Renal Failure最新文献

{"title":"Accessing the relationship between estimated glucose disposal rate and the incidence of the kidney disease: results from the China Health and Retirement Longitudinal Study.","authors":"Xiaolan Ye, Wentong Liu, Qianwen Tang, Hongying Zhao, Wei Zhang","doi":"10.1080/0886022X.2025.2565408","DOIUrl":"10.1080/0886022X.2025.2565408","url":null,"abstract":"<p><p>Recent studies have closely linked estimated glucose disposal rate (eGDR) to cardiovascular events; however, research on eGDR in chronic kidney disease (CKD) is limited. This study aimed to explore the relationship between eGDR and kidney diseases, including rapid kidney function decline (RKFD) and new-onset CKD (NOCKD), in a non-CKD population. We examined 5,679 non-CKD individuals from the China Health and Retirement Longitudinal Study (2011-2015) with complete eGDR data. Participants were categorized into four groups based on eGDR quartiles. Logistic regression and restricted cubic spline (RCS) were utilized to assess the correlation between eGDR and the incidence of RKFD and NOCKD. Subgroup analyses and optimization of predictive models were conducted based on baseline characteristics of participants. During follow-up, 402 RKFD and 220 NOCKD cases were documented. Higher eGDR was associated with reduced risk of RKFD (OR: 0.87, 95% CI: 0.81-0.94, <i>p</i> < 0.001) and NOCKD (OR: 0.88, 95% CI: 0.80-0.97, <i>p</i> = 0.01) per 1.0-SD increment. Restricted cubic splines models showed a linear relationship (non-linear <i>p</i> > 0.05), with increased RKFD/NOCKD risk when eGDR < 10.405 mg/kg/min. Adding eGDR improved predictive ability for RKFD (AUC: 0.659 vs. 0.672, <i>p</i> = 0.012) and NOCKD (AUC: 0.532 vs. 0.539, <i>p</i> = 0.004). This study demonstrated that lower eGDR levels in Chinese participants aged over 45 years without CKD are associated with an increased risk of developing RKFD and NOCKD.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2565408"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12502098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145239435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated concentrations of cardiac troponin T are associated with thoracic aortic calcification in non-dialysis chronic kidney disease patients of stage G3 to G5.","authors":"Wenjiao Zhu, Zhiman Lai, Miaorong Xue, Shaozhen Feng, Pinning Feng, Xiantian Pan, Xiaojie Ke, Xionghui Chen, Zhijian Li, Haiping Mao, Xiao Yang, Fengxian Huang, Wei Chen, Yuanwen Xu, Shurong Li, Qunying Guo","doi":"10.1080/0886022X.2024.2440512","DOIUrl":"10.1080/0886022X.2024.2440512","url":null,"abstract":"<p><strong>Background: </strong>Vascular calcification (VC), especially coronary artery calcification (CAC), serves as a robust predictor of cardiovascular mortality in chronic kidney disease (CKD) patients. Recent studies have revealed that the presence of extra-coronary calcifications (ECCs) contributes to cardiovascular disease (CVD). Elevated myocardial injury markers predict mortality risk in CKD patients and are associated with CVD. Nevertheless, the relationship between VC, including CAC and ECCs, and myocardial injury markers remain unexplored in non-dialysis CKD patients.</p><p><strong>Methods: </strong>In 278 non-dialysis CKD patients of stage G3 to G5, we assessed calcified scores in CAC (Agatston score) and ECCs including thoracic aortic calcification (TAC), abdominal aortic calcification (AAC), carotid artery calcification, and valvular calcification. We analyzed the relationships between VC and myocardial injury markers of cardiac troponin T (cTnT) and creatine kinase-MB (CK-MB).</p><p><strong>Results: </strong>A total of 278 non-dialysis CKD patients (median age 52.4 ± 13.2; male 65.1%; diabetes 33.5%) were enrolled. A total of 71.8% (227) of patients had cTnT levels above the upper limit of normal (> 0.014 ng/mL). Moderate to severe (calcified score ≥100 vs. <100), CAC (OR 6.39; 95% CI 1.03-39.61) and TAC (OR 6.16; 95% CI 1.76-21.55) were significantly associated with higher cTnT concentrations after adjustment for confounders. Additionally, male sex and a lower eGFR were also associated with cTnT elevation. However, when we included CAC and TAC in one model, only moderate to severe TAC (OR 4.85; 95% CI 1.38-16.96) was a risk factor for cTnT elevation, but not CAC. Furthermore, patients with severer TAC presented lower diastolic blood pressure (DBP), wider pulse pressure (<i>p</i> < 0.001) and higher prevalence of left ventricular hypertrophy (LVH).