ArticleScience translational medicine2023
Analysis of the human kidney transcriptome and plasma proteome identifies markers of proximal tubule maladaptation to injury.
Article in Science translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 19 citations in OpenAlex.
- Kidney Transcriptome Sequencing Improves Molecular Diagnosis and Reveals Splicing Complexity Across the Alport Spectrum.Kidney international reports · 2026Article
- HNF4A maintains proximal tubule identity and limits injury-associated cell states in the adult mouse kidney.bioRxiv : the preprint server for biology · 2026Article
- Mechanisms of regeneration and maladaptive repair in acute kidney injury.Nature reviews. Nephrology · 2026Review
- Development of a pediatric pig model of extracorporeal cardiopulmonary resuscitation-induced acute kidney injury.Disease models & mechanisms · 2026Article
- Modelling ischaemic AKI in human kidney organoids reveals injury-associated epithelial states and macrophage-epithelial crosstalk.Genome medicine · 2026Article
- ELF3 links kidney function GWAS loci to maladaptive epithelial inflammation.Science advances · 2026Article
- Spatial Atlas Creation at the Single Cell Level: Unveiling the Human Kidney Metaverse.Clinical journal of the American Society of Nephrology : CJASN · 2026Article
- A novel mouse model for cardiovascular-kidney-metabolic syndrome: Bridging metabolic, renal and cardiac dysfunction.Molecular metabolism · 2026Article
- Association between HALP score and in-hospital outcomes in patients with acute kidney injury: a retrospective cohort study.Scientific reports · 2026Article
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Review
- The mtDNA-cGAS-STING Axis in Acute Kidney Injury and Maladaptive Repair: Preclinical Evidence for Traditional Chinese Medicine and Natural Product-Based Interventions.Journal of inflammation research · 2026Review
- Identification of key biomarkers of telomere-related genes in diabetic nephropathy via bioinformatic analysis.Frontiers in genetics · 2026Article
- Review
- Article
- State of the art: Renal recovery after AKI - from basic science to clinical practice.Intensive care medicine · 2025Review
- Renal tubular GSDME protects cisplatin nephrotoxicity by impeding OGT-STAT3-S100A7A axis in male mice.Nature communications · 2025Article
- Identification of core genes in acute kidney injury: evidence from multi-omics human transcriptomic data andTranslational andrology and urology · 2025Article
- A cross-sectional study of the role of epithelial cell injury in kidney transplant outcomes.JCI insight · 2025Observational
- Multiomic analysis of human kidney disease identifies a tractable inflammatory and pro-fibrotic tubular cell phenotype.Nature communications · 2025Article
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
Acute kidney injury (AKI) is a major risk factor for long-term adverse outcomes, including chronic kidney disease. In mouse models of AKI, maladaptive repair of the injured proximal tubule (PT) prevents complete tissue recovery. However, evidence for PT maladaptation and its etiological relationship with complications of AKI is lacking in humans. We performed single-nucleus RNA sequencing of 120,985 nuclei in kidneys from 17 participants with AKI and seven healthy controls from the Kidney Precision Medicine Project. Maladaptive PT cells, which exhibited transcriptomic features of dedifferentiation and enrichment in pro-inflammatory and profibrotic pathways, were present in participants with AKI of diverse etiologies. To develop plasma markers of PT maladaptation, we analyzed the plasma proteome in two independent cohorts of patients undergoing cardiac surgery and a cohort of marathon runners, linked it to the transcriptomic signatures associated with maladaptive PT, and identified nine proteins whose genes were specifically up- or down-regulated by maladaptive PT. After cardiac surgery, both cohorts of patients had increased transforming growth factor-β2 (TGFB2), collagen type XXIII-α1 (COL23A1), and X-linked neuroligin 4 (NLGN4X) and had decreased plasminogen (PLG), ectonucleotide pyrophosphatase/phosphodiesterase 6 (ENPP6), and protein C (PROC). Similar changes were observed in marathon runners with exercise-associated kidney injury. Postoperative changes in these markers were associated with AKI progression in adults after cardiac surgery and post-AKI kidney atrophy in mouse models of ischemia-reperfusion injury and toxic injury. Our results demonstrate the feasibility of a multiomics approach to discovering noninvasive markers and associating PT maladaptation with adverse clinical outcomes.
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