cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.28319893.v1
title: Prevalence of acute kidney injury in Mexico; a systematic review and meta-analysis of pre-pandemic reports

description: Acute Kidney Injury (AKI) is a health problem worldwide, accounting for high hospital morbidity and mortality. There is little available information regarding the characteristics and incidence of AKI in Latin America (LA), especially in Mexico. Systematically search the literature and perform a meta-analysis of the epidemiology of AKI in Mexico, to provide data on AKI and kidney replacement therapy (KRT) that would contribute to general knowledge in this matter. We performed a systematic search for articles in pediatric and adult patients admitted to the general ward, Emergency Room or Intensive Care Unit published between January 1, 2000, and September 30, 2024. MEDLINE LILIACS, EMBASE and SciELO were searched, as additional reports from supplements, abstracts, and conference sessions. We performed a random-effects meta-analysis for clinically and methodologically comparable studies to estimate the frequency of AKI and KRT. We calculated pooled estimates stratified by age group, year of publication, and setting. 83 full-text articles were included. The percentage of AKI was calculated at 35% (95% CI, 28–42). Mortality for AKI adult patients was 36% (95% CI, 28–45). An overall KRT rate was 7% (95% CI, 6–9), all-cause mortality for AKI requiring KRT was 49% (95% CI, 42–56), with a global Ι2 estimated in 99.87% (<i>p</i> &lt; 0.01). AKI is common in Mexico and remains a main public health problem that needs to be addressed at every level of care. Efforts should be made to reinitiate AKI research and control in Mexico and LA.
DOI: 10.6084/m9.figshare.28579109
title: Effectiveness of abdominal bracing core exercises as rehabilitation therapy for reducing abdominal symptoms in patients with autosomal dominant polycystic kidney disease and significant polycystic liver disease

description: In patients with autosomal dominant polycystic kidney disease (ADPKD) who also have polycystic liver disease (PLD), organomegaly often leads to abdominal symptoms. Abdominal bracing core (ABC) exercises have been validated as effective for alleviating chronic back pain. The purpose of this study was to assess the effectiveness of ABC rehabilitation exercises in reducing pain in ADPKD patients with significant PLD. Significant PLD was defined as a height-adjusted total liver volume (htTLV) exceeding 1,600 mL/m. Both the control groups (<i>n</i> = 11) and intervention (<i>n</i> = 12) and received an outpatient consultation on nutrition and exercise; however, only the intervention group participated in ABC exercises. After a 3-month biweekly intervention, changes in pain assessed by the Korean Oswestry Disability Index, abdominal symptoms, quality of life (QoL) by the second version of the short-form 36-item Health Survey, and bioelectrical impedance analysis (BIA) were analyzed. The participants comprised 23 individuals (male: 4, female: 19). Their mean age was 54, and the mean ± SD of htTLV was 2,706 ± 1,335 mL/m. The mean ± SD of eGFR was 53.9 ± 29.0 mL/min/1.73 m<sup>2</sup>. After the intervention, pain and pressure-related symptoms significantly decreased in some cases; however, gastrointestinal symptoms did not improve. Pain (control vs. intervention: −1.9 vs. 1.0) and QoL (1.20 vs. 0.93) and showed significant improvements. The results of BIA indicated a noticeable change in the soft lean mass of the proximal body (0.4 vs. −0.2). Our study demonstrates that ABC exercise is effective in alleviating pain and increasing soft lean mass in ADPKD patients who have significant PLD.
DOI: 10.6084/m9.figshare.28579109.v1
title: Effectiveness of abdominal bracing core exercises as rehabilitation therapy for reducing abdominal symptoms in patients with autosomal dominant polycystic kidney disease and significant polycystic liver disease

