Analysis of early diagnostic markers for acute kidney injury after cardiac surgery
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE268959 | GEO | 2024/06/08
REPOSITORIES: GEO
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Project description:This study aimed to investigate the molecular mechanism responsible for primary open-angle glaucoma (POAG) progression. We analyzed microRNAs (miRNAs) expression profiling in aqueous humor (AH) of both POAG patients and normal controls, using a microarray-based approach. Subsequently, differentially expressed miRNAs (DEmiRNAs) were identified using Bayes moderated t-test. Next, DEmiRNAs target genes were predicted based on miRNA databases, followed by GO analysis and pathway analysis using DAVID. Furthermore, OAG-related genes analysis for target genes was carried out using CTD database, respectively. Finally, verification of DEmiRNAs expression levels was performed by RT-qPCR. A total of 40 significant DEmiRNAs were identified between control and POAG groups, including 24 up-regulated miRNAs and 16 down-regulated miRNAs. Further, the target genes of hsa-miR-206, including BMP2, SMAD4, ID2, and TNF, were mainly enriched in transforming growth factor-β (TGF-β) signaling pathway. While, target genes of hsa-miR-184, hsa-miR-34c-5p, hsa-miR-7-2-3p and hsa-miR-20b-3p, including BCL2, EPHB2, VEGFA, COL4A1, APC, and TGFBR1, were enriched in eye development. Moreover, FNDC3B, CAV2 and VEGF, target genes of hsa-miR-206 or hsa-miR-34c-5p, were the OAG-related genes. Ultimately, RT-qPCR analysis confirmed that mRNA levels of hsa-miR-206, hsa-miR-7-2-3p, and hsa-miR-20b-3p were increased, while those of hsa-miR-184 and hsa-miR-34c-5p were decreased in POAG compared with normal groups (P < 0.05). Hsa-miR-206, hsa-miR-184, hsa-miR-34c-5p, hsa-miR-7-2-3p and hsa-miR-20b-3p might play a significant role in the pathogenesis of POAG and hsa-miR-206 might be associated with the development of POAG by regulating TGF-β signaling pathway. These results might provide insight toward a better understanding of the pathogenesis of POAG.
2015-08-04 | GSE71639 | GEO
Project description:Objectives: Secretion of extracellular vesicles (EV) and associated micro-RNAs (miR) is altered during cellular stress and may serve as biomarkers of organ injury. We hypothesized that measuring changes in urinary levels of EV and miR will predict the onset of acute kidney injury in cardiac surgery patients. Design: Predictive accuracy biomarker study performed in the cohort of the REVAKI-2 trial Setting: Single center ICU between September 2015 and September 2018 Interventions: Intravenous sildenafil citrate 12.5 mg kg-1 over 150 min or dextrose 5% at the commencement of surgery. Measurements and main results: Urine samples were collected before and 24 hours after the procedure from 93 cardiac surgery patients. Urine EV concentrations and size distribution were assessed using NanoSight. EV derivation and levels were measured using flow cytometry. Samples from 10 selected patients were sequenced to detect differentially expressed miR. Verification was performed with advanced TaqMan assays in samples from all patients. Urine EV concentrations significantly increased in patients with AKI after surgery, with the percentage of EV positive for aquaporin-2 and β1-integrin also increasing. Pre surgery podocalyxin-positive EV were significantly lower, and β1-integrin EV werehigher in patients with AKI. The levels of the former correlated with the severity of theinjury. miR-125a-5p was expressed at higher levels in urine from patients with AKI stage 2/3. Levels of miR-10a-5p decreased after surgery in AKI patients; its levels correlated with the severity of the injury. Preoperative levels of podocalyxin EVs and miR-125a-5p had moderate AKI predictive value and, in a logistic model together with ICU lactate levels, offered good (AUC = 80.9%) AKI prediction. Conclusions: Lower levels of podocalyxin-positive EV at baseline predict the severity of post-surgery AKI. Urine EV concentrations and miR expression offer excellent predictive accuracy when combined with commonly measured biomarkers.
2022-02-26 | GSE197272 | GEO
Project description:Background: Cardiac surgery-associated acute kidney injury (CSA-AKI) may be related to the increase of chronic kidney disease and mortality in critically ill patients, so developing potential biomarkers is particularly important for disease prediction and early diagnosis. The purpose of this study was to investigate the alteration profiles of plasma metabolome and the possible links with urinary metabolome in patients with CSA-AKI. Methods: Non-targeted metabolomics was performed on plasma samples collected from groups of patients with CSA-AKI at different time points, including Before_AKI (uninjured kidney), AKI_Day1 (injured kidney) and AKI_Day14 (recovered kidney). The differential plasma metabolites associated with CSA-AKI were screened out using multivariate and univariate statistical methods, and altered metabolic pathways were identified by examining the Kyoto Encyclopedia of Genes and Genomes database. After receiver operating characteristic analysis to obtain potential biomarkers, the differential plasma metabolites with Level 1 were used for correlation analysis and metabolomic interplay with urinary metabolome. Results: Nearly 1750 plasma metabolites were identified through bioinformatics methods at Annotation Levels 1-3. The plasma metabolome of injured kidney can be well separated from the plasma metabolomes of uninjured or recovered groups, but the plasma samples from the AKI_Day14 and Before_AKI groups cannot be distinguished using statistical analysis. Compared with the uninjured kidney group, the patients with CSA-AKI displayed dramatic changes in plasma metabolism, particularly for amino acid metabolism. As for the potential biomarkers with Level 1 identification in the plasma metabolome, carnitines and amino acid metabolites exhibited a significant positive correlation, while carnitines and organic acids in plasma also involved in the metabolomic interplay with urinary metabolome. Conclusions: Plasma metabolite disorder was observed in patients with CSA-AKI due to ischaemia and medical treatment, and the recovered patients’ systemic status were able to return to normal. This work provides data on plasma metabolite markers on CSA-AKI and possible link to urinary metabolome.
