Increased levels of osteoprotegerin in hemodialysis patients

被引:42
作者
Avbersek-Luznik, I
Malesic, I
Rus, I
Marc, J
机构
[1] Univ Ljubljana, Fac Pharm, Ljubljana 1000, Slovenia
[2] Gen Hosp Jesenice, Dept Clin Biochem, Jesenice, Slovenia
[3] Gen Hosp Jesenice, Dialysis Ctr, Jesenice, Slovenia
关键词
osteoclastogenesis inhibitory factor; receptor activator of nuclear factor-kappa B ligand : RANKL; renal osteodystrophy; beta-CrossLaps; bone alkaline phosphatase;
D O I
10.1515/CCLM.2002.177
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Recently identified soluble circulating osteoprotegerin (OPG), a member of tumor necrosis factor receptor family, is the osteoclastogenesis inhibitory factor (OCIF). It acts as a decoy receptor for receptor activator of NF-kappaB ligand (RANKL) and antagonises RANKL/RANK activity. This way OPG exerts the protective effect on bone, which is also important in hyperparathyroidism. The studies measuring OPG levels in secondary hyperparathyroidism have shown contradictory results and inconsistent conclusions. The aim of our work was to evaluate OPG levels in hemodialysis patients and their correlation with the intensity of bone turnover, bone formation and bone resorption. Serum OPG levels, bone alkaline phosphatase activity (bALP) and beta-CrossLaps (CTx) were measured in a control group (n = 20, age 30+/-6.7 years) and in two groups of dialysis patients: the first group with serum intact parathyroid hormone (iPTH) concentration below 200 pg/ml (n = 28, age 62.6+/-14.8 years) and the second group with iPTH concentration above 200 pg/ml (n = 16, age 63.7+/-14.8 years). Compared to controls, serum OPG levels were 6.4-fold higher in dialysis patients. OPG levels in patients with high PTH were approximately 1.2-fold higher than in the low PTH group. OPG correlated weakly with bALP (r = 0.277, p = 0.153), as well as with CTx (r = 0.018, p = 0.929) in the lowPTH group, and there was an insignificant negative correlation in the highPTH group (r = 0.145, p = 0.593 and r = 0.219, p = 0.416, respectively). In conclusion, 6.4-fold increase in OPG might protect bone against intensive bone loss in hemodialysis patients, but this increase is probably not mediated by the increased bone formation; rather, it seems to be the consequence of the imbalance of bone kinetics in renal disease. The precise role of OPG in the pathogenesis of renal osteodystrophy remains unknown and establishing it requires further studies.
引用
收藏
页码:1019 / 1023
页数:5
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