Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE35487: Expression data from human with IgA nephropathy (IgAN) [HG-U133A] GSE35488: Expression data from human with IgA nephropathy (IgAN) [HG-U133A_ENTREZG_10] Refer to individual Series
2012-02-02 | E-GEOD-35489 | biostudies-arrayexpress
Project description:The current study makes use of NanoString targeted technology to profile urinary exosomal miRNAs from IgA nephropathy affected patients and corresponding healthy controls. Circulatory biomarkers were detected for IgA nephropathy from Indian cohort which can be made used for the diagnostic therapy. 14 miRNAs were detected to be related to the disregulation in miRNome of IgA nephropathy patients using lasso feature selection method, out of which multiple miRNAs like hsa.mir.146b.3p, hsa.mir.599 and many more was resulted with high AUROC values >=0.9 efficient in differentiating between healthy controls and IgA nephropathy condition. These markers can be use further in the diagnosis and treatment of IgAN.
2023-12-13 | GSE244625 | GEO
Project description:IgA nephropathy represents the most prevalent chronic nephrosis worldwide. However, pathogenesis about IgA deposition and end-stage renal failure is still not well defined. Using single-cell RNA-seq, we identified the mesangial membrane receptor for IgA, which collaborates with increased extracellular matrix proteins and protease inhibitor to facilitate IgA deposition. Meanwhile, cell-cell interaction analysis revealed increased communications between mesangium and other cell types, uncovering how morbidity inside glomerulus spreads to whole kidney, which results in the genetic changes of kidney resident immune cells. Prominent interaction decreasing in intercalated cells leads to the discovery of a transitional cell type, which exhibited significant EMT and fibrosis features. Our work comprehensively characterized the pathological mesangial signatures, highlighting the step-by-step pathogenic process of IgA nephropathy from mesangium to epithelium.
2021-07-06 | GSE127136 | GEO
Project description:The comprehensive analysis of kidney biopsy specimen demonstrated different gene expression profile, potential pathologic ligand-receptor crosstalk, signaling pathways in human IgAN. These results offer new insight into pathogenesis and identify new therapeutic targets for patients with IgA nephropathy.
2021-04-02 | GSE171314 | GEO
Project description:By the iTRAQ-PRM proteomics, we found the difference of urinary proteins in IgA nephropathy patients with different progression.
2023-03-13 | PXD040799 |
Project description:Proteinuria is the most important predictor of outcome in glomerulonephritis and experimental data suggest that the tubular cell response to proteinuria is an important determinant of progressive fibrosis in the kidney. However, it is unclear whether proteinuria is a marker of disease severity or has a direct effect on tubular cells in the kidneys of patients with glomerulonephritis. Accordingly we studied an in vitro model of proteinuria, and identified 231 albumin-regulated genes differentially expressed by primary human kidney tubular epithelial cells exposed to albumin. We translated these findings to human disease by studying mRNA levels of these genes in the tubulo-interstitial compartment of kidney biopsies from patients with IgA nephropathy using microarrays. Biopsies from patients with IgAN (n=25) could be distinguished from those of control subjects (n=6) based solely upon the expression of these 231 albumin-regulated genes. The expression of an 11-transcript subset related to the degree of proteinuria, and this 11-mRNA subset was also sufficient to distinguish biopsies of subjects with IgAN from control biopsies. We tested if these findings could be extrapolated to other proteinuric diseases beyond IgAN and found that the all forms of primary glomerulonephritis (n=33) can be distinguished from controls (n=21) based solely on the expression levels of these 11 genes derived from our in vitro proteinuria model. Pathway analysis suggests common regulatory elements shared by these 11 transcripts. In conclusion, we have identified an albumin-regulated 11-gene signature shared between all forms of primary glomerulonephritis. Our findings support the hypothesis that albuminuria may directly promote injury in the tubulo-interstitial compartment of the kidney in patients with glomerulonephritis. We used microarrays to analyze the transcriptome of microdissected renal biopsies from patients with IgA nephropathy (IgAN) RNA from tubulointerstitial compartments was extracted and processed for hybridization on Affymetrix HG-U133A microarrays.
2012-02-02 | E-GEOD-35487 | biostudies-arrayexpress
Project description:Proteinuria is the most important predictor of outcome in glomerulonephritis and experimental data suggest that the tubular cell response to proteinuria is an important determinant of progressive fibrosis in the kidney. However, it is unclear whether proteinuria is a marker of disease severity or has a direct effect on tubular cells in the kidneys of patients with glomerulonephritis. Accordingly we studied an in vitro model of proteinuria, and identified 231 albumin-regulated genes differentially expressed by primary human kidney tubular epithelial cells exposed to albumin. We translated these findings to human disease by studying mRNA levels of these genes in the tubulo-interstitial compartment of kidney biopsies from patients with IgA nephropathy using microarrays. Biopsies from patients with IgAN (n=25) could be distinguished from those of control subjects (n=6) based solely upon the expression of these 231 albumin-regulated genes. The expression of an 11-transcript subset related to the degree of proteinuria, and this 11-mRNA subset was also sufficient to distinguish biopsies of subjects with IgAN from control biopsies. We tested if these findings could be extrapolated to other proteinuric diseases beyond IgAN and found that the all forms of primary glomerulonephritis (n=33) can be distinguished from controls (n=21) based solely on the expression levels of these 11 genes derived from our in vitro proteinuria model. Pathway analysis suggests common regulatory elements shared by these 11 transcripts. In conclusion, we have identified an albumin-regulated 11-gene signature shared between all forms of primary glomerulonephritis. Our findings support the hypothesis that albuminuria may directly promote injury in the tubulo-interstitial compartment of the kidney in patients with glomerulonephritis. We used microarrays to analyze the transcriptome of microdissected renal biopsies from patients with IgA nephropathy (IgAN) RNA from tubulointerstitial compartments was extracted and processed for hybridization on Affymetrix HG-U133A microarrays.
2012-02-02 | E-GEOD-35488 | biostudies-arrayexpress
Project description:We collected glomeruli from biopsy specimens from IgA nephropathy patients with relatively preserved kidney function (eGFR ≥ 60 mL/min/1.73 m2 and urine protein-to-creatinine ratio < 3 g/g) and from normal kidney cortices by hand microdissection and performed RNA-seq. The transcriptomic profiling of IgA nephropathy glomerulus provide insights for intraglomerular pathophysiology of IgAN before reaching profound kidney dysfunction.
2020-09-30 | GSE141295 | GEO
Project description:Single cell sequencing of IgAN patients
| PRJNA783206 | ENA
Project description:We applied scRNAseq analysis to investigate the mouse kidney glomerular injury in IgA nephropathy
2022-02-01 | GSE166793 | GEO