Association of the dietary inflammation index (DII) with the prevalence of chronic kidney disease in patients with type-2 diabetes mellitus.

Chronic kidney disease (CKD) is a major complication of diabetes mellitus (DM). Inflammation is an essential component in the process of CKD progression in patients with DM. Diet is a significant determinant of systemic inflammation levels. However, the association between the dietary inflammatory index (DII) and CKD in individuals with DM remains largely unknown; therefore, the aim of this study was to explore whether the DII is linked to the prevalence of CKD in patients with DM. The research method was as follows: first, data from the National Health and Nutrition Examination Survey (NHANES) between 1999 and 2018 were obtained. There were 7,974 participants in our study. These individuals were then classified into three groups according to DII tertiles (T1-T3), with each group consisting of 2,658 participants. Logistic regression analysis was employed to examine whether there was a connection between the DII and CKD. We observed a significant association between the DII and the prevalence of CKD in individuals with DM. After full adjustment for age, sex, ethnicity, smoking, drinking, body mass index (BMI), triglyceride (TG), total cholesterol (TC), metabolic equivalents (METs), energy intake, hypoglycemic medications, hypertension, and cardiovascular disease (CVD), the group with a higher DII had a greater frequency of CKD (T2 group: OR: 1.40; 95% CI: 1.10-1.76; p = 0.006; T3 group: OR: 1.67; 95% CI: 1.29-2.17; p < 0.001). The implementation of an anti-inflammatory diet could serve as an intervention strategy for patients with DM to prevent the onset of CKD.

Elevated serum procalcitonin level in patients with chronic kidney disease without infection: A case-control study.

BACKGROUND: Inflammation is a necessary component of chronic kidney disease (CKD) that can be attributed to an accumulation of toxins and a reduced clearance of proinflammatory cytokines. Procalcitonin (PCT) is a widely applied biomarker in the diagnosis of infection, and considering the presence of pre-existing inflammation in CKD patients, the PCT level could be high in such a population; however, no reference value for PCT in CKD patients has been available to date. METHODS: During the present study period, 361 CKD patients and 119 healthy controls were included. The PCT level and other biochemistry parameters were assayed by using a COBAS system. Statistical analysis was conducted to compare the differences in PCT levels and other biochemistry parameters between the two groups, and linear regression was used to assess the correlation between two variables. Receiver operating characteristic (ROC) curve analysis was performed to evaluate the performance of PCT and the optimal cutoff value to differentiate between CKD patients and healthy controls. RESULTS: The PCT level in CKD patients was significantly higher than that in healthy controls, and among the CKD patients, the PCT level was increased with advanced clinical stage. Moreover, PCT was moderately correlated with CysC. The optimal off-value was 0.075 with a sensitivity of 94.7% and specificity of 90.8%. CONCLUSION: The PCT level was significantly higher in CKD patients than in healthy controls, and the reference value for CKD patients should be adjusted to avoid unnecessary antibiotic treatments which may pose a negative impact on residual renal function.

Association between Toll-Like Receptor 4 Polymorphisms and Systemic Lupus Erythematosus Susceptibility: A Meta-Analysis.

Family aggregation was observed among systemic lupus erythematosus (SLE) cases, suggesting the genetic factor may contribute to the susceptibility. Toll-like receptors (TLR) play key role in human immune system; in order to gain better insight on the association between TLR4 polymorphisms and SLE risk, a meta-analysis was conducted. In total 4 case-control studies have been included, involving 503 SLE cases and 636 healthy controls. The association between TLR4 polymorphisms and SLE risk was evaluated by calculating pooled odd ratio (OR) and its 95% confidential interval (CI). The Q-test and I (2) statistic were used to estimate the degree of heterogeneity. Publication bias among enrolled studies was examined by using Egger's test and Begg's test. Overall, there was no evidence of positive association between SLE risk and D299G and T399I polymorphisms in TLR4. The meta-analysis reported a null association between TLR4 polymorphisms and SLE risk in included study populations, but the role of TLR4 polymorphisms in developing SLE among other populations remains undetermined. Moreover, some laboratory studies still discovered the involvement of TLR4 in SLE process. Therefore, the association between TLR4 polymorphisms and SLE risk requires further investigation both in laboratory and in epidemiological efforts.