INTRODUCTION:Contrast-induced acute kidney injury (CIAKI) is a leading cause of hospital-acquired kidney dysfunction, yet its immune-mediated pathogenic mechanisms remain poorly defined. Neutrophil extracellular traps (NETs) have been implicated in acute kidney injury. However, whether contrast agents directly induce NETs formation and whether NETs drive tubular ferroptosis through IL-33 has not been investigated. METHODS:A prospective cohort of 330 patients undergoing coronary angiography was enrolled, with serial measurement of circulating NETs markers (myeloperoxidase, neutrophil elastase) and IL-33 at pre-contrast, two- and 12-hour time points. A murine CIAKI model was established in wild-type, peptidyl arginine deaminase 4 (PAD4) -knockout, and IL-33-knockout mice, and single-cell transcriptomic profiling of CIAKI kidneys was performed. In vitro, the serine/threonine kinase IKKα- and β-catenin-overexpressing and knockdown HK-2 cells were stimulated with iodixanol-induced NETs to evaluate how NETs regulate ferroptosis through IL-33-mediated modulation of IKKα and β-catenin. RESULTS:CIAKI occurred in 12.1% (40/330) of patients. Circulating NETs markers and IL-33 were significantly elevated at two and 12 hours post-contrast in CIAKI compared with non-CIAKI patients. Single-cell transcriptomics identified neutrophils as the predominant source of IL-33 in CIAKI kidneys and revealed enrichment of NET formation and ferroptosis pathways. In vivo, PAD4 and IL-33 deficiency each significantly attenuated NETs and ferroptosis in CIAKI mice. Mechanistically, IL-33-enriched NETs suppressed IKKα expression, disrupted IKKα-β-catenin interaction, and impaired β-catenin nuclear translocation, thereby de-repressing long chain acyl CoA synthetase 4 transcription and amplifying ferroptotic injury. Restoration of IKKα stabilized β-catenin and attenuated NET-induced ferroptosis. CONCLUSIONS:Our study demonstrates that IL-33-enriched NETs promote renal tubular ferroptosis in CIAKI by suppressing IKKα and impairing β-catenin nuclear translocation. These findings identify the NETs-IL-33-IKKα-β-catenin pathway as a novel and therapeutically actionable mechanism underlying CIAKI, providing potential targets for its diagnosis and treatment.

Aims The kappa class of glutathione S-transferases 1 (GSTK1) is a vital regulatory factor in metabolic diseases. This study was conducted to investigate the regulatory effects of GSTK1 on renal ectopic fat deposition (EFD) and lipotoxic injury in diabetic nephropathy (DN) . Results HK-2 cells under high glucose(HG) / high fatty acid (HFA) stimulation, diabetic mice and human renal biopsy tissues were used. GSTK1 plasmid, GSTK1 siRNA and OSBPL8 siRNA were applied in vitro. Lipid accumulation was analyzed in the renal tissue of type 2 DN patients, diabetic mice and HK-2 cells under HG/HFA stimulation. The expression of GSTK1, DGAT1, ACAT1, CPT-1, BECLIN1, LC3II, ATG5 and RAB7 in renal tubular cells of diabetic mice and HK-2 cells under HG/HFA condition decreased significantly. Metformin treatment restored the expression of GSTK1 in diabetic mice. Additionally, the GSTK1 pharmacological modulator metformin relieved lipophagy dysfunction and promoted fatty acid (FA) β-oxidation enzyme CPT-1. In vitro, GSTK1 plasmid reduced lipid accumulation, fibrosis and inflammation and up-regulated the expression of CPT1 in HK-2 cells, but GSTK1 plasmid had no effect on lipid metabolizing enzymes (ACAT1, DGAT1) . In addition, GSTK1 plasmid could obviously restore lipophagy. However, pretreatment of HK-2 cells with the AMPK inhibitor Compound C, GSTK1 siRNA or OSBPL8 siRNA negated the activating effects of GSTK1 on lipophagy. Conclusion This study indicated that GSTK1 could contribute to alleviate EFD in DN tubular cell through increasing the expression of FA β-oxidation enzyme CPT-1 and restoring lipophagy via AMPK-OSBPL8 pathway.

