cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.28004430.v1
title: Associations of combined physical activity and dietary quality with all-cause and cardiovascular disease mortality among US adults with chronic kidney disease

description: There is a lack of sufficient information on the impact of physical activity (PA) and dietary quality (DQ) on mortality in patients with chronic kidney disease (CKD), and no study has yet examined the relationship between the combined effects of PA and DQ on the risk of death in patients with CKD in a representative adult population. Adult CKD patients (<i>n</i> = 6,504) from the National Health and Nutrition Examination Survey (NHANES) 1999–2018 were included in the study. Mortality outcomes were assessed by National Death Index records before 2/25/2019. Four lifestyle categories were established: low-PA individuals with unhealthy diets, low-PA individuals with healthy diets, high-PA individuals with unhealthy diets, and high-PA individuals with healthy diets. Cox proportional risk modeling was used to calculate the hazard ratios (HRs) and 95% confidence intervals (CIs) of various lifestyle categories for all-cause and CVD mortality. During a median follow-up period of 111 months, 1,971 participants with CKD died from all-cause mortality, and 567 died from CVD among 6,504 respondents. The high-PA CKD population with a healthier diet had a significantly lower risk of all-cause [0.75, 95% CI (0.64–0.87)] and CVD [0.69, 95% CI (0.51–0.93)] mortality than the low-PA, unhealthy diet participants did. The age and race subgroups showed significant interactions, with the older (≥60 years) and non-Hispanic black subgroups experiencing a more favorable risk-lowering effect for all-cause death. CKD patients with healthy diets and adequate PA had lower risks of CVD and all-cause mortality than did low-PA individuals with unhealthy diets.
DOI: 10.6084/m9.figshare.28039565
title: Research trends and frontiers on risk factors of urinary stones: a bibliometric analysis from 2010 to 2023

description: The occurrence of urinary stone disease (USD) is associated with several factors. However, no conclusive results have been reached regarding the treatment of USD risk factors. This study conducted a detailed bibliometric analysis of USD risk factors to determine research hotspots and provide future development directions. Articles and reviews on the USD risk factors published between 2010 and 2023 were retrieved from the Web of Science Core Collection. Co-occurrence and collaboration analyses of countries, institutions, authors, journals, references, and keywords were conducted using CiteSpace, VOSviewer, and R-Bibliometrix. A total of 436 articles on USD risk factors were included in the study. China and the United States have emerged as the leading countries in this field, with the Mayo Clinic having the highest amount of publication output. Among all the authors, Ferraro PM had the highest number of publications, while Taylor EN was the highly cited author. The journal with the highest number of publications was <i>UROLITHIASIS</i>. Scales reported the reference with the highest burst strength. The current citation themes in research on USD risk factors were ‘multifaceted relationship’ and ‘kidney stone disease recurrence’. ‘Medical-management’ was identified as a major keyword, indicating future research hotspots. This study employed bibliometric methods to conduct a comprehensive visual analysis of USD risk factors to show publication trends and popular topics in this area over the past decade. The results provide a valuable reference for future research on the risk factors of USD.
DOI: 10.6084/m9.figshare.28039565.v1
title: Research trends and frontiers on risk factors of urinary stones: a bibliometric analysis from 2010 to 2023

description: The occurrence of urinary stone disease (USD) is associated with several factors. However, no conclusive results have been reached regarding the treatment of USD risk factors. This study conducted a detailed bibliometric analysis of USD risk factors to determine research hotspots and provide future development directions. Articles and reviews on the USD risk factors published between 2010 and 2023 were retrieved from the Web of Science Core Collection. Co-occurrence and collaboration analyses of countries, institutions, authors, journals, references, and keywords were conducted using CiteSpace, VOSviewer, and R-Bibliometrix. A total of 436 articles on USD risk factors were included in the study. China and the United States have emerged as the leading countries in this field, with the Mayo Clinic having the highest amount of publication output. Among all the authors, Ferraro PM had the highest number of publications, while Taylor EN was the highly cited author. The journal with the highest number of publications was <i>UROLITHIASIS</i>. Scales reported the reference with the highest burst strength. The current citation themes in research on USD risk factors were ‘multifaceted relationship’ and ‘kidney stone disease recurrence’. ‘Medical-management’ was identified as a major keyword, indicating future research hotspots. This study employed bibliometric methods to conduct a comprehensive visual analysis of USD risk factors to show publication trends and popular topics in this area over the past decade. The results provide a valuable reference for future research on the risk factors of USD.
DOI: 10.6084/m9.figshare.26539440
title: Alterations in the gut microbiome and metabolism profiles reveal the possible molecular mechanism of renal injury induced by hyperuricemia in a mouse model of renal insufficiency

