Prognostic Value of Elevated Plasma Galectin-3 for Renal Adverse Events in Dialysis Patients: A Systematic Review and Meta-Analysis.

Context: In prognostic research, Galectin-3 (Gal-3) has gained recognition in renal fibrosis and nephrosis for its characteristics of promoting inflammation and fibrosis. High levels of Gal-3 may function as a predictor of adverse outcomes for patients with end-stage renal disease (ESRD). Objective: The review intended to systematically examine the significance of Gal-3 in the forecast of adverse outcomes for dialysis patients, using a method of evidence-based medicine. Design: The research team performed a systematic narrative review and meta-analysis by searching the Excerpta Medica Database (EMBASE) and the PubMed, Cochrane, and Web of Science databases for pertinent studies published before June 1, 2022. The search contained both meshes and free terms, such as Galectin 3, Gal-3, renal dialysis, hemodialysis, peritoneal dialysis, HD, and PD. Setting: The review took place at First People's Hospital of Linping District in Hangzhou, China. Outcome Measures: The research team used the Newcastle-Ottawa Scale (NOS) for assessment of the quality of the included research. The team created two reports to assess the value of Gal-3 in prediction of risk: (1) one for studies using continuous variables and (2) one for studies using categorical variables, dividing patients into high- and low-level Gal-3 groups with a cut-off value of Gal-3, being Gal-3 < 10.5 ng/mL for the lower tertile, and Gal-3 ≥ 13.4 ng/mL for the higher tertile. The team performed the meta-analysis using Stata 15.0, analyzed publication bias using Egger's test and directly showed it in a funnel plot. Results: The search found 1061 publications, with eight studies with 5194 participants being included in the current review. For the continuous variables, Gal-3 was associated with all-cause risk of death-Hazard ratio (HR) 1.06, 95%CI 1.01-1.12, and P = .024-and cardiovascular (CV) events-HR 1.13, 95%CI 1.07-1.203, and P = .000, but no significant correlation existed between Gal-3 and risk of CV mortality-HR 1.07, 95%CI 0.99-1.16, and P = .091. For the categorical variables, a high level of Gal-3 was correlated with a high risk of dying, from all causes-HR 2.05, 95%CI 1.50-2.80, and P = .000. Conclusions: Clinicians can use Gal-3 as a standalone forecaster of all-cause mortality and CV events for hemodialysis patients because correlates with these outcomes. Further research is necessary to determine its predictive value for CV mortality. Investigators need to perform further research with a large sample size on the predictive value of Gal-3 for dialysis patients, particularly PD patients, from a variety of ethnic backgrounds to improve the precise treatment for high-risk patients.

Identification of potential crosstalk genes and mechanisms between periodontitis and diabetic nephropathy through bioinformatic analysis.

Periodontitis and diabetic nephropathy are significant public health concerns globally and are closely related with each other. This study aimed to identify potential crosstalk genes, pathways, and mechanisms associated with the interaction between periodontitis and diabetic nephropathy. Expression profiles of periodontitis and diabetic nephropathy were retrieved from the Gene expression omnibus gene expression omnibus database, and differentially expressed genes (DEGs) were screened, followed by identification of co-expressed differential genes. Gene ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed using R software. A protein-protein interaction network was constructed via STRING website, and key crosstalk genes were selected using Cytoscape. Subsequent gene ontology and KEGG analyses were conducted for the key genes, and a validation dataset was obtained from the gene expression omnibus database for differential gene validation. The TRRUST website was employed to identify transcription factors (TFs) associated with the key crosstalk genes between periodontitis and diabetic nephropathy, followed by differential analysis of TFs. A total of 17 crosstalk genes were obtained. Among them, SAMSN1, BCL2A1, interleukin-19, IL1B, RGS1, CXCL3, CCR1, CXCR4, CXCL1, and PTGS2 were identified as key crosstalk genes between periodontitis and diabetic nephropathy. Additionally, 16 key TFs were discovered. This bioinformatic analysis revealed potential crosstalk genes between periodontitis and diabetic nephropathy. The identified key genes participate in signaling pathways, including cytokine signaling and chemokine signaling transduction, which might collectively influence these 2 diseases. These genes may serve as potential biomarkers guiding future research in this field.