description: In patients with autosomal dominant polycystic kidney disease (ADPKD) who also have polycystic liver disease (PLD), organomegaly often leads to abdominal symptoms. Abdominal bracing core (ABC) exercises have been validated as effective for alleviating chronic back pain. The purpose of this study was to assess the effectiveness of ABC rehabilitation exercises in reducing pain in ADPKD patients with significant PLD. Significant PLD was defined as a height-adjusted total liver volume (htTLV) exceeding 1,600 mL/m. Both the control groups (<i>n</i> = 11) and intervention (<i>n</i> = 12) and received an outpatient consultation on nutrition and exercise; however, only the intervention group participated in ABC exercises. After a 3-month biweekly intervention, changes in pain assessed by the Korean Oswestry Disability Index, abdominal symptoms, quality of life (QoL) by the second version of the short-form 36-item Health Survey, and bioelectrical impedance analysis (BIA) were analyzed. The participants comprised 23 individuals (male: 4, female: 19). Their mean age was 54, and the mean ± SD of htTLV was 2,706 ± 1,335 mL/m. The mean ± SD of eGFR was 53.9 ± 29.0 mL/min/1.73 m<sup>2</sup>. After the intervention, pain and pressure-related symptoms significantly decreased in some cases; however, gastrointestinal symptoms did not improve. Pain (control vs. intervention: −1.9 vs. 1.0) and QoL (1.20 vs. 0.93) and showed significant improvements. The results of BIA indicated a noticeable change in the soft lean mass of the proximal body (0.4 vs. −0.2). Our study demonstrates that ABC exercise is effective in alleviating pain and increasing soft lean mass in ADPKD patients who have significant PLD.
DOI: 10.6084/m9.figshare.28606790
title: Causal impact of elevated body mass index on diabetic kidney disease: an integrated Mendelian randomization and Global Burden of Disease Study 2021 analysis

description: Elevated body mass index (BMI) has been implicated in the pathogenesis of diabetic kidney disease among patients with type 2 diabetes mellitus (T2DKD). However, establishing a causal relationship and quantifying the resultant global health impact remain challenging. A two-sample Mendelian randomization (MR) analysis was conducted using summary-level data obtained from the IEU database. Multiple MR approaches, including inverse variance weighted (IVW), MR-Egger regression, weighted median, weighted mode, and simple mode methods, were implemented to ensure robust causal inference. In parallel, Global Burden of Disease Study (GBD) 2021 were analyzed to determine the trends in mortality and disability-adjusted life years (DALYs) in T2DKD attributable to high BMI (HBMI-T2DKD) from 1990 to 2021. Joinpoint regression was used to estimate the average annual percent change (AAPC). Bayesian age-period-cohort (BAPC) models were then applied to project the disease burden through 2049. MR analyses provided strong evidence for a causal relationship between elevated BMI and T2DKD. The GBD analysis revealed a sustained global increase in HBMI-T2DKD burden over the past three decades. Between 1990 and 2021, the result of AAPC indicated a persistent upward trend. The burden was particularly high among older adults, with the highest impact observed in East Asia and middle Socio-Demographic Index (SDI) region. By 2049, HBMI-T2DKD-related disease burden were projected to continue rising. Elevated BMI is a significant causal risk factor for T2DKD. The integration of MR and GBD 2021 data underscores the urgent need for targeted public health interventions to reduce BMI levels, especially in high-risk regions and aging populations.
DOI: 10.6084/m9.figshare.28606790.v1
title: Causal impact of elevated body mass index on diabetic kidney disease: an integrated Mendelian randomization and Global Burden of Disease Study 2021 analysis

