Abstract: TH-PO104
Urinary Tubular Epithelial Cells as a Tool for Diagnosis and Prognosis Estimation in AKI
Session Information
- AKI: Biomarkers, Drugs, Onco-Nephrology
November 07, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Kujat, Jacob, Charité Universitätsmedizin Berlin, Berlin, Germany
- Skopnik, Christopher, Charité Universitätsmedizin Berlin, Berlin, Germany
- Freund, Paul, Charité Universitätsmedizin Berlin, Berlin, Germany
- Metzke, Diana, Charité Universitätsmedizin Berlin, Berlin, Germany
- Enghard, Philipp, Charité Universitätsmedizin Berlin, Berlin, Germany
Background
Acute kidney injury (AKI) is a common clinical condition with serious short- and long-term consequences. Present classifications focus on serum creatinine (SCr) and urine output, though these are functional damage markers and only allow indirect conclusions about the actual structural damage taking place. In this project we quantified the amount of tubular epithelial cells (TECs) in urine as a marker for kidney damage at the cellular level.
Methods
Urinary samples were taken from inpatients with AKI according to the KDIGO classification (n=50) and from inpatients with cardiological disease but without AKI according to the KDIGO classification (n=8; control group). Samples were analyzed within 72 hours after the initial SCr increase using flow cytometry. A marker combination of cytokeratin, CD13 and CD10 was used to detect proximal TECs (pTECs) and a combination of cytokeratin, CD326 and CD227 was used to detect distal TECs (dTECs). The cell counts were calculated as cells per 100 ml urine. Patients with renal replacement therapy or with inflammatory cause of the AKI were excluded from this study.
Results
Both the amounts of pTECs and dTECs correlated with the relative increase of SCr from the baseline value to the maximum value within the AKI (pTECs: p=0,0006; dTECs: p=0,0004; Spearman). Samples of the control group contained significantly lower amounts of TECs compared to the AKI cohort (pTECs: p=0,0001; dTECs: p<0,0001; Mann-Whitney-Wilcoxon). Some donors (n=5) with a low relative increase of SCr showed very high amounts of urinary TECs. These donors either did not recover from the AKI or showed acute cardiovascular decompensation on the day of sample uptake.
Furthermore, both the amounts of pTECs and dTECs correlated with the change of the eGFR stage according to KDIGO from baseline value to the value at hospital discharge (pTECs: p=0,0176; dTECs: p=0,0282; Spearman).
Conclusion
Urinary TECs are an innovative, non-invasive possibility to quantify structural kidney damage during an AKI. As a potential new biomarker for prognosis of AKI, TECs additionally allow predictions about the renal filter function during the course of the hospital stay. High amounts of urinary TECs in donors who only had a modest SCr increase may have detected severe structural kidney damage.