Abstract: SA-PO0090
Over-the-Counter and Under-the-Radar: A Tubular Cover-Up for a Covert Interstitial Agent
Session Information
- AKI: Clinical Diagnostics and Biomarkers
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Welch, Briggs Michael, The University of Texas Health Science Center at Houston John P and Katherine G McGovern Medical School, Houston, Texas, United States
- Valdez Cuadra, Margarita, The University of Texas Health Science Center at Houston John P and Katherine G McGovern Medical School, Houston, Texas, United States
- Ziaolhagh, Ali, The University of Texas Health Science Center at Houston John P and Katherine G McGovern Medical School, Houston, Texas, United States
Introduction
Although typically reversible, acute interstitial nephritis (AIN) is a commonly overlooked cause of acute kidney injury (AKI), especially in cases with a clear alternative cause present. Often drug-induced, delayed recognition of AIN can lead to continued use of harmful agents causing ongoing and irreversible damage. With any AKI, a flexible diagnostic approach and frequent reassessment is crucial in guiding appropriate treatment. We present a case where an AKI was initially attributed to acute tubular necrosis (ATN) based on history, with biopsy revealing concurrent and active AIN.
Case Description
A 57-year-old man presented with three days of nausea, vomiting, diarrhea, poor oral intake and generalized weakness. He was afebrile with stable vitals and an exam notable for a erythematous rash involving his lower extremities. With a baseline creatine <1.0 mg/dL, his labs on presentation now showed >5.0 mg/dL. He was admitted for AKI believed secondary to hypovolemic ATN.
Further workup showed normal complement levels, absent eosinophilia, and a bland urinalysis. He was prescribed gabapentin, tramadol, rosuvastatin, aspirin, baclofen, valsartan, amlodipine, and atenolol; he also reported use of esomeprazole and ibuprofen as-need for reflux and back pain. Although ATN secondary to hypovolemia was our running diagnosis, we elected for renal biopsy given the severity of injury with the presence of a rash and known nephrotoxic exposure.
Histologic analysis showed classic features of ATN along with focal areas of interstitial inflammation consistent with AIN. Ibuprofen and esomeprazole were discontinued permanently and the patient steadily improved to near-prior baseline. Corticosteroid treatment was deferred given his recovery and he was discharged. He had stable labs and reported subjective improvement at clinic follow up.
Discussion
This case highlights the need for vigilance with any AKI, even when a cause appears clear. For complex cases, considering alternative or concurrent processes is key to guide proper treatment. While biopsy is still the gold standard for diagnosing AIN, it remains invasive, carries procedural risks, and can be delayed itself due to unforeseen factors. High-clinical suspicion for AIN remains crucial; and continued reaserch on non-invasive tests for reliable detection of AIN is paramount to improve the current quality of management.