description: Elevated body mass index (BMI) has been implicated in the pathogenesis of diabetic kidney disease among patients with type 2 diabetes mellitus (T2DKD). However, establishing a causal relationship and quantifying the resultant global health impact remain challenging. A two-sample Mendelian randomization (MR) analysis was conducted using summary-level data obtained from the IEU database. Multiple MR approaches, including inverse variance weighted (IVW), MR-Egger regression, weighted median, weighted mode, and simple mode methods, were implemented to ensure robust causal inference. In parallel, Global Burden of Disease Study (GBD) 2021 were analyzed to determine the trends in mortality and disability-adjusted life years (DALYs) in T2DKD attributable to high BMI (HBMI-T2DKD) from 1990 to 2021. Joinpoint regression was used to estimate the average annual percent change (AAPC). Bayesian age-period-cohort (BAPC) models were then applied to project the disease burden through 2049. MR analyses provided strong evidence for a causal relationship between elevated BMI and T2DKD. The GBD analysis revealed a sustained global increase in HBMI-T2DKD burden over the past three decades. Between 1990 and 2021, the result of AAPC indicated a persistent upward trend. The burden was particularly high among older adults, with the highest impact observed in East Asia and middle Socio-Demographic Index (SDI) region. By 2049, HBMI-T2DKD-related disease burden were projected to continue rising. Elevated BMI is a significant causal risk factor for T2DKD. The integration of MR and GBD 2021 data underscores the urgent need for targeted public health interventions to reduce BMI levels, especially in high-risk regions and aging populations.
DOI: 10.6084/m9.figshare.29039717
title: Membranous nephropathy concurrent with renal amyloidosis: a six-patient report and literature review

description: The KDIGO 2021 guidelines suggest that individuals who test positive for serum anti-phospholipase A2 receptor (anti-PLA2R) antibodies may not require a renal biopsy to establish a diagnosis of membranous nephropathy (MN). However, it is imperative to acknowledge that MN can coexist with other chronic kidney diseases. In instances where MN is comorbid with IgA nephropathy, diabetic nephropathy, or focal segmental glomerulosclerosis, the therapeutic approach tends to be analogous. Nevertheless, there is a significant disparity in both the treatment regimen and the prognosis between MN and renal amyloidosis, with variations existing even among distinct subtypes of renal amyloidosis. Given that both MN and renal amyloidosis exhibit a predilection for the geriatric population, it is prudent to consider the possibility of MN concurrent with renal amyloidosis in elderly patients who test positive for serum anti-PLA2R antibodies. This consideration should precede a straightforward MN treatment strategy. In this report, we present six patients with MN concurrent with renal amyloidosis identified at our center over the past 14 years; in five of whom were positive for serum anti-PLA2R antibodies. We further elucidated the divergent clinicopathological characteristics and prognostic implications of these cases.
DOI: 10.6084/m9.figshare.29039717.v1
title: Membranous nephropathy concurrent with renal amyloidosis: a six-patient report and literature review

description: The KDIGO 2021 guidelines suggest that individuals who test positive for serum anti-phospholipase A2 receptor (anti-PLA2R) antibodies may not require a renal biopsy to establish a diagnosis of membranous nephropathy (MN). However, it is imperative to acknowledge that MN can coexist with other chronic kidney diseases. In instances where MN is comorbid with IgA nephropathy, diabetic nephropathy, or focal segmental glomerulosclerosis, the therapeutic approach tends to be analogous. Nevertheless, there is a significant disparity in both the treatment regimen and the prognosis between MN and renal amyloidosis, with variations existing even among distinct subtypes of renal amyloidosis. Given that both MN and renal amyloidosis exhibit a predilection for the geriatric population, it is prudent to consider the possibility of MN concurrent with renal amyloidosis in elderly patients who test positive for serum anti-PLA2R antibodies. This consideration should precede a straightforward MN treatment strategy. In this report, we present six patients with MN concurrent with renal amyloidosis identified at our center over the past 14 years; in five of whom were positive for serum anti-PLA2R antibodies. We further elucidated the divergent clinicopathological characteristics and prognostic implications of these cases.
DOI: 10.6084/m9.figshare.29039720
title: miR-29a-3p/<i>Vegfa</i> axis modulates high phosphate-induced vascular smooth muscle cell calcification

