Background: Many studies have evaluated the association between matrix metalloproteinase 9 (MMP9) gene promoter polymorphism and diabetic microvascular complications. However, the results are conflicting and inconclusive. The aim of this meta-analysis was to evaluate the association more precisely. Materials and Methods: Studies were retrieved from the PubMed, Embase, Medline, China National Knowledge Infrastructure, Web of Science, and Cochrane databases. All statistical analyses were performed using Review Manager 5.2. Results: Data were abstracted from four case-control studies that included 446 patients with diabetic microvascular complications and 496 diabetic control subjects. The MMP9-1562 C/T genotype was significantly associated with the risk of diabetic nephropathy after stratification by specific type of microvascular complication (CT + TT vs. CC: OR = 0.42, 95% CI = 0.26–0.69, p = 0.0006; TT vs. CC + CT: OR = 0.37, 95% CI = 0.19–0.76, p = 0.006). Conclusions: This study adds to the evidence that MMP9-1562 T gene mutation might reduce the risk of diabetic nephropathy.

Chemokine ligand 5 (CCL5) is a member of the CC-chemokine family expressed in various organs. It contributes to the migration of monocytes/macrophages into injured vascular walls by binding with its receptor chemokine receptor 5 (CCR5). Many studies have accessed the association between CCL5/CCR5 gene promoter polymorphisms and diabetic microvascular complications (DMI). However, the results are conflicting and inconclusive. The aim of the present study was to evaluate the association more precisely. Trials were retrieved through PubMed, Embase, Medline, China National Knowledge Infrastructure, Web of Science and Cochrane database without restrictions on language. The pooled odds ratio (OR) and 95% confidence interval (CI) were used to describe the strength of association with DMI. Data were obtained from 11 case-control studies that included 2,737 DMI patients and 2,435 diabetic control subjects. In the overall analysis, the CCL5-403 G/A and CCL5-28 C/G gene polymorphisms were not significantly associated with the risk of DMI. However, CCR5-59029 G/A was an independent risk factor of DMI in a dominant model (OR 1.77, 95% CI 1.06-2.97). Subgroup analysis showed that the risk of the CCR5 59029A-positive genotype was significant in Asians (OR 2.08, 95% CI 1.68-2.57). In addition, the CCR5 59029A-positive genotype was associated with increased risk of albuminuria. There were no associations of CCL5 gene promoter polymorphism with the risk of DMI. However, the 59029A polymorphism in CCR5 might affect individual susceptibility for DMI.

Purpose: Uric acid and blood glucose are important indicators of metabolic disorders. Numerous studies have elucidated the association between them, but the focus on their relationship through examination of urinary glucose and uric acid excretion has been limited. In this study, we conducted a comprehensive analysis on these indicators to explain the relationship. Patients and Methods: This study involved the recruitment of 2498 patients who underwent fractional excretion of uric acid (FEUA) testing during their hospitalization at the Health Department of Qilu Hospital (Qingdao), Shandong University, between January 2017 and November 2023, with 1416 subjects being included in the final analysis. The included subjects were analyzed based on different genders. One-way analysis of variance, multiple linear regression analysis, and restricted cubic spline were adopted for data analysis. Results: Higher FEUA and lower serum uric acid (SUA) levels were observed in diabetic patients with urinary glucose than in diabetic patients without urinary glucose and the nondiabetic population. FEUA exhibited a proportional increase with elevated blood glucose levels, even including cases that lacked urinary glucose. After adjustment for potential confounding factors, SUA levels did not increase with the increase in fasting blood glucose (FBG) levels, and once FBG levels surpassed a certain threshold leading to glucosuria, FEUA was further elevated, accompanied with a subsequent reduction in SUA levels. There is a stronger linear relationship between SUA or FEUA and FBG levels in women than that in men after adjusting for confounding factors. Conclusion: Hyperglycemia is not considered a risk factor for hyperuricemia. Regardless of the presence of urinary glucose, elevated blood glucose levels can stimulate renal excretion of uric acid. Upon reaching a threshold that induces glucosuria, the SUA levels decrease substantially. Meanwhile, there are some differences in the relationship between SUA or FEUA and FBG among different genders.