Efficacy and Safety of Rituximab in the Treatment of Idiopathic Membranous Nephropathy: A Meta-Analysis.

Background: Primary membranous nephropathy (MN), sometimes referred to as idiopathic membranous nephropathy (IMN), is a kind of MN whose pathogenesis is yet unclear. According to research reports, the incidence of IMN is about 9.8-26.8%, and it is on the rise. Methods: The computer retrieves eight databases to obtain controlled trials at home and abroad on the rituximab (RTX) actions in IMN management. After a rigorous literature quality evaluation, software called RevMan 5.3 was used for data analysis. Results: This meta-analysis finally contained 8 papers. They were all regarded as controlled trials. Six studies reported serum creatinine (standardized mean difference [SMD]: -6.87; 95% CI: -14.09, 0.35; P = 0.062), ALB (SMD: 1.91; 95% CI: -0.31, 4.14; P = 0.092), and adverse reactions (OR: 0.56; 95% CI: 0.36, 0.90; P < 0.01), all of which were significantly higher in the test group than in the control group (OR: 1.37; 95% CI: 1.07, 1.76; P < 0.01). Conclusion: The overall effective rate, serum creatinine, adverse effects, and ALB of this trial indicate that RTX may be beneficial for individuals with IMN, but further high-quality research is required to confirm these findings.

Meta-Analysis of the Effectiveness and Safety of Glucocorticoid for the Treatment of IgA Kidney Disease.

Purpose: To explore the effect of glucocorticoid on immune globulin A (IgA) nephropathy by meta-analysis. Method: Search the data and literature libraries of ScienceDirect, EBSCO, Wiley, PubMed, CBMdisc, and CNKI and collect the literature on the treatment of IgA nephropathy with glucocorticoids as randomized controlled trials published at home and abroad from 1995 to 2021. The standardized mean difference (SMD) and 95% confidence interval (CI) were calculated by fixed-effects model. RevMan 5.0 software was used for meta-analysis of the subgroups of overall curative effect, different degree of proteinuria, different course of treatment, different creatinine level, and combined ACEI. Result: ① The overall efficacy of glucocorticoid in the treatment of IgA nephropathy was better than that in the control group (P = 0.00001). ② The efficacy of glucocorticoid treatment in patients with IgA nephropathy with proteinuria greater than 1.50 g/d and less than 1.50 g/d was better than that in the control group (P < 0.01). ③ For IgA nephropathy patients with serum creatinine less than 1.50 mg/dl, the curative effect of glucocorticoid treatment was better than that of the control group (P < 0.01). ④ The effects of short-term treatment (<1 year) and long-term treatment (≥1 year) with glucocorticoid were better than those in the control group (P < 0.01). ⑤ The effect of hormone combined with ACEI drugs on IgA nephropathy was more significant (P < 0.01). Conclusion: The overall efficacy of glucocorticoid in the treatment of IgA nephropathy is accurate. Hormone treatment is effective for different degrees of IgA nephropathy. Considering that there is no significant effect on the efficacy of different courses of treatment, it is suggested that the course of hormone treatment can be appropriately shortened. Hormone combined with angiotensin-converting enzyme inhibitors (ACEI) can reduce proteinuria more effectively than ACEI drugs alone.

Automatic epileptic seizure detection via Stein kernel-based sparse representation.

