Systemic lupus erythematosus (SLE) is a common autoimmune disease, which features the secretion of antibodies directed against autoantigens in vivo. In the present study, a peptide microarray was developed to detect the epitopes recognized by autoantibodies in patients with SLE for an effective method of diagnosis. SLE‑associated epitopes in 14 autoantigens were predicted using the antigenic epitope prediction software DNA star. Peptides were synthesized based on the predicted antigenic epitopes and immobilized on a slide surface and developed into a peptide microarray. Using this peptide microarray the autoantibodies in 120 patients with SLE and 110 healthy subjects were detected. A total of 73 potential antigenic epitopes in 14 autoantigens were predicted and screened. The peptide microarray based on the 73 epitopes was used to detect the autoantibodies in patients with SLE. A total of 14 epitopes with potential diagnostic values were screened out. The sensitivity and specificity of the 14 epitopes for the diagnosis of SLE were 71.6 and 85.8%, respectively. An optimal set of epitopes for SLE diagnosis was obtained. As individual patients had a specific autoantibody spectrum it was possible to detect autoantibodies in SLE and perform the diagnosis of SLE using the peptide microarray.

Chronic kidney disease (CKD) progression is driven by a harmful interplay between impaired mitophagy and sustained oxidative stress. Under normal conditions, mitophagy serves as a protective mechanism by removing damaged mitochondria and limiting the production of reactive oxygen species. However, in CKD, a self‑reinforcing cycle of mitochondrial dysfunction, defective mitophagy oxidative stress, and inflammation occurs, which promotes fibrosis. The present review examines the molecular mechanisms governing mitophagy, with a specific focus on the regulatory roles of core signaling pathways, namely the PTEN‑induced kinase l/Parkin, BCL2 interacting protein 3/Nip3‑like protein X and FUN14 domain‑containing protein l pathways, and how their disruption contributes to CKD. The mechanistic crosstalk between mitophagy and oxidative stress is highlighted as a central pathogenic axis in CKD progression. In addition, emerging therapeutic strategies that aim to restore mitophagy and enhance antioxidant capacity are discussed, suggesting new strategies for targeted CKD treatment.

Introduction: Uremic pruritus (UP) is a prevalent symptom in patients suffering from uremia, yet its underlying etiology and mechanisms remain incompletely elucidated. Given the significant incidence of UP, identifying specific alterations in proteins present in the blood of UP patients could offer insights into the potential biological pathways associated with UP and facilitate the exploration of biomarkers.Methods: In this study, we employed LC-MS/MS-based data-independent acquisition (DIA) mode to analyze serum samples obtained from 54 UP patients categorized as DKD-UP, HN-UP, and GN-UP (n = 18 for each subgroup), along with 18 uremic patients without pruritus (Negative) and 18 CKD patients without pruritus (CKD). Through DIA mode analysis, a total of 7075 peptides and 959 proteins were quantified. Within these, we identified four upregulated and 13 downregulated Differentially Expressed Proteins (DEPs) in DKD-UP versus Negative, five upregulated and 22 downregulated DEPs in HN-UP versus Negative, and three upregulated and 23 downregulated DEPs in GN-UP versus Negative. Furthermore, we conducted an intersection analysis of the DEPs across these three comparison groups to derive a set of common DEPs (COMP). Subsequently, a total of 67 common DEPs were identified in the three UP groups when compared to the CKD group, with 40 DEPs showing upregulation and 27 DEPs displaying downregulation.Results: Following Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Protein-Protein Interaction (PPI) analyses, we observed that the DEPs distinguishing UP from CKD were primarily associated with mitochondrial function (MT-CYB, PRDX2, TOMM22), inflammation (CD59, CSF1), renal injury (WFDC2), and neural function (CAP1, VGF).Discussion: Our findings contribute to a potential molecular comprehension of UP pathogenesis, shedding light on the identification of these DEPs as plausible biomarkers for UP.

Pyroptosis, an inflammatory form of lytic programmed cell death intricately linked to innate immunity, is a pivotal driver of renal fibrosis. Its dysregulated activation initiates a self‑amplifying cycle of chronic inflammation and extracellular matrix deposition, ultimately leading to renal failure. The present review integrates current knowledge primarily from preclinical in vivo and in vitro studies with clinical observations to delineate the multifaceted regulatory mechanisms governing renal pyroptosis, with emphasis on molecular triggers and execution pathways. The critical roles of core effectors such as NLRP3 and GSDMD, whose expression levels in patients correlate with fibrosis severity, were highlighted. The article systematically evaluates pharmacological interventions and explores multi‑target synergistic strategies aimed at integrated signaling hubs to circumvent pathway redundancy. Furthermore, advanced therapeutic approaches were discussed, including nanoparticle‑based delivery systems, offering a strategic framework to bridge the gap between bench research and clinical applications in the management of renal fibrosis.

Rhabdomyolysis (RM) induced by electric blankets is exceedingly rare, with only three cases identified in our literature review. Both RM and Guillain–Barré syndrome (GBS) present with similar clinical manifestations of myalgia and muscle weakness, posing a potential challenge for accurate diagnosis in clinical settings. This report presents the case of a 22-year-old man who developed RM subsequent to the use of an electric blanket. Despite undergoing plasma exchange and renal replacement therapy, the patient continued to exhibit poor muscle strength in both lower limbs. Subsequent comprehensive evaluation revealed the presence of concurrent GBS. Following a 5-day course of intravenous gamma globulin treatment, the patient experienced rapid recovery of muscle strength and was discharged. Additionally, we reviewed seven cases from the literature of coexistent RM and GBS. This indicated that investigation of the timing of onset of muscle strength decline in RM patients could help to identify potential concurrent neurological or muscular disorders. In cases in which concurrent GBS and RM cannot be definitively ascertained during early hospitalization, prioritizing plasma exchange treatment may lead to improved patient outcomes.

BACKGROUND Hyperuricemia in patients undergoing maintenance hemodialysis (MHD) has been associated with an increased risk of cardiovascular disease, although its role remains controversial. This study aims to evaluate the prevalence of hyperuricemia and its association with cardiovascular disease risk factors among patients undergoing MHD in Southwest China. MATERIAL AND METHODS This study included 99 patients who underwent MHD at the Blood Purification Center of the Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University. We statistically analyzed the general characteristics, physical indicators, biochemical markers, and cardiac ultrasound parameters. We examined the correlation between serum uric acid levels and cardiovascular risk factors. RESULTS Logistic regression analysis revealed that heavy smoking and higher abdominal fat thickness, waist circumference, and systolic blood pressure were significantly associated with elevated serum uric acid levels. Multivariate linear regression analysis revealed that, compared with patients with normal uric acid levels, those with elevated levels showed gradual increases in triglycerides, C-reactive protein, parathyroid hormone, homocysteine, left ventricular posterior wall thickness, interventricular septum thickness, and left ventricular end-diastolic diameter. In contrast, high-density lipoprotein cholesterol levels and left ventricular ejection fraction progressively decreased. CONCLUSIONS In patients undergoing maintenance hemodialysis, hyperuricemia is closely associated with heavy smoking and abdominal obesity. These associations may increase cardiovascular risk through multiple pathways, including changes in biochemical markers (eg, triglycerides, C-reactive protein) and alterations in cardiac structure. Moreover, this risk increased proportionally with higher serum uric acid levels.