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Flow-cytometric quantification of urine kidney epithelial cells specifically reflects tubular damage in acute kidney diseases

ABSTRACT: Flow-cytometric quantification of urine kidney epithelial cells specifically reflects tubular damage in acute kidney diseases

PROVIDER: PRJNA1188168 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31401861.fastq.gz	Fastqsanger.gz
	SRR31401862.fastq.gz	Fastqsanger.gz
	SRR31401863.fastq.gz	Fastqsanger.gz
	SRR31401864.fastq.gz	Fastqsanger.gz
	SRR31401865.fastq.gz	Fastqsanger.gz

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Flow-cytometric quantification of urine kidney epithelial cells specifically reflects tubular damage in acute kidney diseases

Project description:Despite tubular injury being one of the main mechanisms driving acute kidney injury (AKI), clinicians still have a limited diagnostic repertoire to precisely monitor damage to tubular epithelial cells (TEC). In our previous work we used single cell sequencing to identify TEC subsets as main component of the urine signature in AKI. The aim of this study was to establish TEC as a clinical marker for tubular damage. In total 243 patients were analyzed. For sequencing, we collected eight urine samples of patients with AKI and glomerular disease. By aligning urinary single-cell transcriptomes and TEC-surface proteins using Cellular Indexing of Transcriptome and Epitope Sequencing (CITE-Seq), we developed a protocol for flow cytometric quantification of CD10/CD13+ proximal and CD227/CD326+ distal TEC in urine. The marker combinations were confirmed in kidney biopsies. We validated our approach across four cohorts totaling 235 patients, consisting of patients with AKI (n=63), SARS-CoV-2 infection (n=47), ANCA-associated vasculitis (AAV) with active disease and stable remission (n=110) and healthy controls (n=15). Our findings demonstrate that CD10/CD13 and CD227/CD326 adequately identify proximal and distal urinary TEC, respectively. Distal urinary TEC counts correlate with the severity of AKI based on KDIGO stage and acute eGFR loss in two separate cohorts and can successfully discriminate AKI from healthy controls as well as glomerular disease. We propose urinary CD227/CD326+ TEC counts as a specific, non-invasive marker for tubular injury in AKI. Our protocol provides the basis for a deeper phenotypic analysis of urinary TECs

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Expression data from mice overexpressing Tcfeb specifically in P0 kidney

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Generation of human kidney organoids from urine cells

Project description:Kidney organoids are ideal models to study the complex process of human kidney development. Here we report the generation of functional kidney organoids by reprogramming human urine epithelial cells (hUCs). RNA-seq and ATAC-seq revealed the three-stage process of the 2D U-iRO induction. Single cell RNA-seq further reveals the cell types in 2D and 3D organoids, 2D U-iRO dominated with mesenchyme and 3D U-iRO with tubule.

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Vanin-1 in Renal Pelvic Urine Reflects Kidney Injury in a Rat Model of Hydronephrosis.

Project description:Urinary tract obstruction and the subsequent development of hydronephrosis can cause kidney injuries, which results in chronic kidney disease. Although it is important to detect kidney injuries at an early stage, new biomarkers of hydronephrosis have not been identified. In this study, we examined whether vanin-1 could be a potential biomarker for hydronephrosis. Male Sprague-Dawley rats were subjected to unilateral ureteral obstruction (UUO). On day 7 after UUO, when the histopathological renal tubular injuries became obvious, the vanin-1 level in the renal pelvic urine was significantly higher than that in voided urine from sham-operated rats. Furthermore, vanin-1 remained at the same level until day 14. There was no significant difference in the serum vanin-1 level between sham-operated rats and rats with UUO. In the kidney tissue, the mRNA and protein expressions of vanin-1 significantly decreased, whereas there was increased expression of transforming growth factor (TGF)-?1 and Snail-1, which plays a pivotal role in the pathogenesis of renal fibrosis via epithelial-to-mesenchymal transition (EMT). These results suggest that vanin-1 in the renal pelvic urine is released from the renal tubular cells of UUO rats and reflects renal tubular injuries at an early stage. Urinary vanin-1 may serve as a candidate biomarker of renal tubular injury due to hydronephrosis.

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Generation of human kidney organoids from urine cells

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