Rationale & Objective:Secondary hyperparathyroidism (SHPT) is a common health problem among patients receiving maintenance hemodialysis. SHR6508, an allosteric modulator of calcium-sensing receptors, was developed to reduce parathyroid hormone secretion among Chinese hemodialysis patients with SHPT. This study aimed to evaluate the safety, pharmacokinetics, and pharmacodynamics of SHR6508 administered intravenously. Study Design:This was a multicenter, randomized, double-blind, placebo-controlled single and multiple ascending dose phase 1 trial. Setting & Participants:This study was conducted at 18 sites in China. Hemodialysis patients who had serum intact parathyroid hormone (iPTH) concentration 400-1,300 pg/mL and corrected calcium ≥8.4 mg/dL (2.1 mmol/L) were enrolled. Interventions:Patients were randomized in a 4:1 ratio to receive SHR6508 or placebo by intravenous injection after hemodialysis. Outcomes:The primary outcomes were pharmacokinetic parameters and changes in iPTH and corrected calcium concentrations. Results:The plasma drug exposures (mean maximum plasma concentration, area under the concentration-time curve) increased proportionally with the dose after the administration of SHR6508. iPTH level declined markedly after a single dose of SHR6508 in all cohorts (5-30 mg). After multiple doses of 5-15 mg, the percentage of patients achieving a reduction in iPTH concentration ≥30% from baseline to week 2 (25.0%-90.9%) and week 4 (36.4%-100.0%) in the 5, 10, and 15 mg groups was higher than those observed in the placebo group (12.5% and 14.3%, respectively). Treatment-emergent adverse events, which were mostly mild or moderate, occurred in 41 (95.3%) SHR6508-treated patients and in all patients treated with placebo. Limitations:This study had a relatively small sample size and short treatment and follow-up period. Conclusions:SHR6508 showed promising efficacy and safety in Chinese hemodialysis patients with SHPT. A starting dose of 5 mg for titration was the best dose and will be used in the phase 2 study.

Kidney fibrosis is a hallmark of chronic kidney disease (CKD) and a major contributor to progression toward end-stage renal disease. Here, we identify 8-oxoguanine DNA glycosylase 1 (Ogg1), a DNA repair enzyme, as a regulator of kidney fibrosis. Ogg1 expression is upregulated in experimental fibrosis models in male mice, including unilateral ureteral obstruction (UUO) and aristolochic acid (AA) nephropathy, as well as in kidney tissues from CKD patients. Genetic deletion of Ogg1 reduces fibrosis, tubular atrophy and fibrotic marker expression, and improves renal function in AA nephropathy. Mechanistically, Ogg1 interacts with phosphorylated Smad3 in the nucleus and promotes transcriptional regulation of profibrotic genes. Pharmacological inhibition of Ogg1 with TH5487 alleviates fibrosis in both UUO and AA nephropathy models, supporting Ogg1 as a potential therapeutic target in CKD.

Cisplatin-induced acute kidney injury (CP-AKI) often limits its clinical utility in treating various solid tumors. However, the underlying pathogenesis of CP-AKI is still unclear. Lyn, a member of Src family kinases, is predominantly implicated in regulating immune response and inflammation. This study investigates the functional role of Lyn in CP-AKI, as well as the possible mechanism. Here, we found that Lyn was down-regulated in mice with CP-AKI. Knockout of Lyn exacerbated renal damage, increased inflammatory cytokine expression, and promoted tubular cell apoptosis and necroptosis in the kidneys of CP-AKI mice. Conversely, both Lyn agonist MLR-1023 and RIPK1 inhibitor Necrostatin-1 (Nec-1) attenuated cisplatin-triggered kidney injury, tubular cell apoptosis and necroptosis. Moreover, in vitro study showed that Lyn knockout/knockdown aggravated cisplatin-induced apoptosis and necroptosis in renal tubular epithelial cells, while Lyn overexpression alleviated them. Mechanistically, Lyn interacted with RIPK1 and inhibited the phosphorylation activation of RIPK1. In conclusion, our study revealed that Lyn protects from cisplatin-induced nephrotoxicity by suppressing RIPK1-mediated apoptosis, necroptosis and inflammation. Thus, Lyn kinase may serve as a promising therapeutic target for CP-AKI.