description: <b>Objectives:</b> To investigate the role of the intestinal flora and metabolites in the development of hyperuricemic renal injury in chronic kidney disease (CKD).<b>Methods:</b> Unilaterally nephrectomized mice were fed with adenine and potassium oxonate for 9 weeks. HE staining combined with plasma biochemical indicators was used to evaluate renal pathological and functional changes. We conducted 16S rRNA sequencing and untargeted metabolomics on feces and plasma samples to reveale changes in intestinal microbiota and metabolites.<b>Result:</b> Our analysis revealed significant differences in 15 bacterial genera, with 7 being upregulated and 8 being downregulated. Furthermore, metabolomic analysis revealed changes in the distribution of amino acid and biotin metabolites in basic metabolic pathways in both feces and serum. Specifically, differentially abundant metabolites in feces were associated primarily with histidine metabolism; the biosynthesis of phenylalanine, tyrosine, and tryptophan; and tyrosine metabolism. In plasma, the differentially abundant metabolites were involved in multiple metabolic pathways, including aminoacyl-tRNA biosynthesis; glycine, serine, and threonine amino acid metabolism; valine, leucine, and isoleucine biosynthesis; tyrosine biosynthesis and metabolism; biotin metabolism; and taurine and hypotaurine metabolism. Furthermore, correlation analysis revealed that <i>Akkermansia, UCG-005, Lachnospiraceae_NK4A136_group, Lactococcus, and Butymonas</i> were associated with various differentially abundant metabolites as well as renal function, oxidative stress, and mitophagy. The changes in the intestinal flora observed in hyperuricemia may lead to imbalances in amino acid and biotin metabolism in both the intestine and host, ultimately affecting oxidative stress and mitophagy in mice and accelerating the progression of CKD.<b>Conclusion: </b>Our findings provide insights into a potential pathogenic mechanism by which hyperuricemia exacerbates renal injury in mice with renal insufficiency. Understanding these pathways may offer new therapeutic strategies for managing hyperuricemic renal injury in CKD patients.
DOI: 10.6084/m9.figshare.26539440.v1
title: Alterations in the gut microbiome and metabolism profiles reveal the possible molecular mechanism of renal injury induced by hyperuricemia in a mouse model of renal insufficiency

description: <b>Objectives:</b> To investigate the role of the intestinal flora and metabolites in the development of hyperuricemic renal injury in chronic kidney disease (CKD).<b>Methods:</b> Unilaterally nephrectomized mice were fed with adenine and potassium oxonate for 9 weeks. HE staining combined with plasma biochemical indicators was used to evaluate renal pathological and functional changes. We conducted 16S rRNA sequencing and untargeted metabolomics on feces and plasma samples to reveale changes in intestinal microbiota and metabolites.<b>Result:</b> Our analysis revealed significant differences in 15 bacterial genera, with 7 being upregulated and 8 being downregulated. Furthermore, metabolomic analysis revealed changes in the distribution of amino acid and biotin metabolites in basic metabolic pathways in both feces and serum. Specifically, differentially abundant metabolites in feces were associated primarily with histidine metabolism; the biosynthesis of phenylalanine, tyrosine, and tryptophan; and tyrosine metabolism. In plasma, the differentially abundant metabolites were involved in multiple metabolic pathways, including aminoacyl-tRNA biosynthesis; glycine, serine, and threonine amino acid metabolism; valine, leucine, and isoleucine biosynthesis; tyrosine biosynthesis and metabolism; biotin metabolism; and taurine and hypotaurine metabolism. Furthermore, correlation analysis revealed that <i>Akkermansia, UCG-005, Lachnospiraceae_NK4A136_group, Lactococcus, and Butymonas</i> were associated with various differentially abundant metabolites as well as renal function, oxidative stress, and mitophagy. The changes in the intestinal flora observed in hyperuricemia may lead to imbalances in amino acid and biotin metabolism in both the intestine and host, ultimately affecting oxidative stress and mitophagy in mice and accelerating the progression of CKD.<b>Conclusion: </b>Our findings provide insights into a potential pathogenic mechanism by which hyperuricemia exacerbates renal injury in mice with renal insufficiency. Understanding these pathways may offer new therapeutic strategies for managing hyperuricemic renal injury in CKD patients.
DOI: 10.6084/m9.figshare.27367452
title: Systematic review of microRNAs in human acute kidney injury