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Project description:Low cardiac output and kidney congestion are related to cardiac surgery-associated acute kidney injury (CSA-AKI), which is one of the most prevalent complications of cardiac surgery. This pathological process may be connected with a great risk of developing chronic kidney disease and mortality. This study aimed to investigate the possible correlations between gut microbiota metabolism and CSA-AKI.
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2009-09-15 | GSE14857 | GEO
Project description:Friedreich’s ataxia (FRDA; OMIM 229300), an autosomal recessive neurodegenerative mitochondrial disease, is the most prevalent hereditary ataxia. In addition, FRDA patients showed additional non-neurological features such as scoliosis, diabetes and cardiac complications. Hypertrophic cardiomyopathy, which is found in two thirds of patients at the time of diagnosis, is the primary cause of death in these patients. In this data set, using small RNA-sequencing of small RNA purified from plasma samples of FRDA patients and controls we identified differential expression of miRNAs (hsa-miR-128-3p, hsa-miR-625-3p, hsa-miR-130b-5p, hsa-miR-151a-5p, hsa-miR-330-3p, hsa-miR-323a-3p, and hsa-miR-142-3p) between both groups. In addition, we found that miR-323a-3p can be used as a biomarker for differentiation of FRDA patients with cardiac problems. Identification of miRNA signatures could therefore provide new molecular explanation for pathological mechanisms occurring during the natural history of the FRDA. Since miRNA levels change with disease progression and pharmacological interventions, miRNAs will contribute to design new therapeutic strategies and improve clinical decisions.
2017-10-18 | GSE105052 | GEO
Project description:Background: Cardiac surgery-associated acute kidney injury (CS-AKI) is reported in 20-30% of patients undergoing cardiac surgery and, leading to poor outcomes and increased healthcare costs. Because the pathophysiology of CS-AKI is complex and has not been fully elucidated, no effective preventive and interventional strategy has been reported. Nitrite, a nitric oxide (NO) donor under hypoxic conditions, has shown to exert organ-protective effects in various kind of preclinical models, however, its efficacy in CS-AKI remains unclear. Objectives: This study aimed to generate a rat cardiopulmonary bypass (CPB) model to induce AKI, identify key molecular pathways involved in its pathophysiology, and evaluate the renoprotective effects of nitrite. Methods: A CPB model was established using rats and AKI was confirmed through molecular and histological analysis. RNA-seq was performed to identify differentially expressed genes and enriched pathway. Nitrite (2 mg/kg) was intravenously administered prior to CPB, and its effects on kidney injury markers and inflammation-related pathways were evaluated. Results: AKI was successfully produced in our rat CPB model, as evidenced by increased KIM-1 and NGAL expression and renal histological damage. RNA-seq revealed significant activation of multiple inflammation-related pathways, including TNF and NFκB signaling pathway. Nitrite administration significantly reduced KIM-1 and NGAL expression and suppressed these pathways associated with development of AKI. Conclusion: This study underscores the role of inflammation in CS-AKI pathophysiology and demonstrates the renoprotective potential of nitrite. These findings provide a foundation for further investigations into nitrite's mechanisms and its potential clinical application in cardiac surgery.
2025-03-01 | GSE290044 | GEO
Project description:Friedreich’s ataxia (FRDA; OMIM 229300), an autosomal recessive neurodegenerative mitochondrial disease, is the most prevalent hereditary ataxia. In addition, FRDA patients showed additional non-neurological features such as scoliosis, diabetes and cardiac complications. Hypertrophic cardiomyopathy, which is found in two thirds of patients at the time of diagnosis, is the primary cause of death in these patients. In this data set, using small RNA-sequencing of small RNA purified from plasma samples of FRDA patients and controls we identified differential expression of miRNAs (hsa-miR-128-3p, hsa-miR-625-3p, hsa-miR-130b-5p, hsa-miR-151a-5p, hsa-miR-330-3p, hsa-miR-323a-3p, and hsa-miR-142-3p) between both groups. In addition, we found that miR-323a-3p can be used as a biomarker for differentiation of FRDA patients with cardiac problems. Identification of miRNA signatures could therefore provide new molecular explanation for pathological mechanisms occurring during the natural history of the FRDA. Since miRNA levels change with disease progression and pharmacological interventions, miRNAs will contribute to design new therapeutic strategies and improve clinical decisions. Plama miRNA profiles of 25 Friedreich's ataxia patients and 17 healthy subjects were generated by deep sequencing using Illumina HiScan SQ.
2017-10-18 | E-GEOD-105052 | biostudies-arrayexpress