Decreased urine uric acid excretion is an independent risk factor for chronic kidney disease but not for carotid atherosclerosis in hospital-based patients with type 2 diabetes: A cross-sectional study
Li L.-X.,Shanghai JiaoTong University |
Wang A.-P.,The 454th Hospital of Chinese PLA |
Zhang R.,Shanghai JiaoTong University |
Li T.-T.,Shanghai JiaoTong University |
And 3 more authors.
Cardiovascular Diabetology | Year: 2015
Background: The associations between urine uric acid excretion (UUAE) and chronic kidney disease (CKD)/atherosclerosis have not been investigated. Our aims were to investigate the relationships between UUAE and CKD and carotid atherosclerotic lesions in hospitalized Chinese patients with type 2 diabetes. Methods: This was a cross-sectional study that was conducted with 2627 Chinese inpatients with type 2 diabetes. UUAE was determined enzymatically using a single 24-h urine collection. The subjects were stratified into quartiles according to their UUAE levels. Carotid atherosclerotic lesions, including carotid intima-media thickness (CIMT), plaque and stenosis, were assessed by Doppler ultrasound. Both CKD and carotid atherosclerotic lesions were compared between the UUAE quartile groups. Results: After adjustment for confounding factors, there was a significant decrease in the prevalence of CKD in the patients with type 2 diabetes across the UUAE quartiles (16.9%, 8.5%, 5.9%, and 4.9%; p < 0.001). Multiple logistic regression analyses revealed that the UUAE quartiles were significantly and inversely associated with the presence of CKD (p < 0.001). Compared with the diabetics in the highest UUAE quartile, those in the lowest quartile exhibited a nearly 4.2-fold increase in the risk of CKD (95% CI: 2.272-7.568; p < 0.001). The CIMT value (0.91 ± 0.22 mm for the diabetics with CKD and 0.82 ± 0.20 mm for the diabetics without CKD, p = 0.001) and the prevalence of carotid plaques (62.1% for the diabetics with CKD and 41.8% for the diabetics without CKD, p = 0.025) were significantly higher in the diabetics with CKD than in those without CKD. However, there was no obvious difference in carotid atherosclerotic lesions across the UUAE quartiles after controlling for the confounding factors. Conclusions: Decreased UUAE was closely associated with the presence of CKD but not with carotid atherosclerotic lesions in hospitalized Chinese patients with type 2 diabetes. Our results suggest that UUAE is an independent risk factor for CKD in type 2 diabetes. In selected populations, such as patient with type 2 diabetes, the role of uric acid in atherosclerosis might be the result of other concomitant atherosclerotic risk factors, such as CKD. © Li et al.; licensee BioMed Central. Source
Gu X.-Y.,The 454th Hospital of Chinese PLA |
Shen S.-E.,The 454th Hospital of Chinese PLA |
Huang C.-F.,The 454th Hospital of Chinese PLA |
Liu Y.-N.,The 454th Hospital of Chinese PLA |
And 4 more authors.
Diabetes Research and Clinical Practice | Year: 2013
Aim: We aimed to evaluate the effectiveness of the application of activated autologous monocytes/macrophages (Mo/Mp) on wound healing in diabetic rats. Methods: Sixty male SD rats were equally divided into the following: control group (normal, nondiabetic), PBS-treated diabetic group, and tumor necrotic factor alpha (TNF-α) plus interferon-γ (IFN-γ)-stimulated or unstimulated Mo/Mp-treated diabetic group. Full-thickness round wounds (1. cm. ×. 1. cm) were created in the right hind foot of rats and the wounds were treated with PBS or Mo/Mp on day 1 after injury. In the following 14 days, the percentage of wound contraction was measured, histologic examination was performed with hematoxylin and eosin staining, and vascular endothelial growth factor (VEGF) in the wound was evaluated by Western blot analysis. Results: Diabetic rats exhibited impaired wound healing with delayed angiogenesis and VEGF expression. The early application of TNF-α plus IFN-γ-stimulated autologous Mo/Mp to diabetic wounds significantly improved the delayed wound healing through the stimulation of angiogenesis and re-epithelization, as well as restoring the defect in VEGF expression. Conclusions: Mo/Mp activated by TNF-α and IFN-γ promotes diabetic wound healing and normalizes the defect in VEGF regulation associated with diabetes-induced skin-repair disorders. © 2013 Elsevier Ireland Ltd. Source