description: Vascular calcification (VC) is a major contributor to the progression of cardiovascular disease (CVD). The VC is characterized by arterial stiffness and impaired blood flow. This pathology is especially prevalent in chronic kidney disease (CKD), where dysregulated mineral metabolism and elevated phosphate levels accelerate calcification of vascular smooth muscle cells (VSMCs). Emerging evidence suggests that microRNAs (miRNAs) are key regulators of VC, with the miR-29 family implicated in extracellular matrix remodeling and calcification. We investigated the role of the miR-29a-3p/vascular endothelial growth factor A (<i>Vegfa</i>) axis in CKD-associated VC. Dual-luciferase assays and bioinformatic analysis confirmed that miR-29a-3p directly targets <i>Vegfa</i>, a critical regulator of vascular homeostasis. miR-29a-3p overexpression significantly attenuated VSMC calcification under high phosphate conditions, as indicated by significantly reduced Alizarin Red staining (ARS, <i>P</i> &lt; 0.0001) and intracellular calcium content (ICC, <i>P</i> = 0.0235). Conversely, <i>Vegfa</i> overexpression exacerbated calcification (<i>P</i> = 0.0010 for ICC and <i>P</i> = 0.0001 for ARS). <i>Vegfa</i> knockdown mitigated these effects (<i>P</i> &lt; 0.0001 for both ARS and ICC). Notably, miR-29a-3p counteracted calcification even in <i>Vegfa</i>-overexpressing cells (<i>P</i> &lt; 0.0001 for ARS and <i>P</i> = 0.0235 for ICC), underscoring its protective role in vascular integrity. These findings highlight the therapeutic potential of targeting the miR-29a-3p/<i>Vegfa</i> axis for VC management in patients with CKD. miRNA-based interventions may offer a promising strategy for preventing pathological calcification and reducing the risk of CVD in affected patients.
DOI: 10.6084/m9.figshare.29039720.v1
title: miR-29a-3p/<i>Vegfa</i> axis modulates high phosphate-induced vascular smooth muscle cell calcification

description: Vascular calcification (VC) is a major contributor to the progression of cardiovascular disease (CVD). The VC is characterized by arterial stiffness and impaired blood flow. This pathology is especially prevalent in chronic kidney disease (CKD), where dysregulated mineral metabolism and elevated phosphate levels accelerate calcification of vascular smooth muscle cells (VSMCs). Emerging evidence suggests that microRNAs (miRNAs) are key regulators of VC, with the miR-29 family implicated in extracellular matrix remodeling and calcification. We investigated the role of the miR-29a-3p/vascular endothelial growth factor A (<i>Vegfa</i>) axis in CKD-associated VC. Dual-luciferase assays and bioinformatic analysis confirmed that miR-29a-3p directly targets <i>Vegfa</i>, a critical regulator of vascular homeostasis. miR-29a-3p overexpression significantly attenuated VSMC calcification under high phosphate conditions, as indicated by significantly reduced Alizarin Red staining (ARS, <i>P</i> &lt; 0.0001) and intracellular calcium content (ICC, <i>P</i> = 0.0235). Conversely, <i>Vegfa</i> overexpression exacerbated calcification (<i>P</i> = 0.0010 for ICC and <i>P</i> = 0.0001 for ARS). <i>Vegfa</i> knockdown mitigated these effects (<i>P</i> &lt; 0.0001 for both ARS and ICC). Notably, miR-29a-3p counteracted calcification even in <i>Vegfa</i>-overexpressing cells (<i>P</i> &lt; 0.0001 for ARS and <i>P</i> = 0.0235 for ICC), underscoring its protective role in vascular integrity. These findings highlight the therapeutic potential of targeting the miR-29a-3p/<i>Vegfa</i> axis for VC management in patients with CKD. miRNA-based interventions may offer a promising strategy for preventing pathological calcification and reducing the risk of CVD in affected patients.
DOI: 10.6084/m9.figshare.28171331
title: Identification of biomarkers for chronic renal fibrosis and their relationship with immune infiltration and cell death