Targeted therapy has emerged as a promising precision medicine strategy for immunoglobulin A nephropathy (IgAN) through the modulation of specific pathogenic pathways. Although research in this area has accelerated, the literature remains scattered, and no bibliometric study has mapped its global knowledge structure or evolving hotspots. We conducted a bibliometric and visualization analysis of 678 publications indexed in the Web of Science Core Collection (1999–2025). CiteSpace 6.4R1, VOSviewer 1.6.20, and the R‑based bibliometric package were used to assess publication and citation trends; identify prolific countries, institutions, authors, and journals; and generate co‑authorship, co‑citation, and keyword co‑occurrence networks. Research frontiers were explored through thematic evolution mapping and keyword burst detection. Annual publications increased notably after 2015, indicating a shift from supportive care to molecularly targeted interventions. China and the United States produce over 60

Objectives:Atypical pulmonary carcinoid (AC) is a rare intermediate-grade neuroendocrine tumor with substantial clinical heterogeneity and an unpredictable prognosis. Accurate estimation of fixed-horizon mortality risk remains challenging because of its rarity and limited AC-specific prediction tools. This study aimed to develop and evaluate an interpretable model for estimating 3-year all-cause mortality in patients with AC. Methods:Clinical data for patients with AC diagnosed between 2000 and 2021 were retrospectively obtained from the Surveillance, Epidemiology, and End Results (SEER) database. Patients diagnosed during 2000-2018 (n=1, 301) were randomly divided into a training set (n=910) and an internal test set (n=391). Patients diagnosed during 2019-2021 (n=446) constituted a temporal validation cohort within the same registry, and 45 patients treated at the General Hospital of Ningxia Medical University during 2015-2024 were used for preliminary independent single-center evaluation. Demographic, clinicopathological, and treatment variables were considered. LASSO regression and the Boruta algorithm selected 11 predictors: Grade, N_stage, M_stage, Bone_metastasis, Brain_metastasis, Liver_metastasis, Marital_status, Radiation, Chemotherapy, Age, and Tumor_Size. Seven machine learning models were developed to evaluate predictive performance, including Logistic Regression (LR), Extreme Gradient Boosting (XGBoost), Light Gradient Boosting Machine (LightGBM), Gradient Boosting Decision Tree (GBDT), Support Vector Machine (SVM), K-Nearest Neighbors (KNN), and Adaptive Boosting (AdaBoost). The SHapley Additive exPlanations (SHAP) approach was used to interpret feature importance. Results:LR showed the most consistent held-out performance, with an area under the receiver operating characteristic curve of 0.802 (95% CI: 0.751-0.852) in the internal test set, 0.839 (95% CI: 0.796-0.882) in the temporal validation cohort, and 0.904 (95% CI: 0.808-1.000) in the single-center cohort. Boosting models showed larger declines from apparent training to held-out performance. Decision curve analysis (DCA) suggested potential net benefit across selected threshold probabilities. SHAP identified Age as the largest contributor to model predictions. Conclusion:The LR-based model showed consistent discrimination and interpretability in internal and same-registry temporal evaluation, with promising but imprecise results in the small single-center cohort. Geographic transportability remains unestablished. Independent multi-institutional validation with fully separated preprocessing is required before clinical use.

