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World J Nephrol. Mar 25, 2026; 15(1): 117950
Published online Mar 25, 2026. doi: 10.5527/wjn.v15.i1.117950
Published online Mar 25, 2026. doi: 10.5527/wjn.v15.i1.117950
Renal tubular acidosis complication of non-steroidal anti-inflammatory drugs induced interstitial nephritis and its complete resolution with steroids: A case report
Abhisekh Sinha Ray, Department of Nephrology and Critical Care, Creighton University School of Medicine, Kearney, NE 68847, United States
Praveen Errabelli, Department of Nephrology, Allina Health, St Paul, MN 55125, United States
Neeharik Mareedu, Department of Nephrology, UPMC Western Maryland, Cumberland, MD 21502, United States
Maulik K Lathiya, Department of Nephrology, Mayo Clinic, Rochester, MN 55905, United States
Author contributions: Sinha Ray A contributed to the original concept; Errabelli PK contributed to the submission; Sinha Ray A and Errabelli PK contributed to writing; Mareedu N and Maulik L contributed to review and revision.
Informed consent statement: Written informed consent was obtained from the patient for publication of this report and any accompanying images.
Conflict-of-interest statement: All authors declare that they have no conflict of interest to disclose.
CARE Checklist (2016) statement: The authors have read the CARE Checklist (2016), and the manuscript was prepared and revised according to the CARE Checklist (2016).
Corresponding author: Abhisekh Sinha Ray, Assistant Professor, Department of Nephrology and Critical Care, Creighton University School of Medicine, 3219 Central Ave #200, Kearney, NE 68847, United States. abhisekh.sinharay@commonspirit.org
Received: December 25, 2025
Revised: January 27, 2026
Accepted: February 26, 2026
Published online: March 25, 2026
Processing time: 85 Days and 3.3 Hours
Revised: January 27, 2026
Accepted: February 26, 2026
Published online: March 25, 2026
Processing time: 85 Days and 3.3 Hours
Core Tip
Core Tip: This article underscores the importance of maintaining a high level of clinical suspicion for interstitial nephritis (IN) in case of non-steroidal anti-inflammatory drugs (NSAID)-induced persistent renal injury and dyselectrolytemia suggestive of renal tubular acidosis, and the critical role of biopsy in NSAID-induced IN. Role of steroids in drug-induced IN is debated; some study suggests their role only in early cases before fibrosis ensues. Our article emphasizes the potential role of steroids in persistent renal impairment and metabolic disturbances, even after discontinuation of NSAIDs, provided there is evidence of active interstitial inflammation and tubulitis on renal biopsy.