description: Chronic kidney disease (CKD) represents a significant global public health challenge. This study aims to identify biomarkers of renal fibrosis and elucidate the relationship between unilateral ureteral obstruction (UUO), immune infiltration, and cell death. Gene expression matrices for UUO were retrieved from the gene expression omnibus (GSE36496, GSE79443, GSE217650, and GSE217654). Seven genes identified through Protein-Protein Interaction (PPI) network and Support Vector Machine-Recursive Feature Elimination (SVM-RFE) analysis were validated using qRT-PCR in both <i>in vivo</i> and <i>in vitro</i> UUO experiments. WB assays were employed to investigate the role of Clec4n within NF-κB signaling pathway in renal fibrosis. The composition of immune cells in UUO was assessed using CIBERSORT, and gene set variant analysis (GSVA) was utilized to evaluate prevalent signaling pathways and cell death indices. GO and KEGG enrichment analyses revealed numerous inflammation-related pathways significantly enriched in UUO conditions. Bcl2a1b, Clec4n, and Col1a1 were identified as potential diagnostic biomarkers for UUO. Analysis of immune cell infiltration indicated a correlation between UUO and enhanced mast cell activation. Silencing Clec4n expression appeared to mitigate the inflammatory response in renal fibrosis. GSVA results indicated elevated inflammatory pathway scores in UUO, with significant differences in disulfiram and cuproptosis scores compared to those in the normal murine kidney group. Bcl2a1b, Clec4n, and Col1a1 may serve as biomarkers for diagnosing UUO. UUO development is closely linked to immune cell infiltration, activation of inflammatory pathways, disulfiram, and cuproptosis processes.
DOI: 10.6084/m9.figshare.28171331.v1
title: Identification of biomarkers for chronic renal fibrosis and their relationship with immune infiltration and cell death

description: Chronic kidney disease (CKD) represents a significant global public health challenge. This study aims to identify biomarkers of renal fibrosis and elucidate the relationship between unilateral ureteral obstruction (UUO), immune infiltration, and cell death. Gene expression matrices for UUO were retrieved from the gene expression omnibus (GSE36496, GSE79443, GSE217650, and GSE217654). Seven genes identified through Protein-Protein Interaction (PPI) network and Support Vector Machine-Recursive Feature Elimination (SVM-RFE) analysis were validated using qRT-PCR in both <i>in vivo</i> and <i>in vitro</i> UUO experiments. WB assays were employed to investigate the role of Clec4n within NF-κB signaling pathway in renal fibrosis. The composition of immune cells in UUO was assessed using CIBERSORT, and gene set variant analysis (GSVA) was utilized to evaluate prevalent signaling pathways and cell death indices. GO and KEGG enrichment analyses revealed numerous inflammation-related pathways significantly enriched in UUO conditions. Bcl2a1b, Clec4n, and Col1a1 were identified as potential diagnostic biomarkers for UUO. Analysis of immune cell infiltration indicated a correlation between UUO and enhanced mast cell activation. Silencing Clec4n expression appeared to mitigate the inflammatory response in renal fibrosis. GSVA results indicated elevated inflammatory pathway scores in UUO, with significant differences in disulfiram and cuproptosis scores compared to those in the normal murine kidney group. Bcl2a1b, Clec4n, and Col1a1 may serve as biomarkers for diagnosing UUO. UUO development is closely linked to immune cell infiltration, activation of inflammatory pathways, disulfiram, and cuproptosis processes.
DOI: 10.6084/m9.figshare.28776692
title: miR-1225-3p regulates fibrosis in mesangial cells via SMURF2-mediated ubiquitination of ChREBP in diabetic kidney disease