Background Emerging evidence supports the presence of microbial signatures in the blood, yet their clinical relevance remains poorly understood. In this study, we profiled blood microbial signatures in patients with Parkinson's disease (PD) and investigated their associations with disease progression. Methods We analysed 4018 whole-genome sequencing (WGS) data of blood samples from two independent cohorts. The high-quality non-human reads were extracted for microbial annotation using Kraken 2 and Bracken software with the PlusPF database. To identify PD-associated signatures, we implemented a population-based, cross-cohort filtration process with resequencing validation to minimise noise and putative contaminants. Findings Microbial DNA signals, predominantly bacterial, were extensively detected in the sequencing data and were more abundant in individuals with PD than in controls. Across the two cohorts, 126 bacterial species were identified as key signatures, nearly two-thirds of which are known to colonise human body sites. Among these, 19 species exhibited increased abundance and higher prevalence in PD, and could serve as features to discriminate effectively patients from controls. Furthermore, several microbial signatures were correlated with more severe clinical manifestations, such as motor dysfunction and cognitive impairment. Interpretation Our findings supported blood microbial signatures as promising biomarkers in PD, although their origin and functional relevance remain to be validated. The analytical framework may facilitate future investigations into the potential clinical implications of blood microbial signatures in disease contexts. Funding This work was supported by Hunan Innovative Province Construction Project, National Natural Science Foundation of China, and Natural Science Foundation of Hunan Province.

Introduction Aldosterone synthase inhibitors (ASIs) have emerged as a promising therapeutic approach for blood pressure (BP) management.Materials and Methods We searched the PubMed, Web of Science, EMBASE and Cochrane Library databases until July 11, 2025. We expressed continuous outcome data as mean differences (MDs) with 95% confidence intervals (CIs) and dichotomous outcome data as risk ratios (RRs) with 95% CIs.Results Five randomized controlled trials involving 1958 patients (mean age, 60 years; 54% men) were included. The pooled results showed that ASIs significantly reduced SBP compared with placebo, with a mean difference of -7.08 mmHg (95% CI: -9.24 to -4.93). There was no significant difference between patients assigned to ASIs treatment and placebo on serious adverse events (RR,1.16; 95% CI,0.47-2.88). Additionally, significant reductions were observed among patients receiving ASIs treatment compared with receiving placebo on the change in diastolic blood pressure (DBP), with a mean difference of -2.96 mmHg (95% CI: -4.6 to -1.32).Conclusions ASIs effectively reduce SBP and DBP in patients with resistant hypertension (RHT) and demonstrate a generally favorable safety profile, although the increased risk of hyperkalemia and other adverse events warrants consideration. These results support the potential of ASIs as a therapeutic option for RHT, requiring confirmation in larger-scale studies.

Ischemia-reperfusion injury stands as a primary instigator of acute kidney injury (AKI), prominently driven by oxidative stress. Among the critical antioxidant defenses is glutathione peroxidase 3 (GPX3), an enzyme generated by renal tubular epithelial cells. Our prior investigations have unveiled a substantial downregulation of GPX3 in renal tissues gleaned from AKI patients and murine models. This study aims to investigate the role of tubular cell-specific Gpx3 deletion on ischemia-reperfusion injury-induced AKI (IRI-AKI) in a murine model and delineate the potential underlying mechanisms. By generating renal tubular epithelial cell-specific Gpx3 knockout mice and inducing IRI-AKI, we assessed a spectrum of kidney injury indices including renal function, oxidative stress, apoptosis and mitochondrial dynamics. Additionally, we conducted transcriptome sequencing and bioinformatics analyses. The outcomes underscore that the deficiency of GPX3 in tubular cells exacerbates tubular injury, renal dysfunction, oxidative stress, apoptosis, and mitochondrial dynamic disturbances in the context of IRI-AKI. Sequencing and bioinformatics analysis suggest that the Gpx3 deletion predominantly impacts pathways associated with metabolism and inflammation. In conclusion, the tubular cell-specific deficiency of GPX3 exacerbates renal injury by intensifying oxidative stress, fostering mitochondrial impairment, perturbing metabolic processes and fueling inflammation. The targeted restoration of GPX3 in the renal tubular emerges as a potential therapeutic avenue for mitigating IRI-AKI.

