#2140 Association between bone mineral density and C-reactive protein in patients with kidney failure

Abstract Background and Aims Mounting evidence suggests that inflammation contributes to bone mineral density (BMD) loss, not only in patients with chronic autoimmune conditions but also in postmenopausal women. Chronic kidney disease (CKD) is also a state of low-grade systemic inflammation. A plethora of endogenous and exogenous mediators seems to be involved, with metabolic endotoxemia gaining much interest in recent years. This study explores the association between metabolic endotoxemia, inflammation and bone mass in patients with kidney failure. Method This cross-sectional observational study included patients with kidney failure eligible for kidney transplantation. Data on demographics, comorbidities, parameters of mineral and bone disorder, high-sensitivity C-reactive protein (CRP, as a marker of inflammation), lipopolysaccharide-binding protein (LBP, as a marker of metabolic endotoxemia), plasma bone turnover markers (BALP, iPINP and TRAP5b by IDS-iSYS) and bone mineral density (BMD), assessed by Dual-energy X-ray absorptiometry (DXA) at lumbar spine (LS), total hip (TH), femoral neck (FN), 1/3 distal radius and ultradistal radius, were collected. Univariate and multivariate analyses were conducted to investigate the determinants of bone loss and inflammation. Results The cohort included 649 patients (age 57 ± 12 years, 63% male). Median CRP was 3 (IQR 1, 7) mg/L and median LBP (subset only, n = 190) was 19 (14, 23) . Higher BMI and elevated LBP were associated with increased CRP (P < 0.01), independently of age and sex. High CRP was a risk factor for low BMD at all skeletal sites, after adjustment for traditional risk factors (age, BMI, sex) and PTH, remaining significant at all sites except LS after additional adjusting for any of the bone turnover markers BALP, iPINP or TRAP5b. Interestingly, the inverse association between CRP and BMD was only revealed after adjusting for BMI (Table 1 ). Conclusion CRP emerged as a significant risk factor for low bone mass in patients with kidney failure, particularly when adjusting for BMI. While obesity is linked to higher BMD, through estrogen production from adipocytes and increased skeletal loading, obesity is also associated with chronic low-grade inflammation, underscoring the complex relationship between inflammation, BMI, and bone mass (Fig. 1 ). Present findings call for additional studies exploring the link between metabolic endotoxemia and bone health.