description: Early diagnosis of acute kidney injury (AKI) is limited with current tools. MicroRNAs (miRNAs) are implicated in AKI pathogenesis in preclinical models, but less is known about their role in humans. We conducted a systematic review to identify dysregulated miRNAs in humans with AKI. We searched Ovid MEDLINE, Embase, Web of Science, and CENTRAL (August 21, 2023) for studies of human subjects with AKI. We excluded reviews and pre-clinical studies without human data. The primary outcome was dysregulated miRNAs in AKI. Two reviewers screened abstracts, reviewed full texts, performed data extraction and quality assessment (Newcastle Ottawa Scale). We screened 2,456 reports and included 92 for synthesis without meta-analysis. All studies except one were observational. Studies were grouped by etiology of AKI: cardiac surgery-associated (CS-AKI, <i>n</i> = 13 studies), sepsis (<i>n</i> = 25), nephrotoxic (<i>n</i> = 9), kidney transplant (<i>n</i> = 26), and other causes (<i>n</i> = 19). In total, 128 miRNAs were identified to be dysregulated across AKI studies (45 miRNAs upregulated, 55 downregulated, 28 both). miR-21 was the most frequently reported (<i>n</i> = 17 studies) and it was increased in all etiologies except CS-AKI where it was decreased (<i>n</i> = 3 studies). Study limitations included bias due to targeted approaches, absence of clinical data/controls, and miRNA normalization methods. Overall study quality was fair (median 5/9, range 2-8 points). Dysregulated miRNAs, particularly miR-21, have potential as AKI biomarkers. These results should be interpreted cautiously due to methodological limitations. Standardized methods and unbiased approaches are needed to validate candidate miRNA biomarkers. <b>Registration:</b> International Prospective Register of Systematic Reviews (PROSPERO CRD42020201253)
DOI: 10.6084/m9.figshare.27367452.v1
title: Systematic review of microRNAs in human acute kidney injury

description: Early diagnosis of acute kidney injury (AKI) is limited with current tools. MicroRNAs (miRNAs) are implicated in AKI pathogenesis in preclinical models, but less is known about their role in humans. We conducted a systematic review to identify dysregulated miRNAs in humans with AKI. We searched Ovid MEDLINE, Embase, Web of Science, and CENTRAL (August 21, 2023) for studies of human subjects with AKI. We excluded reviews and pre-clinical studies without human data. The primary outcome was dysregulated miRNAs in AKI. Two reviewers screened abstracts, reviewed full texts, performed data extraction and quality assessment (Newcastle Ottawa Scale). We screened 2,456 reports and included 92 for synthesis without meta-analysis. All studies except one were observational. Studies were grouped by etiology of AKI: cardiac surgery-associated (CS-AKI, <i>n</i> = 13 studies), sepsis (<i>n</i> = 25), nephrotoxic (<i>n</i> = 9), kidney transplant (<i>n</i> = 26), and other causes (<i>n</i> = 19). In total, 128 miRNAs were identified to be dysregulated across AKI studies (45 miRNAs upregulated, 55 downregulated, 28 both). miR-21 was the most frequently reported (<i>n</i> = 17 studies) and it was increased in all etiologies except CS-AKI where it was decreased (<i>n</i> = 3 studies). Study limitations included bias due to targeted approaches, absence of clinical data/controls, and miRNA normalization methods. Overall study quality was fair (median 5/9, range 2-8 points). Dysregulated miRNAs, particularly miR-21, have potential as AKI biomarkers. These results should be interpreted cautiously due to methodological limitations. Standardized methods and unbiased approaches are needed to validate candidate miRNA biomarkers. <b>Registration:</b> International Prospective Register of Systematic Reviews (PROSPERO CRD42020201253)
DOI: 10.6084/m9.figshare.26354710
title: Causal role of immune cells in IgA nephropathy: a mendelian randomization study

