Abstract
Background: The prevalence of low- turnover bone disease (LTBD) in peritoneal dialysis (PD) patients is higher than in hemodialysis (HD) patients. LTBD patients may be at risk for vascular calcification, and cardiovascular disease. Current therapy for chronic kidney disease metabolic bone disorders (CKD-MBD) is guided by biochemical parameters, as bone biopsy is not used in routine clinical care.Methods: We assessed intact PTH (iPTH: 1-84PTH plus non-1-84PTH), 1-84PTH, and the 1-84PTH/non-1-84PTH ratio in 129 hemodialysis and 73 PD prevalent patients dialyzed with solutions containing 1.75 mmol/L calcium.Results: Hemodialysis and PD patients presented similar iPTH and tCa values and prevalence of putative LTBD as defined according to KDOQI iPTH cut-off levels or 1-84 PTH levels. However, iCa accounted for a higher percentage of tCa in PD (53%) than in hemodialysis (39%) p < 0.001, and the 1-84PTH/non-1-84PTH ratio was lower in PD than in hemodialysis patients (0.44 ± 0.12) vs. (0.60 ± 0.10), p < 0.001. The prevalence of putative LTBD when using the coexistence of 1-84PTH/non-1-84PTH ratio < 1.0 and iPTH < 420 pg/m, was higher in PD than in hemodialysis patients (73 vs. 16% respectively, p < 0.001). In a multivariate logistic regression analysis, dialysis modality was the main determinant of the 1-84PTH/non-1-84PTH ratio.Conclusion: Solutions containing 1.75 mmol/L calciums are associated to a higher proportion of non-1-84PTH fragments in PD than in HD patients. Different analytical criteria result in widely different estimates of LTBD prevalence, thus impairing the ability of clinicians to optimize therapy for CKD-MBD.
Highlights
Bone disorders in patients with chronic kidney disease (CKD) encompass high and low turnover bone disease (HTBD and low- turnover bone disease (LTBD)) (Moe et al, 2006)
Intraglandular aminoterminal degradation is regulated by extracellular ionic calcium concentration, which suppresses the release of 1-84 PTH and increases the release of 7-84 PTH fragments from parathyroid cells (Kawata et al, 2005; Friedman and Goodman, 2006)
The aims of the present study were to investigate whether there are any differences in the distribution of circulating PTH fragments in peritoneal dialysis (PD) vs. HD patients, and we wanted to determine any relationship between PTH fragments and metabolic markers of bone turnover such as the serum Carboxy-terminal telopeptides of collagen type I, a marker of bone resorption (Bonde et al, 1995); as well as the possible role of PTH fragments in bone remodeling
Summary
Bone disorders in patients with chronic kidney disease (CKD) encompass high and low turnover bone disease (HTBD and LTBD) (Moe et al, 2006). It has been established knowledge that PTH is present in uremic serum in different PTH fragments with variable half-life (Martin et al, 1979). Some of these fragments may even behave as antagonists of the PTH receptor (Langub et al, 2003; Huan et al, 2006). Second-generation iPTH assays in widespread clinical use recognize both the full-length molecule (1-84 PTH) and PTH fragments of different sizes missing N-terminal aminoacids, including a 7-84 PTH molecule. Current therapy for chronic kidney disease metabolic bone disorders (CKD-MBD) is guided by biochemical parameters, as bone biopsy is not used in routine clinical care
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
