Bone turnover correlates with bone quantity but not bone microarchitecture in chronic hemodialysis.

INTRODUCTION: In chronic hemodialysis, high-turnover bone disease was associated with decreased bone mineral density (BMD), poor bone quality (chemical and structural), and increased fracture risk. Our aim was to correlate bone turnover markers (BTMs) with bone microarchitecture measured by trabecular bone score (TBS) before and after correction for BMD. MATERIALS AND METHODS: We measured lumbar spine (LS), femoral neck, and 1/3 radius BMD and LS TBS by dual X-ray absorptiometry in 81 patients on permanent hemodialysis. Bone turnover was assessed using serum parathyroid hormone, osteocalcin, C-terminal crosslaps of type 1 collagen, procollagen 1 N-terminal propeptide (P1NP), and alkaline phosphatase (ALP). No patient had any partial or total parathyroidectomy and no previous or current treatment with anti-osteoporotic drugs. RESULTS: All BTMs correlated significantly with each other. Univariate regressions showed significant negative correlations between BTMs and BMD (best r = - 0.53, between P1NP and 1/3 radius Z-score) or BTMs and TBS (best r = - 0.27, p < 0.05 between ALP and TBS T-score). TBS correlated significantly with BMD at all three sites (best r = 0.5, between LS BMD and TBS T-score). Multivariate regression showed that TBS, crude or adjusted, correlated with LS BMD. No model retained any of the BTMs as independent variables due to the better prediction of BMD and multicollinearity. CONCLUSION: We showed a progressively impaired bone microarchitecture with increasing bone turnover in chronic hemodialysis. However, this correlation is no longer present when controlling for bone mass. This suggests that impaired bone microarchitecture and increased fracture risk are dependent upon factors other than high bone turnover.

Chronic hemodialysis is associated with lower trabecular bone score, independent of bone mineral density: a case-control study.

We measured trabecular bone score (TBS) in 98 patients on permanent hemodialysis (HD) and 98 subjects with similar bone mineral density and normal kidney function. TBS was significantly lower in HD patients, indicating deteriorated bone microarchitecture, independent of bone mass. This might partially explain the increased fracture risk in HD. PURPOSE: In the general population, trabecular bone score (TBS) was shown to predict fracture independent of bone mineral density (BMD). In end-stage renal disease patients on hemodialysis (HD), the value of TBS is beyond that of BMD in currently unclear. Our aim was to assess lumbar spine (LS) TBS in HD patients compared with subjects with normal kidney function matched for age, sex, and LS BMD. METHODS: We assessed TBS and LS and femoral neck (FN) BMD in 98 patient on permanent HD (42.8% males; mean age 57.5 ± 11.3 years; dialysis vintage 5.5 ± 3.8 years) and 98 control subjects (glomerular filtration rate > 60 mL/min) using DXA. We simultaneously controlled for sex, age (± 3 years), and LS BMD (± 0.03 g/cm2). RESULTS: HD patients had significantly lower LS TBS (0.07 [95% CI 0.03-0.1]; p = 0.0004), TBS T-score (0.83 SD [95% CI 0.42-1.24]; p = 0.0001)) and TBS Z-score (0.81 SD [95% CI 0.41-1.20]; p = 0.0001) than matched controls. TBS significantly correlated with LS BMD in both HD patients (r = 0.382; p = 0.001) and controls (r = 0.36; p = 0.002). The two regression lines had similar slopes (0.3 vs. 0.28; p = 0.84) with different intercepts (0.88 vs. 0.98). TBS adjustment significantly increased the 10-year fracture risk from 3.7 to 5.3 for major osteoporotic fracture and from 0.9 to 1.5 for hip fracture. CONCLUSIONS: HD patients have lower TBS than controls matched for LS BMD, indicating altered bone microarchitecture. Also, the magnitude of TBS reduction in HD patients is constant at any LS BMD. Adjustment for TBS partially corrects the absolute 10-year fracture risk.

The impact of basal insulin analogues on glucose variability in patients with type 2 diabetes undergoing renal replacement therapy for end-stage renal disease.

PURPOSE: We aimed to analyze the impact of basal insulin analogues on glucose variability (GV) in patients with type 2 diabetes (DM) undergoing renal replacement therapy. METHODS: Fourteen subjects on insulin therapy for at least 6 months (detemir, n = 7 vs. glargine, n = 7) were sequentially enrolled in this prospective study. Continuous glucose monitoring system (CGMS Gold, Dex Com 7+) was applied for 5 days, over 3 consecutive sessions of hemodialysis (HD). Various glycemic profiles (coefficient of variation-CV of mean glucose) were compared between the day on (HD-on) and the day off (HD-off) dialysis. The CV of at least 3 values of HbA1c (HPLC) since replacement therapy has been applied to assay the long-term GV. Endogenous insulin and insulin resistance (HOMA using fasting glucose and C-peptide levels), fasting lipid profile, quantitative C-reactive protein (CRP) and ferritin (values adjusted for Hb) were measured in serum at inclusion. RESULTS: The overnight HD-off and HD-on short-term (CV CGMS) GV, overall long-term (CV of HbA1c) GV, CRP and ferritin were reduced in subjects treated with detemir (paired t test, p = 0.0001, 0.0011, 0.036, <0.001, and <0.001 between groups). All participants were insulin-resistant (HOMA-IR > 3). CONCLUSIONS: Insulin-resistant patients with type 2 diabetes undergoing hemodialysis for end-stage renal disease on insulin detemir exhibit lower glycemic variability and pro-inflammatory profile than with insulin glargine.