description: Diabetic kidney disease (DKD), characterized by mesangial fibrosis and renal dysfunction, is a major microvascular complication of diabetes. Studies have shown that miRNAs are closely related to the progression of DKD. Therefore, in this study, we aimed to explore whether miR-1225-3p can regulate Smad ubiquitin regulatory factor 2 (SMURF2)-mediated carbohydrate response element binding protein (ChREBP) ubiquitination through Rho GTPase-activating protein 5 (ARHGAP5) to affect fibrosis in DKD. DKD mice were established by intraperitoneally injecting streptozocin (STZ), and a DKD cell model was generated by culturing in media supplemented with 25 mmol/L glucose (high glucose, HG). StarBase was used to predict the target binding sites between miR-1225-3p and ARHGAP5, and a dual-luciferase reporter gene assay was used to verify this relationship. Western blotting, RT–qPCR, flow cytometry, immunoprecipitation, ELISAs, HE staining, and Masson staining were used to detect relevant indicators. ARHGAP5 and SMURF2 expression was decreased, but ChREBP was highly expressed in the renal tissue of DKD mice and HG-induced mouse mesangial cells (MMCs). miR-1225-3p could target and regulate the transcription of ARHGAP5, and an association between ARHGAP5 and SMURF2 was revealed. miR-1225-3p facilitated fibrosis and oxidative stress in MCCs by inhibiting ARHGAP5. In addition, SMURF2 promoted the ubiquitination of HA-ChREBP, and miR-1225-3p facilitated fibrosis and oxidative stress by mediating the ARHGAP5/SMURF2-mediated ubiquitination of ChREBP in MCCs. Furthermore, the miR-1225-3p inhibitor inhibited fibrosis and inflammation in the renal tissues of DKD mice. miR-1225-3p facilitates fibrosis and oxidative stress by mediating ARHGAP5/SMURF2-mediated ubiquitination of ChREBP.
DOI: 10.6084/m9.figshare.28776692.v1
title: miR-1225-3p regulates fibrosis in mesangial cells via SMURF2-mediated ubiquitination of ChREBP in diabetic kidney disease

description: Diabetic kidney disease (DKD), characterized by mesangial fibrosis and renal dysfunction, is a major microvascular complication of diabetes. Studies have shown that miRNAs are closely related to the progression of DKD. Therefore, in this study, we aimed to explore whether miR-1225-3p can regulate Smad ubiquitin regulatory factor 2 (SMURF2)-mediated carbohydrate response element binding protein (ChREBP) ubiquitination through Rho GTPase-activating protein 5 (ARHGAP5) to affect fibrosis in DKD. DKD mice were established by intraperitoneally injecting streptozocin (STZ), and a DKD cell model was generated by culturing in media supplemented with 25 mmol/L glucose (high glucose, HG). StarBase was used to predict the target binding sites between miR-1225-3p and ARHGAP5, and a dual-luciferase reporter gene assay was used to verify this relationship. Western blotting, RT–qPCR, flow cytometry, immunoprecipitation, ELISAs, HE staining, and Masson staining were used to detect relevant indicators. ARHGAP5 and SMURF2 expression was decreased, but ChREBP was highly expressed in the renal tissue of DKD mice and HG-induced mouse mesangial cells (MMCs). miR-1225-3p could target and regulate the transcription of ARHGAP5, and an association between ARHGAP5 and SMURF2 was revealed. miR-1225-3p facilitated fibrosis and oxidative stress in MCCs by inhibiting ARHGAP5. In addition, SMURF2 promoted the ubiquitination of HA-ChREBP, and miR-1225-3p facilitated fibrosis and oxidative stress by mediating the ARHGAP5/SMURF2-mediated ubiquitination of ChREBP in MCCs. Furthermore, the miR-1225-3p inhibitor inhibited fibrosis and inflammation in the renal tissues of DKD mice. miR-1225-3p facilitates fibrosis and oxidative stress by mediating ARHGAP5/SMURF2-mediated ubiquitination of ChREBP.