BACKGROUND Autoimmune hemolytic anemia (AIHA) is a hemolytic anemia characterized by autoantibodies against red blood cells. Patients with AIHA can have 4 subtypes of IgG-type red blood cell antibodies: IgG1, IgG2, IgG3, and IgG4. The development of this disease is closely related to IgG 1 and IgG 3, and the combination with high IgG4 is rare. A patient with autoimmune hemolytic anemia who had a poor response to the steroid combined with immunosuppressive regimen (methylprednisolone and cyclophosphamide) received 4 sessions of protein A immunosorbent therapy with good results and is still under continued follow-up. CASE REPORT A 60-year-old woman had recurrent dizziness, weakness, darkening of urine, and jaundice for 2 months. Five years ago, she underwent a lymph node biopsy for "pelvic lymph node enlargement", which indicated "reactive lymph node hyperplasia". Bone marrow aspiration indicated "myelodysplasia", excluding leukemia and plasma cell disease. This patient was first treated with the steroid combination immunosuppressive regimen (methylprednisolone and cyclophosphamide), but she had a poor outcome and an increase in progressive anemia. She was treated with methylprednisolone and cyclophosphamide combined with protein A immunoadsorption therapy. She responded well and her clinical symptoms improved after 2 weeks of treatment. Her malaise was significantly reduced, jaundice decreased, Hb rose to 76 g/L, and IgG4 decreased to 12.4 g/L. At the outpatient review after 2 months, the patient's clinical symptoms had disappeared, hemoglobin (Hb) increased to 136 g/L, and IgG4 decreased to 6.72 g/L. CONCLUSIONS Protein A immunosorbent therapy may be an effective treatment option for patients with AIHA who have a poor response to conventional therapy.

Although docetaxel (DTX) is a first-line chemotherapeutic agent for treating prostate cancer (PCa), its clinical effectiveness is hampered by patients developing resistance following long-term, high-dose use. Additionally, its low bioavailability and significant toxicity further restrict its therapeutic potential. To address these issues, we developed hyaluronan (HA)-modified Prussian blue nanoparticles (PB NPs) that co-load DTX and chitosan-encased silver nanoparticles (Chi-Ag NPs), aimed at enhancing solubility, targeting capability, and therapeutic efficacy. In vitro assays demonstrated that HA-Ag-PB@DTX NPs could synergistically kill PC-3 cells by effectively targeting tumor cells and inducing cell apoptosis. In vivo studies showed that HA-Ag-PB@DTX NPs significantly inhibited tumor growth in heterotopic tumor-bearing mice through enhanced penetrability in tumor tissues and synergistic effects. Furthermore, these NPs markedly reduced the toxicity of DTX due to their controlled release and targeted delivery mechanisms. In conclusion, we have successfully developed novel nanocomplexes that improve the dosage of DTX and provide a synergistic approach for PCa therapy.

The chemotherapeutic agent cisplatin is widely utilized for the treatment of various solid tumors. However, its clinical utility is limited by nephrotoxicity. Although numerous studies have demonstrated the potential of enhancing macroautophagy/autophagy in alleviating cisplatin-induced acute kidney injury (AKI), the dynamics of the autophagic process during renal tubular injury remain to be elucidated. In our investigation, we observed that cisplatin treatment leads to increased expression of LC3-II, GABARAPL1, SQSTM1/p62 and NBR1 in mouse renal tubular epithelial cells and BUMPT cells. Moreover, ultrastructurally, there is extensive accumulation of autophagic vacuoles in AKI mice. These findings imply that cisplatin-induced AKI results in impaired autophagic flow within renal tubular cells. Furthermore, LGALS3 (galectin 3) was found to be enriched in lysosomes after cisplatin treatment, revealing a close association between autophagy dysfunction and impaired lysosomal membrane integrity. Given the damaging contents of lysosomes, lysosomal membrane permeabilization must be rapidly resolved. Our findings showed that ESCRT III subunit CHMP4A-mediated lysosomal membrane repair significantly ameliorates autophagic defects and protects against lysosomal damage-induced cell death in a cisplatin-induced AKI model. In conclusion, our study indicates that ESCRT III-mediated lysosomal repair can relieve cisplatin-induced cell apoptosis and restore normal autophagy function in renal tubular epithelial cells. This mechanism plays a protective role against cisplatin-induced AKI.Abbreviations: AAV: adeno-associated virus; AKI: acute kidney injury; CQ: chloroquine; ESCRT: endosomal sorting complex required for transport; LMP: lysosomal membrane permeabilization; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MTOR: mechanistic target of rapamycin kinase; PAS: periodic acid Schiff; PTECs: proximal renal tubule epithelial cells; TEM: transmission electron microscopy; TUNEL: terminal deoxynucleotidyl transferase dUTP nick end labeling.

