence of an inappropriate PTH secretion in renal transplant recipients. Furthermore, in subgroups of 25 recipients and 25 healthy controls matched for
creatinine clearance, the results superimposed those obtained in the whole groups, suggesting that excessive PTH secretion and high bone turnover in renal transplant recipients did not merely reflect the moderately reduced renal function of some recipients. In the whole group of transplant recipients, PTH correlated positively with
osteocalcin (r = 0.40; P < 0.001), suggesting that PTH contributes at least partly to posttransplant
bone disease. Conversely, there was no correlation between serum PTH or
osteocalcin and the delay from grafting. Therefore, our results provide no evidence for a spontaneous improvement of either persistent
hyperparathyroidism or high bone turnover in normocalcemic long-term renal transplant recipients.