We do not appreciate a significant relationship between 25 (OH) D3 levels and glucose control or OPF. Therefore, more studies are needed to identify the specific effect of 25 (OH) D3 in T2DM physiopathology.

Background The 2017 KDIGO guidelines establish a 2B grade recommendation in favor of testing Bone Mineral Density (BMD) by DXA to assess osteoporotic fracture (OPF) risk in patients with CKD G3a-G5D. Still, controversy remains because large studies evaluating it for this particular population are lacking. Aim To establish the clinical performance of BMD measured by DXA in the evaluation of fracture risk in women with CKD. Methods We conducted a 43 year retrospective cohort study with 218 women ≥18 years-old with CKD and BMD measurement by DXA of total hip and lumbar spine. Clinical (age, year of CKD onset, comorbidities, BMI, transplant status, treatment), and biochemical (PTH, corrected calcium, phosphate, vitamin D [25 (OH) D3], creatinine, and albumin), parameters were collected from hospital records. All osteoporotic fractures (as defined by the WHO) found in the clinical and radiologic files were registered. Results 218 women with a median age of 60 years (40–73 IQ range) and a CKD evolution time of 12 years (7–18 IQ range) were evaluated. Forty-eight (28.23%) presented an OPF. These women were older (57 vs 69 years, p =0.0072) and had a lower BMD. CKD stage did not influence fracture incidence. In the multivariate analysis we found that for each standard deviation decrease in hip and lumbar spine T-Score, the overall fracture risk was 2.7 and 2.04 times higher, respectively. More than 50% of fractures took place within the first ten years of follow-up, especially with GFR <30 mL/min/m 2 and osteoporosis. Diabetes and hypothyroidism accelerated fracture onset, while renal transplant delayed it. In the ROC analysis, the AUC was largest with the total hip (0.7098, p = 0.000 ) and lumbar spine (0.6916, p = 0 .000 ). Conclusions BMD measured by DXA is a useful fracture prediction tool for women with CKD, having a sensibility and specificity similar to that in the general population. It seems to be appropriate for the diagnosis, treatment decisions, and follow-up of patients with renal failure.

This cohort study analyzes the association of grit scores with treatment adherence, as measured with a survey and biomarker levels, among patients with type 2 diabetes.

Background: Various studies suggest that perioperative concentrations of high-sensitivity troponins are incremental and predictive factors of a major adverse cardiac event (MACE) and all-cause mortality. Objective: The objective of the study was to evaluate the predictive value of high-sensitivity cardiac troponin I (hs-cTnI) in the development of MACE and all-cause mortality, within 30-days and 1-year follow-up after noncardiac surgery. Methods: In this prospective cohort study, we included men ≥ 45 years and women ≥ 55 years with ≥ 2 cardiovascular risk factors and undergoing intermediate or high-risk noncardiac surgery. Demographic and clinical information was collected from clinical charts. We measured baseline hs-cTnI 24 h before surgery, and its post-operative concentration 24 h after surgery. Results: In the entire sample, 8 patients (8.6%) developed MACE at 30-days follow-up (4 deaths), 12 (12.9%) within the 1 st year (7 deaths), and 17 (18.2%) after complete post-surgical follow-up (10 deaths). We observed higher baseline and post-operative concentrations in patients who presented MACE (12 pg/ml vs. 3.5 pg/ml; p = 0.001 and 18.3 pg/ml vs. 5.45 pg/ml; p = 0.009, respectively). The hazard ratios (HRs) calculated by Cox regression analysis between the hs-cTnI baseline concentration and the post-operative development of MACE at 30-days and 1-year were 5.70 (95% confidence interval [CI], 1.10-29.40) with hs-cTnI > 6.2 pg/ml and 12.86 (95% CI, 1.42-116.34) with hs-cTnI > 3.3 pg/ml, respectively. The estimated post-operative HR death risk at 1-year was 14.43 (95% CI, 1.37-151.61) with hs-cTnI > 4.5 pg/ml. Conclusions: Pre-operative hs-cTnI was an independent predictive risk factor for MACE at 30-days and 1-year after noncardiac surgery and for all-cause mortality at 1-year after noncardiac surgery. (REV INVEST CLIN. 2020;72(2):110-8)