Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13964700_1.fastq.gz | Fastqsanger.gz | |||
| SRR13964700_2.fastq.gz | Fastqsanger.gz | |||
| SRR13964701_1.fastq.gz | Fastqsanger.gz | |||
| SRR13964701_2.fastq.gz | Fastqsanger.gz | |||
| SRR13964702_1.fastq.gz | Fastqsanger.gz |
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Project description:Secondary hyperparathyroidism is well known complication manifested in end-stage renal disease (ESRD). Both nodular and diffuse parathyreoid hyperplasia occur in ESRD patients. Distinct molecular mechanisms involved in parathyreoid hyperplasia remain poorly understood. Microarray screening proved homogeneity of gene transcripts in hemodialysis patients as compared to transplant cohort and primary hyperparathyreoidism, therefore further studies were performed in hemodialysis patints only. Enrichment analysis conducted on 485 differentially expressed genes between nodular and diffuse parathyreoid hyperplasia revealed highly significant differences in GO terms and KEGG database in ribosome structure (p=3.70-18). Next, RT-qPCR validation of microarray analysis proved higher expression of RAN guanine nucleotide release factor (RANGRF, p<0.001), calcyclin binding protein (CACYBP, p<0.05) and exocyst complex component 8 (EXOC8, p<0.05) and lower expression of peptidylprolyl cis/trans isomerase, NIMA-interacting 1 (PIN1, p<0.01) mRNA in nodular hyperplasia. Multivariate analysis revealed RANGRF and PIN1 expression along with parathyroid weight to be associated with nodular hyperplasia. Higher expression of genes associated with ribosomal structure and function underline extended translation mechanisms involved in parathyreoid nodular formation in long-term hemodialysis treated patients. Parathyroid tissue obtained from ESRD hyperparathyroidism patients who had undergone parathyroidectomy were used for transcriptome screening (Illumina HumanHT-12 v4.0 Expression BeadChips) and subsequently for discriminatory gene analysis, pathway mapping and gene-annotation enrichment analyses. Results were verified on enlarged group of hemodialysis patients with nodular (n=20) and diffuse (n=20) hyperplasia using RT-qPCR method.
2015-12-12 | E-GEOD-75886 | biostudies-arrayexpress
Project description:Hemodialysis patients experience persistent inflammation due to increased production of pro-inflammatory monocytes. We hypothesized that the persistent hyper-responsiveness of innate immune cells in these patients is driven by trained immunity, a form of innate immune memory. This observational study aimed to investigate the presence of trained immunity responses in hemodialysis patients and to elucidate the molecular mechanisms underlying it. We profiled innate immune cell subsets by flow cytometry and cytokine responses of hemodialysis patients and healthy controls following ex vivo stimulation of peripheral blood mononuclear cells with Toll-like receptor (TLR) agonists. Plasma concentrations of inflammatory markers were assessed using the Olink Proximity Extension Assay, while whole-genome RNA sequencing was performed on circulating monocytes to identify genes associated with trained immunity. In vitro assays were conducted to explore the role of interferon gamma (IFN-γ) in mediating trained immunity. Hemodialysis patients displayed elevated monocyte counts and their cells showed significantly heightened cytokine responses to TLR stimulation, indicative of trained immunity. Importantly, plasma IFN-γ concentrations positively correlated with these cytokine responses. Gene expression analysis revealed enrichment of interferon response pathways, particularly in patients whose monocytes exhibited the most pronounced cytokine production upon restimulation. In vitro experiments confirmed that trained immunity induction depends on IFN-γ, produced by CD4+ T cells. Our findings demonstrate that hemodialysis patients display a dysregulated immune response characterized by trained immunity and that this might be mediated by IFN-γ. These insights suggest that targeting IFN-γ could be a promising strategy to mitigate damaging immune hyperactivity in dialysis patients.
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Project description:Integrated metabolomic and proteomic profiling of end stage kidney disease patients undergo hemodialysis
2023-03-28 | MSV000091579 | MassIVE
Project description:End-stage renal disease patients experience uremia-driven immune compromise characterized by complex alterations of both innate and adaptive immunity, and results in higher susceptibility to infection and lower response to vaccination. This immune compromise, coupled with greater risk of exposure to infectious disease at hemodialysis (HD) centers, motivates an examination of immune response to the COVID-19 mRNA-based BTN162b2 vaccine. We performed gene expression profiling by RNA-seq across 6 time points to assess vaccine response in healthy controls and hemodialysis patients over time.