description: Previous observational studies have shown that immune cells play an important role in IgA nephropathy. However, the specific causal relationship between the two is inconsistent. We used a two-sample mendelian randomization(MR) analysis to investigate the causal association between 731 immune cell signatures and IgA nephropathy in this study. Based on published GWAS data, immune cells were characterized by four immune types absolute cell (AC) counts, median fluorescence intensity (MFI), morphological parameters (MP), relative cell (RC) counts. Meanwhile, heterogeneity test, horizontal pleiotropy and sensitivity test were used to evaluate the robustness and reliability of the results. An important causal association was achieved for 14 RC traits/IgA nephropathy, 3 AC traits/IgA nephropathy, 10 MFI traits/IgA nephropathy, and 1 MP trait/IgA nephropathy. However, after false discovery rate (FDR) correction, only one immunophenotype was found to be protective against IgA nephropathy. The OR of herpesvirus entry mediator (HVEM) on terminally differentiated CD4+ T cell (maturation stages of T-cell panel) on IgA nephropathy risk was estimated to be 0.727 (95%CI: 0.624-0.847, <i>p</i> = 4.20e − 05, P<sub>FDR</sub> = 0.023) according to inverse variance weighting (IVW) method, and the weighted-median method yielded similar results (OR = 0.743, 95% CI: 0.596-0.927, <i>p</i> = 0.008). Although not statistically significant, the association was consistent with MR-Egger, simple mode and weighted mode. Our study further confirmed that immune cells play a complex and important role in the pathogenesis of IgA nephropathy, providing evidence for clinical research.
DOI: 10.6084/m9.figshare.26354710.v1
title: Causal role of immune cells in IgA nephropathy: a mendelian randomization study

description: Previous observational studies have shown that immune cells play an important role in IgA nephropathy. However, the specific causal relationship between the two is inconsistent. We used a two-sample mendelian randomization(MR) analysis to investigate the causal association between 731 immune cell signatures and IgA nephropathy in this study. Based on published GWAS data, immune cells were characterized by four immune types absolute cell (AC) counts, median fluorescence intensity (MFI), morphological parameters (MP), relative cell (RC) counts. Meanwhile, heterogeneity test, horizontal pleiotropy and sensitivity test were used to evaluate the robustness and reliability of the results. An important causal association was achieved for 14 RC traits/IgA nephropathy, 3 AC traits/IgA nephropathy, 10 MFI traits/IgA nephropathy, and 1 MP trait/IgA nephropathy. However, after false discovery rate (FDR) correction, only one immunophenotype was found to be protective against IgA nephropathy. The OR of herpesvirus entry mediator (HVEM) on terminally differentiated CD4+ T cell (maturation stages of T-cell panel) on IgA nephropathy risk was estimated to be 0.727 (95%CI: 0.624-0.847, <i>p</i> = 4.20e − 05, P<sub>FDR</sub> = 0.023) according to inverse variance weighting (IVW) method, and the weighted-median method yielded similar results (OR = 0.743, 95% CI: 0.596-0.927, <i>p</i> = 0.008). Although not statistically significant, the association was consistent with MR-Egger, simple mode and weighted mode. Our study further confirmed that immune cells play a complex and important role in the pathogenesis of IgA nephropathy, providing evidence for clinical research.
DOI: 10.6084/m9.figshare.26207266
title: Predictive nomogram model for severe coronary artery calcification in end-stage kidney disease patients