Sepsis-associated acute kidney injury (SA-AKI) is a severe clinical condition with a high mortality. Currently, there is no specific therapy for SA-AKI, and clinicians can only rely on extensive supportive treatment. Therefore, finding effective methods for SA-AKI therapy is crucial to delay the progression of sepsis. Our previous studies have found that paricalcitol, an active vitamin D analog, can reduce renal inflammation and delay the progression of SA-AKI. However, expression inhibition of megalin caused by endotoxins can reduce the entry of active vitamin D into renal tubular epithelial cells and weakening its renal protective efficacy. Therefore, how to enhance the enrichment of paricalcitol in the kidney is a challenge. In this study, we constructed a nanodrug delivery system to enhance the enrichment of paricalcitol in the kidney by encapsulating paricalcitol into a poly lactic-co-glycolic acid (PLGA) nanosystem, forming PLGA@paricalcitol nanoparticles (PLGA@pari NPs). In vivo experiments demonstrated that PLGA@pari NPs exhibited higher accumulation in the kidneys and significantly improve renal function in septic mice. The study indicates that PLGA@pari NPs represent a simple, safe, and efficient drug delivery system that enhances the therapeutic efficacy for SA-AKI by improving renal accumulation. This study provides new insights for clinical treatment of SA-AKI.

Introduction: Anemia is a common complication in patients undergoing peritoneal dialysis (PD), significantly impacting quality of life and increasing cardiovascular risk. Enarodustat, an oral hypoxia-inducible factor-prolyl hydroxylase inhibitor, has been developed for the treatment of anemia in chronic kidney disease (CKD) patients, but evidence for its use in PD patients is limited. This study aimed to evaluate the efficacy and safety of enarodustat in PD patients with anemia. Methods: This was an open-label, multicenter, phase 3 trial. PD patients with anemia received enarodustat at an initial dose of 2 mg orally once daily for 4 weeks with dose adjustments every 4 weeks thereafter to achieve the target hemoglobin (Hb) range of 100–120 g/L. The primary efficacy endpoint was the mean Hb level and its 95% confidence interval (CI) during the evaluation period (weeks 20–24 or the end of the treatment). Secondary endpoints included several Hb and treatment-related parameters, as well as iron supplementation use. Exploratory endpoints assessed parameters related to red blood cell indices and iron metabolism. Results: A total of 37 patients enrolled in this study, with a mean ± SD adherence of 99.21 ± 3.03%. The mean Hb level (95% CI) during the evaluation period was 110.50 g/L (95% CI: 107.72, 113.28), with 83.8% (31/37) patients achieving target Hb levels (≥100 and ≤120 g/L) during the evaluation period. The change from baseline in Hb level at week 4 was −3.1 g/L. Enarodustat improved iron-related parameters compared to baseline, including serum iron, total iron-binding capacity, transferrin, and hepcidin levels. Drug-related AEs occurred in 21.6% (8/37) of patients, with no grade 3 or higher drug-related AEs reported. Serious AEs occurred in 21.6% (8/37), none were considered related to enarodustat. Conclusion: Enarodustat effectively maintained target Hb levels in PD patients with anemia, demonstrating favorable safety and tolerability. Its convenient once-daily oral dosing regimen may enhance patient adherence, highlighting its potential as a promising therapeutic option for anemia management in PD patients.