Epileptic seizure detection is of great significance in the diagnosis of epilepsy and relieving the heavy workload of visual inspection of electroencephalogram (EEG) recordings. This paper presents a novel method for seizure detection using the Stein kernel-based sparse representation (SR) for EEG recordings. Different from the traditional SR scheme that works with vector data in Euclidean space, the Stein kernel-based SR framework is constructed for seizure detection in the space of the symmetric positive definite (SPD) matrices, which form a Riemannian manifold. Due to the non-Euclidean geometry of the Riemannian manifold, the Stein kernel on the manifold permits the embedding of the manifold in a high-dimensional reproducing kernel Hilbert space (RKHS) to perform SR. In the Stein kernel-based SR framework, EEG samples are described by SPD matrices in the form of covariance descriptors (CovDs). Then, a test EEG sample is sparsely represented on the training set, and the test sample is classified as a member of the class, which leads to the minimum reconstructed residual. Finally, by using three widely used EEG datasets to evaluate the detection performance of the proposed method, the experimental results demonstrate that it achieves good classification accuracy on each dataset. Furthermore, the fast computational speed of the Stein kernel-based SR also meets the basic requirements for real-time seizure detection.

Ameliorative effects of aspirin against lipopolysaccharide-induced preeclampsia-like symptoms in rats by inhibiting the pro-inflammatory pathway.

Preeclampsia is an inflammatory disease and has connection with increased pro-inflammatory cytokines. Aspirin reduces the incidence of preeclampsia complications. However, the effects of aspirin on lipopolysaccharide-induced preeclampsia-like symptoms in rats have not been reported and the underlying molecular mechanism has not been illuminated. Hence, we investigated the anti-inflammatory effects of aspirin on lipopolysaccharide-induced preeclampsia-like phenotypes in pregnant rats and elucidated the potential molecular mechanism. Preeclampsia-like phenotypes were induced by tail vein injection of lipopolysaccharide (1 µg/kg) on gestational day 14. Aspirin (2 mg/kg per day) were administered from gestational day 14 to 19. Clinical phenotypes were recorded. Placenta tissues and serum were obtained to measure inflammatory cytokines levels using ELISA kit on gestational day 20. The mRNA expressions of IL-6, IL-1ß, and MCP-1 were measured by real-time PCR. Protein expressions including TLR4, MyD88, NF-κBp65, and TLR2 were determined by Western blot analysis in the rat placentas of each group. Aspirin obviously assuaged lipopolysaccharide-induced preeclampsia-like phenotypes in pregnant rats. Aspirin treatment significantly decreased the levels of pro-inflammatory cytokines in serum and placenta tissues of preeclampsia rats. Aspirin also obviously downregulated the mRNA expressions of IL-6, IL-1ß, and MCP-1 and assuaged the activation of TLR4, MyD88, NF-κBp65, and TLR2 in the placental tissue. Our results indicated that aspirin could assuage preeclampsia-like phenotypes, and this improvement effect is possibly the result of the suppression of pro-inflammatory cytokines via the TLR4, MyD88, NF-κBp65, and TLR2 signaling pathway.

CCL20 secreted from IgA1-stimulated human mesangial cells recruits inflammatory Th17 cells in IgA nephropathy.

IgA nephropathy (IgAN) is the most common primary glomerulonephritis characterized by human mesangial cells (HMC) proliferation and extracellular matrix expansion associated with immune deposits consisting of galactose-deficient IgA1. However, how IgA1 contributes to IgAN has yet to be completely elucidated. In this study, the expression profile of chemokines was more altered in IgA1-treated HMC than in the control group. CCL20 was significantly higher either in the serum of IgAN patients or in IgA1-treated HMC. Further experiments demonstrated that CCR6, the only receptor of CCL20, was highly expressed in activated T cells. Intracellular staining assay and cytokine expression profile implied that CCR6+ T cells produced high IL-17 levels. Transwell experiment immunohistochemistry and immunofluorescence experiments extensively demonstrated that CCL20 could recruit inflammatory Th17 cells to the kidneys. These phenomena caused a series of immune inflammatory responses and further damaged the kidneys. Therefore, HMC stimulated by IgA1 could produce CCL20 and consequently recruit inflammatory Th17 cells to the kidneys to induce further lesion in IgA nephropathy.