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Kidney Week

Abstract: SA-PO0338

Biopsy-Proven Acute Tubular Injury Associated with Semaglutide Use

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical, Outcomes, and Trials

Authors

  • Nair, Rohan, Herricks High School, New Hyde Park, New York, United States
  • Bhuiyan, Md Refayat, Northwell Health, New Hyde Park, New York, United States
  • Wang, Xiaotong, Northwell Health, New Hyde Park, New York, United States
  • Jhaveri, Kenar D., Northwell Health, New Hyde Park, New York, United States
Introduction

GLP-1RAs are widely used for diabetes and obesity, with established cardiovascular and kidney benefits. While AKI is often attributed to volume depletion from gastrointestinal side effects, biopsy-proven intrinsic kidney lesions—including acute interstitial nephritis (AIN) and podocytopathies—are increasingly recognized. Acute tubular injury (ATI) associated with GLP-1RAs has not been reported.

Case Description

A 72-year-old woman with type 2 diabetes, hypertension, and stage 3 chronic kidney disease (baseline creatinine ~1.5 mg/dL) presented with vomiting and dizziness two months after initiation of semaglutide. Medications included metformin and losartan. She denied NSAID use, hypotension, or contrast exposure. On admission, creatinine was 6.2 mg/dL, potassium 6.9 mmol/L, bicarbonate 11 mmol/L, and pH 7.21. Despite fluid resuscitation and preserved urine output, kidney function worsened with a peak creatinine of 9.8 mg/dL. Serologic workup was negative. Kidney biopsy demonstrated acute tubular injury with mild chronic changes, without interstitial inflammation or immune complex deposition(Figure). Semaglutide, metformin, and losartan were discontinued. The patient improved without dialysis or immunosuppression, with creatinine declining to 2.4 mg/dL at two months. The patient was never re-challenged with semaglutide but restarted on losartan.

Discussion

This case highlights biopsy-proven ATI in association with semaglutide use. While GLP-1RA-associated kidney injury is most commonly linked to AIN or podocytopathies, ATI represents an underrecognized entity. Mechanistically, gastrointestinal intolerance leading to volume depletion—especially in patients with baseline CKD and concurrent renin–angiotensin system inhibition—may predispose to tubular injury. Clinicians should provide “sick-day” counseling and consider early drug interruption during gastrointestinal illness.

Light microscopy (Periodic acid–Schiff. Magnification: X100) demonstrates : Attenuation of tubular epithelial cells and loss of brush borders (arrows). No significant interstitial inflammation.