</p><p><strong>Conclusion: </strong>Moderate to severe thoracic aortic calcification (TAC score ≥ 100) is significantly associated with elevated cTnT concentrations in non-dialysis CKD patients of stage G3 to G5. The linkage may result from decreased coronary perfusion and relative myocardial ischemia.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2440512"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11656758/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142855241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The natural immune molecules urinary Tamm-Horsfall protein and pentraxin 3 as predictors for recurrent urinary tract infection severity: a single-center self-control study.","authors":"Zongping Li, Yingru Xu, Qian Wang, Gang Yuan, Jing Shu, Shiwei Liu, Xuezhong Gong","doi":"10.1080/0886022X.2024.2449574","DOIUrl":"10.1080/0886022X.2024.2449574","url":null,"abstract":"<p><strong>Objective: </strong>The innate immune defense plays a pivotal role in protecting the urinary tract from uropathogenic invasion and maintaining immune homeostasis. Dysregulation of the innate immune system can result in recurrent urinary tract infections (RUTI) due to heightened susceptibility to uropathogens. Despite this, predicting the risk of recurrence and the degree of immune compromise in patients who have had one urinary tract infection remains challenging. Also identifying which patients are more susceptible to developing pyelonephritis rather than the more local disease of cystitis is imperfect, although delayed diagnosis of a UTI is a good indicator for developing pyelonephritis. This study aims to assess the potential of urinary Tamm-Horsfall protein (THP) and Pentraxin 3 (PTX3) as predictors of RUTI symptom severity and recurrence, while also evaluating the efficacy of the Chinese herbal formulation Tailin Formula (TLF) as a clinical therapeutic intervention for RUTI.</p><p><strong>Methods: </strong>A single-center cohort study was conducted involving 142 participants, consisting of 31 healthy individuals (non-RUTI group, <i>n</i> = 31) and 111 patients with RUTI. The RUTI patients were divided into two groups: one group received continuous low-dose antibiotic therapy (CLAT group, <i>n</i> = 55), and the other group received herbal preparations (Tailin formula) (TLF group, <i>n</i> = 56). All patients received consistent lifestyle guidance. Descriptive analysis was performed on the RUTI cohort.</p><p><strong>Results: </strong>Urinary THP levels were significantly lower in RUTI patients (TLF and CLAT groups) compared to the non-RUTI, whereas PTX3 levels showed a tendency toward elevation. After treatment, urinary THP levels were markedly higher in the TLF group (27.43 ± 7.07) compared to pretreatment levels (10.00 ± 2.79), while levels remained lower in the CLAT group (8.91 ± 2.23) than in the TLF group. Urinary PTX3 levels decreased post-treatment in both groups after treatment than before (CLAT: 0.30 ± 0.13 vs. 1.04 ± 0.38; TLF: 0.29 ± 0.12 vs. 1.15 ± 0.36). Additionally, THP was negatively correlated with renal tubular injury markers NAG/Cr and β2-MG in RUTI patients (<i>r</i> = -0.5041 and -0.6169, respectively), while PTX3 showed a positive correlation with NAG/Cr and β2-MG (<i>r</i> = 0.28 and 0.498, respectively). Notably, as RUTI symptoms improved and recurrence rates decreased, urinary THP levels increased, while PTX3 levels decreased.</p><p><strong>Conclusion: </strong>This study suggests that urinary THP and PTX3 are likely involved in the pathogenesis of RUTI. These biomarkers may serve as valuable predictors for assessing symptom severity, recurrence risk, and therapeutic efficacy in patients with RUTI at risk of disease progression.