ArticleKidney international reports2025
Flow-Cytometric Quantification of Urine Kidney Epithelial Cells Specifically Reflects Tubular Damage in Acute Kidney Diseases.
Article in Kidney international reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Urinary Cells Flow Cytometry in Renal Disease: A Systematic Review of Diagnostic and Prognostic Applications.Biomedicines · 2026Review
- Research progress in single‑cell omics technologies for kidney disease (Review).International journal of molecular medicine · 2026Review
- Response to the Letter to the Editor Entitled "Renal Tubular Epithelial Cells as Marker of Tubular Damage in Acute Kidney Disease".Kidney international reports · 2025Article
- Renal Tubular Epithelial Cells as Marker of Tubular Damage in Acute Kidney Disease.Kidney international reports · 2025Article
Corrections and comments
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Authors and funding
19 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Tubular injury is one of the main mechanisms driving acute kidney injury (AKI); however, clinicians still have a limited diagnostic repertoire to precisely monitor damage to tubular epithelial cells (TECs). In our previous study, we used single-cell sequencing to identify TEC subsets as the main components of the urine signature of AKI. This study aimed to establish TECs as clinical markers of tubular damage. Methods: A total of 243 patients were analyzed. For sequencing, we collected 8 urine samples from patients with AKI and glomerular disease. We developed a protocol for the flow cytometric quantification of CD10/CD13 Results: Our findings demonstrated that CD10/CD13 and CD227/CD326 adequately identified PTECs and DTECs, respectively. Distal urinary TEC counts correlate with the severity of AKI based on Kidney Disease: Improving Global Outcomes (KDIGO) stage and acute estimated glomerular filtration rate (GFR) loss in 2 separate cohorts and can successfully discriminate AKI from healthy controls and glomerular disease. Conclusion: We propose that urinary CD227/CD326
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