NO TREND TOWARD A SPONTANEOUS IMPROVEMENT OF HYPERPARATHYROIDISM AND HIGH BONE TURNOVER IN NORMOCALCEMIC LONG-TERM RENAL-TRANSPLANT RECIPIENTS

Citation
G. Dumoulin et al., NO TREND TOWARD A SPONTANEOUS IMPROVEMENT OF HYPERPARATHYROIDISM AND HIGH BONE TURNOVER IN NORMOCALCEMIC LONG-TERM RENAL-TRANSPLANT RECIPIENTS, American journal of kidney diseases, 29(5), 1997, pp. 746-753
Citations number
50
Categorie Soggetti
Urology & Nephrology
ISSN journal
02726386
Volume
29
Issue
5
Year of publication
1997
Pages
746 - 753
Database
ISI
SICI code
0272-6386(1997)29:5<746:NTTASI>2.0.ZU;2-B
Abstract
Although hyperparathyroidism is a common feature in renal transplant r ecipients, the long-term course of parathyroid hormone (PTH) secretion in these patients is not well established, and the actual contributio n of PTH to posttransplant bone disease remains incompletely understoo d. Therefore, we studied calcium-regulating hormones and serum osteoca lcin, as a marker of bone remodeling, in 82 normocalcemic renal transp lant recipients with good renal function who had received a graft 6 to 73 months previously and in 82 healthy subjects matched for age and s ex. In all subjects, fasting serum and 24-hour urinary samples were co llected. 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 mu g/L v 8.0 +/- 0.3 mu g/L; P < 0.001). (Values are mean +/- SEM.) I n addition, transplant recipients had a slightly higher ionized calciu m than the healthy subjects, providing definite evidence of an inappro priate PTH secretion in renal transplant recipients. Furthermore, in s ubgroups of 25 recipients and 25 healthy controls matched for creatini ne clearance, the results superimposed those obtained in the whole gro ups, suggesting that excessive PTH secretion and high bone turnover in renal transplant recipients did not merely reflect the moderately red uced renal function of some recipients. In the whole group of transpla nt recipients, PTH correlated positively with osteocalcin (r = 0.40; P < 0.001), suggesting that PTH contributes at least partly to posttran splant bone disease. Conversely, there was no correlation between seru m PTH or osteocalcin and the delay from grafting. Therefore, our resul ts provide no evidence for a spontaneous improvement of either persist ent hyperparathyroidism or high bone turnover in normocalcemic long-te rm renal transplant recipients. (C) 1997 by the National Kidney Founda tion, Inc.