Backgroundand Aims: Calcium-containing phosphate binders have been shown to increase the progression of vascular calcification in hemodialysis patients. This is a prospective study that compares the effects of calcium acetate and sevelamer on coronary calcification (CAC) and bone histology. Methods: 101 hemodialysis patients were randomized for each phosphate binder and submitted to multislice coronary tomographies and bone biopsies at entry and 12 months. Results: The 71 patients who concluded the study had similar baseline characteristics. On follow-up, the sevelamer group had higher levels of intact parathyroid hormone (498 ± 352 vs. 326 ± 236 pg/ml, p = 0.017), bone alkaline phosphatase (38 ± 24 vs. 28 ± 15 U/l, p = 0.03) and deoxypyridinoline (135 ± 107 vs. 89 ± 71 nmol/l, p = 0.03) and lower LDL cholesterol (74 ± 21 vs. 91 ± 28 mg/dl, p = 0.015). Phosphorus (5.8 ± 1.0 vs. 6 ± 1.0 mg/dl, p = 0.47) and calcium (1.27 ± 0.07 vs. 1.23 ± 0.08 mmol/l, p = 0.68) levels did not differ between groups. CAC progression (35 vs. 24%, p = 0.94) and bone histological diagnosis at baseline and 12 months were similar in both groups. Patients of the sevelamer group with a high turnover at baseline had an increase in bone resorption (eroded surface, ES/BS = 9.0 ± 5.9 vs. 13.1 ± 9.5%, p = 0.05), whereas patients of both groups with low turnover at baseline had an improvement in bone formation rate (BFR/BS = 0.015 ± 0.016 vs. 0.062 ± 0.078, p = 0.003 for calcium and 0.017 ± 0.016 vs. 0.071 ± 0.084 μm³/μm²/day, p = 0.010 for sevelamer). Conclusions: There was no difference in CAC progression or changes in bone remodeling between the calcium and the sevelamer groups.

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Diabetes complications and osteoporotic fractures are two of the most important causes of morbidity and mortality in older patients and share many features including genetic susceptibility, molecular mechanisms, and environmental factors. Type 2 diabetes mellitus (T2DM) compromises bone microarchitecture by inducing abnormal bone cell function and matrix structure, with increased osteoblast apoptosis, diminished osteoblast differentiation, and enhanced osteoclast-mediated bone resorption. The linkage between these two chronic diseases creates a possibility that certain antidiabetic therapies may affect bone quality. Both glycemic and bone homeostasis are under control of common regulatory factors. These factors include insulin, accumulation of advanced glycation end products, peroxisome proliferator-activated receptor gamma, gastrointestinal hormones (such as the glucose-dependent insulinotropic peptide and the glucagon-like peptides 1 and 2), and bone-derived hormone osteocalcin. This background allows individual pharmacological targets for antidiabetic therapies to affect the bone quality due to their indirect effects on bone cell differentiation and bone remodeling process. Moreover, it’s important to consider the fragility fractures as another diabetes complication and discuss more deeply about the requirement for adequate screening and preventive measures. This review aims to briefly explore the impact of T2DM on bone metabolic and mechanical proprieties and fracture risk.

Background and objectives: As well as being a marker of body iron stores, serum ferritin (sFerritin) has also been shown to be a marker of inflammation in hemodialysis (HD) patients. The aim of this study was to analyze whether sFerritin is a reliable marker of the iron stores present in bone marrow of HD patients.Design: Histomorphometric analysis of stored transiliac bone biopsies was used to assess iron stores by determining the number of iron-stained cells per square millimeter of bone marrow.Results: In 96 patients, the laboratory parameters were hemoglobin ‫؍‬ 11.3 ؎ 1.6 g/dl, hematocrit ‫؍‬ 34.3 ؎ 5%, sFerritin ‫؍‬ 609 ؎ 305 ng/ml, transferrin saturation ‫؍‬ 32.7 ؎ 22.5%, and C-reactive protein (CRP) ‫؍‬ 0.9 ؎ 1.4 mg/dl. sFerritin correlated significantly with CRP, bone marrow iron, and time on HD treatment (P ‫؍‬ 0.006, 0.001, and 0.048, respectively). The independent determinants of sFerritin were CRP (␤-coef ‫؍‬ 0.26; 95% CI ‫؍‬ 24.6 to 132.3) and bone marrow iron (␤-coef ‫؍‬ 0.32; 95% CI ‫؍‬ 0.54 to 2.09). Bone marrow iron was higher in patients with sFerritin >500 ng/ml than in those with sFerritin <500 ng/ml. In the group of patients with sFerritin <500 ng/ml, the independent determinant of sFerritin was bone marrow iron (␤-coef ‫؍‬ 0.48, 95% CI ‫؍‬ 0.48 to 1.78), but in the group of patients with sFerritin >500 ng/ml, no independent determinant of sFerritin was found.Conclusions: sFerritin adequately reflects iron stores in bone marrow of HD patients.

1.000pg/mL foi de 3.463 (10,7%). Em 49 (21,7%) CD não é possível encaminhar os pacientes para PTx. Cerca de 40% dos serviços que realizam PTx são ligados a centros universitários. Em 74 (33%) CD o tempo de espera para que um paciente seja operado é superior a 6 meses. Foram contabilizados 68 serviços que realizam PTx. Os principais problemas relacionados para a realização de PTx foram: dificuldades com a realização dos exames pré-operatórios, escassez de cirurgiões de cabeça e pescoço, e longa fila de espera. CONCLUSÕES: a prevalência de HPS grave é elevada em nosso meio. Uma parcela significativa de pacientes não tem acesso ao tratamento cirúrgico. Uma melhor organização das políticas de saúde pública, além de um maior entrosamento entre nefrologistas e cirurgiões de cabeça e pescoço, em torno dessa questão, são necessários para a mudança dessa realidade.]]>