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2449574"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11721855/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142953550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Letter to the Editor regarding 'triglyceride glucose index: a significant prognostic marker of heart failure in patients with chronic kidney disease'.","authors":"Yao Yin, Si Jin","doi":"10.1080/0886022X.2024.2448579","DOIUrl":"https://doi.org/10.1080/0886022X.2024.2448579","url":null,"abstract":"","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2448579"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11721626/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142966276","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Simple methods for estimating the maximum 24-hour urinary potassium excretion in kidney failure without replacement therapy patients.","authors":"Danyang Zhang, Yukun Wang, Shimin Jiang, Wenge Li","doi":"10.1080/0886022X.2024.2445157","DOIUrl":"10.1080/0886022X.2024.2445157","url":null,"abstract":"<p><strong>Background: </strong>Adjusting dietary potassium intake based on 24-hour urinary potassium excretion is the primary method of preventing hyperkalemia. Currently, there is no accurate and convenient method for calculating maximum 24-hour urinary potassium excretion in kidney failure without replacement therapy patients. We developed and validated two new models to assess the upper limit of dietary potassium consumption in this high-risk cohort, using the maximum 24-hour urinary potassium excretion as a proxy.</p><p><strong>Methods: </strong>The data of 145 kidney failure without replacement therapy patients with hyperkalemia was gathered. The prediction models were developed using multilayer perceptron and stepwise multiple linear regression utilizing a stochastic sample of 102 (70%) patients. Within the rest 43 (30%), the performance of various models was independently verified.</p><p><strong>Results: </strong>The two new models had low bias (-0.02 and -0.57 mmol/24h vs 66.74 and 79.91 mmol/24h, mean absolute error = 5.57 and 5.22 vs 68.95 and 81.37), high accuracy (percentage of calculated values within_±30% of measured values = 83.45% and 84.14% vs 0.00% and 0.00%), high correlation with measured values (Spearman correlation coefficient = 0.72 and 0.72 vs 0.46 and 0.45, intraclass correlation coefficient = 0.67 and 0.70 vs 0.03 and 0.03) and high agreement with 24-hour urine potassium measurements (95% limits of agreement of Bland-Altman plot = 13.70 and 13.20 mmol/24h vs 113.8 and 191.3 mmol/24h).</p><p><strong>Conclusion: </strong>These new models show high clinical application value for the calculation of maximum 24-hour urinary potassium excretion in kidney failure without replacement therapy patients with hyperkalemia.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2445157"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11721948/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142953543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A hidden gem on the banks of the Danube River-our experience at the 28^th Budapest Nephrology School.","authors":"Joshua H Lipschutz, Mihály Tapolyai","doi":"10.1080/0886022X.2025.2453010","DOIUrl":"10.1080/0886022X.2025.2453010","url":null,"abstract":"","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2453010"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11792129/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143080782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immune cells mediate the effect of plasma lipidomes on IgA nephropathy: a Mendelian randomization study.","authors":"Quanxin Li, Ye Chen, Yahan Zhu, Xiaoyang Cui, Jichen Pan, Xiao Li, Xiaolin Liu","doi":"10.1080/0886022X.2025.2498631","DOIUrl":"https://doi.org/10.1080/0886022X.2025.2498631","url":null,"abstract":"<p><strong>Background: </strong>IgA nephropathy (IgAN) is a leading cause of chronic kidney disease, often associated with dyslipidemia and immune dysfunction. This study employs Mendelian randomization (MR) to investigate the causal relationship between plasma lipidomes and IgAN, with a focus on the potential mediating role of immune cells.