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Project description:Introduction: COVID-19 has been shown to increase the risk of extracorporeal coagulation during hemodialysis in patients, but the mechanism is unclear. This study aims to investigate the effect and mechanism of COVID-19 on the risk of extracorporeal coagulation during hemodialysis. Methods: A retrospective analysis was performed on the extracorporeal coagulation status of 339 hemodialysis patients at our hemodialysis center before and after COVID-19 infection. Protein spectroscopy was used to analyze blood composition differences between asymptomatic/mild and severe/critical patients after infection. Results: In comparison to the pre-COVID-19 infection period, a notable increase in the risk of extracorporeal coagulation during hemodialysis after infection has been observed. The grade of coagulation was directly proportional to the severity of infection symptoms, especially in severe and critically symptoms patients. In addition, proteomic analysis has demonstrated that in severe/critical cases, the coagulation cascade reaction, platelet activation, inflammation, and oxidative stress-related signals were significantly amplified as compared to asymptomatic/mild cases. Notably, the coagulation-related signaling pathway vWF/FBNL5 was significantly upregulated. Conclusions: In conclusion, this study revealing the potential role of vWF/FBNL5 in COVID-19-induced coagulation, which can have severe implications for patients undergoing hemodialysis. The findings highlight the critical importance of early initiation of anticoagulant therapy for COVID-19 patients, particularly those undergoing hemodialysis.
2023-08-03 | PXD044377 |
Project description:Integrated metabolomic and proteomic profiling of end stage kidney disease patients undergo hemodialysis
2023-03-28 | MSV000091579 | GNPS
Project description:Secondary hyperparathyroidism is well known complication manifested in end-stage renal disease (ESRD). Both nodular and diffuse parathyreoid hyperplasia occur in ESRD patients. Distinct molecular mechanisms involved in parathyreoid hyperplasia remain poorly understood. Microarray screening proved homogeneity of gene transcripts in hemodialysis patients as compared to transplant cohort and primary hyperparathyreoidism, therefore further studies were performed in hemodialysis patints only. Enrichment analysis conducted on 485 differentially expressed genes between nodular and diffuse parathyreoid hyperplasia revealed highly significant differences in GO terms and KEGG database in ribosome structure (p=3.70-18). Next, RT-qPCR validation of microarray analysis proved higher expression of RAN guanine nucleotide release factor (RANGRF, p<0.001), calcyclin binding protein (CACYBP, p<0.05) and exocyst complex component 8 (EXOC8, p<0.05) and lower expression of peptidylprolyl cis/trans isomerase, NIMA-interacting 1 (PIN1, p<0.01) mRNA in nodular hyperplasia. Multivariate analysis revealed RANGRF and PIN1 expression along with parathyroid weight to be associated with nodular hyperplasia. Higher expression of genes associated with ribosomal structure and function underline extended translation mechanisms involved in parathyreoid nodular formation in long-term hemodialysis treated patients.
2015-12-12 | GSE75886 | GEO
Project description:A systems biology approach was used to comprehensively examine the impact of renal disease and hemodialysis (HD) on host response during critical illness. We examined the metabolome, proteome, and transcriptome of 150 patients with critical illness, stratified by renal function. Plasma metabolite values showed greater changes as renal function declined, with the greatest derangements in patients receiving chronic HD. Specifically, 6 uremic retention molecules, 17 other protein catabolites, 7 modified nucleosides, and 7 pentose phosphate sugars increased as renal function declined, consistent with decreased excretion or increased catabolism of amino acids and ribonucleotides. Similarly, the proteome showed increased levels of low-molecular weight proteins and acute phase reactants. The transcriptome revealed a broad-based decrease in mRNA levels among HD patients. Systems integration revealed an unrecognized association between plasma RNASE1 and several RNA catabolites and modified nucleosides. Further, allantoin, N1-methyl-4-pyridone-3-carboxamide, and n-acetylaspartate showed inverse correlations with the majority of significantly down-regulated genes. In conclusion, renal function broadly affected the plasma metabolome, proteome, and peripheral blood transcriptome during critical illness. These changes were not effectively mitigated by hemodialysis. These studies suggest several novel mechanisms whereby renal dysfunction contributes to critical illness. We sequenced peripheral blood RNA of 133 representative subjects with systemic inflammatory response syndrome that had Acute Kidney Injury (AKI) or Hemodialysis (HD). No injury (AKI0; n= 58); AKI Stage 1 (AKI1; n= 36); AKI stage 2 and 3 (AKI23; n= 17); HD (N=22).
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Project description:Patients with aortic stenosis (AS) undergoing hemodialysis (HD) often experience faster disease progression and poorer prognosis than non-dialysis patients, yet the underlying mechanisms remain unclear. This study aimed to elucidate clinical and molecular differences between HD and non-HD patients with AS, focusing on transcriptomic profiling of resected aortic valves.
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Project description:Purpose: Heart failure (HF) has a very high prevalence in patients with maintenance hemodialysis (MHD). However, there is still a lack of effective and reliable HF diagnostic markers and therapeutic targets for patients with MHD. Patients and methods: In this study, we analyzed transcriptome profiles of 28 patients with MHD by high-throughput sequencing.
2025-01-01 | GSE253498 | GEO