BACKGROUND:Chronic kidney disease (CKD) is a significant global health challenge with a multifaceted etiology. Risk stratification and timely intervention are crucial for mitigating CKD progression. Trimethylamine N-oxide (TMAO), a gut microbiota metabolite, has been implicated in CKD pathogenesis. However, the lack of standardized diagnostic assays for TMAO has limited its clinical applicability. METHODS:We conducted a multicenter observational study in Southern China. Plasma TMAO levels were quantified using a newly developed liquid chromatography-mass spectrometry (LC-MS)-based diagnostic kit in a cohort of 272 participants, including healthy controls and CKD patients. We analyzed the correlation between TMAO levels and renal function indicators, evaluated the utility of TMAO for risk stratification in CKD, and assessed its independent association with reduced eGFR using multivariable logistic regression. RESULTS:Plasma TMAO levels were significantly elevated in CKD patients compared to healthy controls. TMAO levels increased with CKD severity and exhibited a strong positive correlation with serum creatinine (Scr) and a negative correlation with estimated glomerular filtration rate (eGFR). TMAO levels demonstrated excellent consistency with eGFR in both the full analysis set (FAS) and per protocol set (PPS) populations. Receiver operating characteristic (ROC) curve analysis indicated that TMAO could identify reduced eGFR with high accuracy (AUC: 0.916), which was confirmed by bootstrap validation. After adjusting for age, sex, hypertension, and diabetes, TMAO remained independently associated with reduced eGFR. CONCLUSIONS:Our findings suggest that TMAO is a promising and independent complementary biomarker for the risk stratification of CKD, though its prognostic value requires validation in longitudinal studies. The developed LC-MS kit enables robust clinical application. Further research is warranted to validate these findings in larger cohorts and explore TMAO's potential as a therapeutic target for CKD management. TRIAL REGISTRATION:Clinical Trails.gov identifier, ChiCTR2400089774 (retrospectively registered in 14/09/2024).

Sepsis is a life-threatening clinical syndrome, and renal impairment associated with sepsis significantly increases patient mortality. Blood purification techniques are crucial in managing sepsis by removing inflammatory mediators and toxic substances from the bloodstream, thereby improving outcomes. Traditional modalities, including continuous renal replacement therapy, hemodialysis, and hemoperfusion, have demonstrated clinical efficacy in this context. Recent advancements in blood purification filters have enhanced sepsis treatment strategies. This review assesses the mechanisms and clinical applications of novel filters such as the oXiris filter, AN69ST membrane, CytoSorb, Hemopurifier, and others, focusing on their effectiveness in eliminating toxins and inflammatory mediators. The oXiris filter has demonstrated superior capacity to remove small molecular toxins, pro-inflammatory cytokines, and endotoxins while promoting renal protection and enhancing microcirculation. In contrast, the AN69ST membrane and CytoSorb filters have shown promising efficacy in cytokine clearance, though their ability to remove endotoxins is limited. The Hemopurifier specifically targets endotoxins like lipopolysaccharides, effectively suppressing inflammatory responses and mitigating renal damage. Furthermore, the integration of Extracorporeal Carbon Dioxide Removal (ECCO2R) with continuous renal replacement therapy (CRRT) offers benefits, including the regulation of carbon dioxide levels, maintenance of acid-base balance, and enhanced clearance of inflammatory factors from circulation. Additionally, selective removal of lipopolysaccharides (LPS) can alleviate leukopenia and immune dysregulation, preserving renal function. This review aims to provide clinical guidance for optimizing individualized treatment protocols to enhance survival rates and improve the quality of life for patients with sepsis-related AKI. Incorporating these advanced filtration technologies into routine clinical practice can transform sepsis management and pave the way for innovative therapeutic strategies in critical care.