ArticlePloS one2010
A molecular signature of proteinuria in glomerulonephritis.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 84 citations in OpenAlex.
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- Decoding vascular calcification-neutrophil signature in pathogenesis of chronic IgA nephropathy: evidence from artificial intelligence-driven multi-omics andFrontiers in physiology · 2026Article
- Arp2/3-dependent regulation of ciliogenesis governs adaptive distal tubular epithelial cell states in kidney disease.Science advances · 2025Article
- Integrative bioinformatics analysis unveils hub transcription factors and their interacting drugs in immunoglobulin A nephropathy: Implications for pathogenesis and treatments.Journal, genetic engineering & biotechnology · 2025Article
- Cytoskeleton-associated protein 4 affects podocyte cytoskeleton dynamics in diabetic kidney disease.JCI insight · 2025Article
- To establish and validate autophagy related biomarkers for the diagnosis of IgA nephropathy.Scientific reports · 2025Article
- Collagen V regulates renal function after kidney injury and can be pharmacologically targeted to enhance kidney repair in mice.Science translational medicine · 2025Article
- Integrated multiomic analyses: An approach to improve understanding of diabetic kidney disease.Diabetic medicine : a journal of the British Diabetic Association · 2025Review
- GPX4 expression changes in proximal tubule cells highlight the role of ferroptosis in IgAN.Scientific reports · 2025Article
- System failure: Systemic inflammation following spinal cord injury.European journal of immunology · 2024Review
- Cathepsin S (CTSS) in IgA nephropathy: an exploratory study on its role as a potential diagnostic biomarker and therapeutic target.Frontiers in immunology · 2024Article
- Development and evaluation of a chronic kidney disease risk prediction model using random forest.Frontiers in genetics · 2024Article
- Neuroblastoma suppressor of tumorigenicity 1 is associated with the severity of interstitial fibrosis and kidney function decline in IgA nephropathy.Journal of nephrology · 2023Article
- TIMP-2 and IGFBP7 in human kidney biopsies in renal disease.Clinical kidney journal · 2023Article
- Present and Future of IgA Nephropathy and Membranous Nephropathy Immune Monitoring: Insights from Molecular Studies.International journal of molecular sciences · 2023Review
- Omics are Getting Us Closer to Understanding IgA Nephropathy.Archivum immunologiae et therapiae experimentalis · 2023Review
- Single-cell transcriptomics reveals a mechanosensitive injury signaling pathway in early diabetic nephropathy.Genome medicine · 2023Article
- Assessment of Fibrinogen-like 2 (FGL2) in Human Chronic Kidney Disease through Transcriptomics Data Analysis.Biomolecules · 2022Article
- Identification of key candidate genes for IgA nephropathy using machine learning and statistics based bioinformatics models.Scientific reports · 2022Article
- Identification of blood-based key biomarker and immune infiltration in Immunoglobulin A nephropathy by comprehensive bioinformatics analysis and a cohort validation.Journal of translational medicine · 2022Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
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 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.
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