Author/Editor     Avberšek-Lužnik, Ivica; Malešič, Ivan; Rus, Igor; Marc, Janja
Title     Increased levels of osteoprotegerin in hemodialysis patients
Type     članek
Source     Clin Chem Lab Med
Vol. and No.     Letnik 40, št. 10
Publication year     2002
Volume     str. 1019-23
Language     eng
Abstract     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-KB 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 yearsl. 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 lowPTH group. OPG correlated weakly with bALP (r = 0.277, p= 0.1531, as well as with CTx (r = 0.018, p = 0.929) in the low-PTH group, and there was an insignificant negative correlation in the high-PTH group (r = -0.145, p 0.593 and r =-0.279, p = 0.416, respectivelyl. 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.
Descriptors     KIDNEY FAILURE, CHRONIC
GLYCOPROTEINS
HEMODIALYSIS
RENAL OSTEODYSTROPHY
RECEPTORS, CYTOPLASMIC AND NUCLEAR
AGE FACTORS
SEX FACTORS
ALKALINE PHOSPHATASE
COLLAGEN
PARATHYROID HORMONES
PEPTIDE FRAGMENTS