</p><p><strong>Methods: </strong>We analyzed the 179 genetically predicted plasma lipidomes and the IgAN gene using two-sample Mendelian randomization (TSMR) and multivariable MR based on summary-level data from a genome-wide association study, and the results were validated by liquid chromatography-mass spectrometry. Furthermore, we quantified the proportional effect of immune cell-mediated lipidomes on IgAN using TSMR.</p><p><strong>Results: </strong>This study identified significant causal relationships of 3 lipidomes on IgAN risk by examining 179 lipidome traits as exposures. To investigate whether the impact of the 3 lipid groups on IgAN is specific, we performed TSMR analyses using 3 lipidomes as exposure factors and 4 nephritides as outcomes. Specifically, only phosphatidylinositol (18:1_20:4) was found to have a significant negative relationship with IgAN incidence (IVW method, <i>p</i> = 0.01, OR = 0.71, 95% CI = 0.55 - 0.92). Our further analysis focused on 8 immune cells associated with IgAN. We identified 2 immune cell phenotypes that may contribute to phosphatidylinositol (18:1_20:4)-mediated IgAN by careful screening.</p><p><strong>Conclusions: </strong>Our findings provide robust genetic evidence supporting a causal link between plasma lipidomes and IgAN, with immune cells acting as potential mediators. Phosphatidylinositol (18:1_20:4) emerges as a promising biomarker for IgAN risk stratification, early detection, and therapeutic intervention. Modulating its plasma levels may offer novel avenues for IgAN management.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2498631"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12057791/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144050776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammatory markers mediate association of AIP with kidney failure risk: data from National Health and Nutrition Examination Survey (NHANES) 2005-2018.","authors":"Chengjing Guan, Ruixue Chen, Yu Wang","doi":"10.1080/0886022X.2025.2486565","DOIUrl":"https://doi.org/10.1080/0886022X.2025.2486565","url":null,"abstract":"<p><p>Dyslipidemia and inflammation often coexist in the progression of kidney failure, with the atherosclerosis index of plasma (AIP) serving as a valuable marker for monitoring dyslipidemia. This cross-sectional study analyzed data from the National Health and Nutrition Examination Survey (NHANES) spanning 2005 to 2018, involving a total of 10,358 participants. AIP was calculated as the logarithmic ratio (base 10) of triglycerides to high-density lipoprotein cholesterol (log10[TG/HDL-C]), while kidney failure was assessed through self-reported physician diagnosis. Logistic regression models and restricted cubic splines (RCS) were utilized to examine the association between AIP and the risk of kidney failure, with additional subgroup analyses performed to explore potential interactions. Mediation analyses were conducted to investigate whether inflammatory markers mediated the relationship between AIP and kidney failure. In logistic regression, after adjusting for all covariates, AIP was found to be positively associated with the risk of kidney failure [OR = 1.74 (95% CI: 1.04-2.92)], and a linear relationship between AIP and kidney failure risk was observed (P-non-linear = 0.4050). Mediation analysis revealed that segmented neutrophils, eosinophils, and monocytes partially mediated the association between AIP and kidney failure, with mediation proportions of 19.65%, 2.44%, and 7.25%, respectively. These findings suggest that Higher AIP was associated with an increased risk of kidney failure, with segmented neutrophils, eosinophils, and monocytes serving as partial mediators. The results provide valuable insights into the role of inflammation in kidney failure and highlight potential avenues for its prevention.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2486565"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12001854/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144029009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Causal relationship between chronic kidney disease, renal function, and venous thromboembolism: a bidirectional Mendelian randomization study.","authors":"Rongping Yang, Shuanglan Xu, Qian Liu, Xifeng Zhang, Huilin He, Yue Xu, Linna Chen, Xiqian Xing, Jiao Yang","doi":"10.1080/0886022X.2025.2496803","DOIUrl":"https://doi.org/10.1080/0886022X.2025.2496803","url":null,"abstract":"<p><strong>Background: </strong>Chronic kidney disease (CKD) and impaired renal function have been implicated in venous thromboembolism (VTE), but their causal relationships remain uncertain. This study employs Mendelian randomization (MR) to elucidate the potential bidirectional causal effects between CKD, renal function biomarkers, and VTE.