RESUMO
Background: Blood eosinophils can increase in response to infection, inflammation, and hypersensitivity reactions, yet their involvement in the progression of chronic kidney disease (CKD) is poorly understood. This study explores the relationship between blood eosinophils and CKD progression among patients in a real-world setting. Methods: This retrospective study analyzed data obtained from the Optum® de-identified electronic health records dataset in the United States. Patients diagnosed with CKD stage 3 or 4 (International Classification of Diseases diagnosis code or estimated glomerular filtration rate [eGFR] <60 mL/min) between January 2011 and March 2018 were included and followed until progression to the next CKD stage, death, or dropout. The primary objective of this study was to assess the relationship between blood eosinophil counts (bEOS) and CKD progression, adjusting for clinical and demographic features as well as known risk factors for CKD stages 3-4. The primary outcomes were CKD progression and all-cause mortality. Results: We found that high eosinophilic levels (bEOS ≥300 cells/µL) were associated with CKD progression from stage 3 to stages 4 or 5 (hazard ratio [HR] ranging from 1.30 to 1.50) and from stages 4 to 5 (HR ranging from 1.28 to 1.50). Among patients with CKD progression, those with blood eosinophils ≥300 cells/µL appeared to have a relatively lower eGFR, higher all-cause mortality, and reduced time to CKD progression and death than those with <300 cells/µL. Factors including sex, race, hypertension, anemia, and treatments for cardiovascular and hematopoietic drugs were associated with CKD progression. Conclusion: Elevated eosinophils may increase the risk for CKD progression. Larger studies are needed to assess whether the risk of mortality is increased among patients with elevated eosinophils.
RESUMO
To evaluate the efficacy of the polylactide-polyglycolide copolymer Fisiograft® as a bone graft material in the treatment of interproximal intrabony defects clinically and radiographically. Methods: A total of 22 intrabony defects in 8 patients with chronic periodontitis (4 males and 4 females) aged 20 to 55 years were recruited and divided equally into two groups: control (open flap debridementalone) and experimental (open flap debridement with Fisiograft®). Recordings of probing pocket depth (PPD), clinical attachment level (CAL), gingival margin position (GMP) and radiovisiographic assessment was done at baseline and 6 months. Results: Statistical analysis was done by Wilcoxon Signed Rank test for intra-group comparisons and Mann-Whitney U-test for inter-group comparisons. The clinical parameters PPD, CAL and GMP were found to be statistically significant(p<0.05) within each group. Inter-group comparison showed only the CAL gain to be statistically significant (p<0.01). In relation to hard tissue changes, statistically significant (p=0.05) result was seen for the percent filling of the original defect, comparing the experimental and control groups 6 months postoperatively. Conclusions: Placement of Fisiograft® resulted in better healing of intrabony defects as assessed clinically and radiographically when compared to open flap debridement alone.