Kidney Week

Abstract: SA-PO1283

Urinary CD4+ EM CD38+ HLA DR+ T Cells Are a Potential Biomarker for Diagnosis of Immune Checkpoint Inhibitor-Associated Acute Interstitial Nephritis

Session Information

• Onconephrology: Epidemiological Trends, Risk Stratification, and Clinical Outcomes
  October 24, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Onconephrology

• 1600 Onconephrology

Authors

• Mirkheshti, Pouneh, Charite - Universitatsmedizin Berlin, Berlin, BE, Germany

Pouneh Mirkheshti

• Barbarini, Michele, Universita degli Studi di Parma Dipartimento di Medicina e Chirurgia, Parma, Emilia-Romagna, Italy

Michele Barbarini, MD, MBBS

• Nava Chavez, Coraima Claudia, Mayo Clinic Division of Nephrology and Hypertension, Rochester, Minnesota, United States

Coraima Claudia Nava Chavez, MD

• Cuenca Narvaez, Victor, Mayo Clinic Division of Nephrology and Hypertension, Rochester, Minnesota, United States

Victor Cuenca Narvaez, MD

• Enghard, Philipp, Charite - Universitatsmedizin Berlin, Berlin, BE, Germany

Philipp Enghard, DrMed

• Herrmann, Sandra, Mayo Clinic Division of Nephrology and Hypertension, Rochester, Minnesota, United States

Sandra Herrmann, MD, FASN

Background

Acute interstitial nephritis (AIN) is the most common cause of acute kidney injury (AKI) in patients treated with immune checkpoint inhibitors (ICI). Clinical presentation is often nonspecific, and diagnosis relies on kidney biopsy. While previous studies in immune checkpoint inhibitor associated AIN (ICI AIN) have focused on soluble urinary biomarkers such as CXCL9 and the urine retinol binding protein to creatinine ratio (uRBP/Cr), increasing evidence suggests a central role of T cells in ICI AIN pathogenesis. We therefore investigated urinary T cells as a non invasive biomarker for ICI AIN.

Methods

In this prospective cohort, 30 urine samples from ICI treated patients were analyzed by flow cytometry. Five patients had biopsy proven ICI AIN, 13 developed AKI without AIN (ICI non AIN AKI), and 10 were ICI treated without AKI. Follow up urine samples were obtained from two ICI AIN patients 12 weeks after diagnosis. Serum CRP and uRBP/Cr were measured, and urinary T cells were phenotyped for CD4 and CD8 and subdivided into naïve, effector memory (EM), central memory, and TEMRA subsets. Expression of HLA DR and CD38 was assessed (F1A).

Results

Patients with ICI AIN had significantly higher urinary counts of CD4+ EM CD38+ HLA DR+ T cells than ICI non AIN AKI patients and ICI treated controls (p < 0.05). This T cell population showed superior discrimination of ICI AIN compared with serum CRP and uRBP/Cr (F1B). In longitudinal follow up, both ICI AIN patients demonstrated declining urinary CD4+ EM CD38+ HLA-DR+ T cell counts at 12 weeks, paralleling improvements in serum creatinine, serum CRP, and uRBP/Cr (F1C).

Conclusion

Urinary CD4+ EM CD38+ HLA-DR+ T cells show promise as a biomarker for non invasive diagnosis of ICI AIN and for longitudinal monitoring of treatment response.

Acknowledgment

We thank the Flow Cytometry Core Facility for technical support.

Funding

• Other NIH Support