description: The Agatston coronary artery calcification score (CACS) is an assessment index for coronary artery calcification (CAC). This study aims to explore the characteristics of CAC in end-stage kidney disease (ESKD) patients and establish a predictive model to assess the risk of severe CAC in patients. CACS of ESKD patients was assessed using an electrocardiogram-gated coronary computed tomography (CT) scan with the Agatston scoring method. A predictive nomogram model was established based on stepwise regression. An independent validation cohort comprised of patients with ESKD from multicentres. 369 ESKD patients were enrolled in the training set, and 127 patients were included in the validation set. In the training set, the patients were divided into three subgroups: no calcification (CACS = 0, <i>n</i> = 98), mild calcification (0 &lt; CACS ≤ 400, <i>n</i> = 141) and severe calcification (CACS &gt; 400, <i>n</i> = 130). Among the four coronary branches, the left anterior descending branch (LAD) accounted for the highest proportion of calcification. Stepwise regression analysis showed that age, dialysis vintage, β-receptor blocker, calcium-phosphorus product (Ca × P), and alkaline phosphatase (ALP) level were independent risk factors for severe CAC. A nomogram that predicts the risk of severe CAC in ESKD patients has been internally and externally validated, demonstrating high sensitivity and specificity. CAC is both prevalent and severe in ESKD patients. In the four branches of the coronary arteries, LAD calcification is the most common. Our validated nomogram model, based on clinical risk factors, can help predict the risk of severe coronary calcification in ESKD patients who cannot undergo coronary CT analysis.
DOI: 10.6084/m9.figshare.26207266.v1
title: Predictive nomogram model for severe coronary artery calcification in end-stage kidney disease patients

description: The Agatston coronary artery calcification score (CACS) is an assessment index for coronary artery calcification (CAC). This study aims to explore the characteristics of CAC in end-stage kidney disease (ESKD) patients and establish a predictive model to assess the risk of severe CAC in patients. CACS of ESKD patients was assessed using an electrocardiogram-gated coronary computed tomography (CT) scan with the Agatston scoring method. A predictive nomogram model was established based on stepwise regression. An independent validation cohort comprised of patients with ESKD from multicentres. 369 ESKD patients were enrolled in the training set, and 127 patients were included in the validation set. In the training set, the patients were divided into three subgroups: no calcification (CACS = 0, <i>n</i> = 98), mild calcification (0 &lt; CACS ≤ 400, <i>n</i> = 141) and severe calcification (CACS &gt; 400, <i>n</i> = 130). Among the four coronary branches, the left anterior descending branch (LAD) accounted for the highest proportion of calcification. Stepwise regression analysis showed that age, dialysis vintage, β-receptor blocker, calcium-phosphorus product (Ca × P), and alkaline phosphatase (ALP) level were independent risk factors for severe CAC. A nomogram that predicts the risk of severe CAC in ESKD patients has been internally and externally validated, demonstrating high sensitivity and specificity. CAC is both prevalent and severe in ESKD patients. In the four branches of the coronary arteries, LAD calcification is the most common. Our validated nomogram model, based on clinical risk factors, can help predict the risk of severe coronary calcification in ESKD patients who cannot undergo coronary CT analysis.
DOI: 10.6084/m9.figshare.26879647
title: Early reduction in total cholesterol to high-density lipoprotein cholesterol ratio predicts hydroxychloroquine efficacy in treating IgA nephropathy

description: Hydroxychloroquine (HCQ) effectively improves lipid levels in patients with autoimmune diseases. This study aimed to examine the effect of HCQ on lipid profiles in patients with immunoglobulin A (IgA) nephropathy (IgAN) and determine whether alterations in lipid profiles can predict the efficacy of HCQ. This study retrospectively analyzed 77 patients, and the total cholesterol to high-density lipoprotein cholesterol (TC/HDL-C) decline rate after 3 months of HCQ treatment was selected as a predictor based on receiver operating curve analysis. Patients were then divided into low and high TC/HDL-C decline rate groups based on the optimal cutoff value. The Cox proportional hazard model and Kaplan–Meier curve were used to evaluate the value of the TC/HDL-C decline rate in predicting the efficacy of HCQ in patients with IgAN. Patients in the high TC/HDL-C decline rate group with ≥50% decrease in proteinuria from baseline experienced a significant improvement during the follow-up. Kaplan–Meier analysis revealed that a high TC/HDL-C decline rate was strongly associated with a higher proteinuria reduction rate in patients with IgAN. Furthermore, multivariate Cox analysis indicated that a higher reduction in the TC/HDL-C ratio (hazard ratio: 2.314; 95% confidence interval: 1.234–4.340; <i>p</i> = 0.009) was an independent predictive indicator for achieving ≥50% reduction in proteinuria with HCQ therapy in IgAN. HCQ effectively improves lipid profiles in patients with IgAN, and an early decrease in the TC/HDL-C ratio serves as a predictor of better outcomes in patients treated with HCQ.