</p><p><strong>Methods: </strong>We collated datasets from genome-wide association studies conducted among European individuals to perform MR analyses. The primary method utilized was the random-effect inverse variance-weighted (IVW) approach, with MR-Egger and the weighted median approaches employed as supplemental techniques. Several sensitivity studies were performed to assess the findings' robustness.</p><p><strong>Results: </strong>We identified a link between elevated serum creatinine levels and both VTE (OR: 1.14, 95% CI: 1.05-1.24, <i>p</i> = 0.001) and PE (OR: 1.20, 95% CI: 1.08-1.33, <i>p</i> = 0.001). After outlier removal and Bonferroni correction, the Cr-VTE association lost significance (<i>p</i> = 0.005). A suggestive causal relationship was found between eGFR and VTE (OR: 0.38, 95% CI: 0.20-0.73, <i>p</i> = 0.004), DVT (OR: 0.37, 95% CI: 0.16-0.87, <i>p</i> = 0.022), and PE (OR: 0.29, 95% CI: 0.12-0.66, <i>p</i> = 0.004). No causal effects of CKD or BUN on VTE or its subtypes were observed. Reverse causality inferences did not reveal any meaningful results.</p><p><strong>Conclusions: </strong>This MR analysis provides evidence that elevated serum creatinine is associated with a higher risk of VTE and PE, while reduced eGFR may be a potential risk factor for VTE and its subtypes. These findings highlight the need for proactive monitoring and preventive strategies in individuals with impaired renal function. Further studies are warranted to confirm these associations and explore underlying mechanisms.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2496803"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12054574/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144030674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathophysiological changes in patients during hemodialysis and blood reinfusion predict potential development of hemodialysis reactions.","authors":"Ákos Géza Pethő, Csaba Révész, Tamás Mészáros, Orsolya Sáfár, László Rosivall, József Domán, Gábor Szénási, Tünde Gigacz, László Dézsi","doi":"10.1080/0886022X.2025.2500662","DOIUrl":"https://doi.org/10.1080/0886022X.2025.2500662","url":null,"abstract":"<p><p>Hemodialysis reactions (HDRs) are a type of hypersensitivity reactions (HSRs), such as complement activation-related pseudoallergy (CARPA) observed during nanoparticle infusions. Our study aimed to elucidate the mechanisms of human HDRs by focusing on hemodynamic and clinical chemistry changes of HSR-related or biocompatibility issues during human hemodialysis (HD) and the reinfusion of blood. Based on our recent animal experiments, we hypothesize that increased pulmonary arterial pressure (PAP), and increases in thromboxane B2 (TXB2) and complement 3a (C3a) plasma concentrations will likely manifest in, or at least predict, human HDRs during HD and blood reinfusion. To verify our hypothesis, we measured these parameters during high-flux HD in patients. Since direct PAP measurement was not possible, the plasma concentration of the N-terminal fragment of the brain natriuretic peptide (NT-proBNP) was determined for the noninvasive estimation of PAP. Our results show an increase in NT-proBNP and TXB2 during the reinfusion of extracorporeal blood. The plasma concentration of C3a increased in early HD already and remained elevated up to blood reinfusion. In conclusion, the observed changes in HSR-related parameters or biocompatibility issues in otherwise asymptomatic patients may suggest that a greater activation of these mechanisms could explain the development of human hemodialysis reactions.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2500662"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12057777/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144034701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}