Kidney Week

Abstract: SA-PO0339

When Protection Meets Injury: A Case Report of SGLT2 Inhibitor-Associated Acute Tubular Necrosis

Session Information

• AKI: Case Reports - Drug/Toxin Injury, Crystals, Obstruction, and Unusual Presentations
  October 24, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

• 102 AKI: Clinical, Outcomes, and Trials

Authors

• Bali, Prateek, Jamaica Hospital Medical Center, Jamaica, New York, United States

Prateek Bali, MBBS

• Ahmadi, Ali, Jamaica Hospital Medical Center, Jamaica, New York, United States

Ali Ahmadi, MD

• Kumar, Rahul, Ross University School of Medicine - Barbados Campus, Bridgetown, Saint Michael, Barbados

Rahul Kumar, MD

• Chang, Michael, Jamaica Hospital Medical Center, Jamaica, New York, United States

Michael Chang, MD

• Cabezas, Fausto, Jamaica Hospital Medical Center, Jamaica, New York, United States

Fausto Cabezas, MD

• Thomas, David B., UNC Medical Center North Carolina Memorial Hospital, Chapel Hill, North Carolina, United States

David B. Thomas, MD

Group or Team Name

• JHMC Renal Hemodynamics Research Collaborative

Introduction

SGLT2 inhibitors are widely used in chronic kidney disease and provide established cardiorenal benefits. Although they reduce AKI risk at the population level, individual AKI cases have been reported, most attributed to volume depletion. SGLT2 inhibitor initiation commonly causes eGFR decline through tubuloglomerular feedback and reduced intraglomerular pressure. Biopsy-proven interstitial nephritis and osmotic nephrosis have been described, but acute tubular necrosis (ATN) has not previously been reported with SGLT2 inhibitor use.

Case Description

A 61-year-old male with CKD stage 3b, type 2 diabetes, and heart failure developed significant AKI (creatinine levels escalating from 1.5 to 7.3 mg/dL) following SGLT2 inhibitor exposure and ARB initiation. Renal biopsy of 26-30 glomeruli demonstrated severe ATN, moderate interstitial fibrosis, and 28% global glomerulosclerosis. After discontinuation of the ARB and SGLT2 inhibitor, creatinine improved to 1.4 mg/dL over 3 months.

Discussion

SGLT2 inhibitors may induce ATN, representing a previously unreported association. RAS blockade and SGLT2 inhibition likely initiated tubular injury through reduced intraglomerular perfusion pressure. Additional injury may have resulted from renal medullary hypoxia due to increased distal tubular workload in the setting of low medullary oxygen tension. Notably, this occurred without traditional “second hits” such as volume depletions or NSAID exposure, suggesting increased metabolic demand alone may precipitate injury in susceptible individuals. This case demonstrated reversibility after medication discontinuation.