# Interstitial Nephritis Induced by Repeated Nonsteroidal Anti-inflammatory Drugs (NSAIDs) Use for Persistent Fever: A Case Report

## TL;DR

A 46-year-old man developed kidney damage from long-term ibuprofen use, showing how early treatment with steroids can help before a biopsy confirms the diagnosis.

## Contribution

This case highlights the use of urinary biomarkers and early steroid therapy in managing suspected NSAID-induced kidney injury.

## Key findings

- Elevated urinary tubular markers (NAG, β2MG, L-FABP) were key in suspecting drug-induced acute interstitial nephritis.
- Empirical steroid therapy improved kidney function before biopsy confirmation.
- Kidney biopsy confirmed the diagnosis and supported the effectiveness of early treatment.

## Abstract

Nonsteroidal anti-inflammatory drugs (NSAIDs) are extensively utilized for their analgesic and anti-inflammatory efficacy, yet they pose a significant risk for renal adverse events, notably drug-induced acute interstitial nephritis (DI-AIN). Prompt recognition and appropriate management are paramount to prevent irreversible kidney damage. We present the case of a 46-year-old male with NSAID-induced DI-AIN, emphasizing the diagnostic utility of a specific urinary biomarker profile and the rationale for empirical steroid therapy initiated before histopathological confirmation.

Our patient developed acute kidney injury (AKI) following daily ibuprofen administration for persistent fever. Despite ibuprofen discontinuation on day eight, renal function failed to improve, necessitating hospital admission on day 14. On day 15, his serum creatinine (Cr) level was 1.86 mg/dL. Urinalysis revealed mild proteinuria [urine protein-to-creatinine ratio (UPCR): 0.24 g/gCr] but strikingly elevated urinary tubular injury markers: N-acetyl-β-D-glucosaminidase (NAG): 20.9 U/L (on day one), β2-microglobulin (β2MG): 6028 μg/L, and L-type fatty acid-binding protein (L-FABP): 27.75 ng/mL. Based on a strong clinical suspicion of DI-AIN, a kidney biopsy was performed on day 15, and oral prednisolone (PSL, 0.8 mg/kg/day) was commenced the same evening before biopsy results were available. Serum creatinine improved to 1.56 mg/dL by discharge on day 23. Post-discharge, kidney biopsy results confirmed AIN. PSL was gradually tapered and discontinued after approximately 10 months, with sustained renal function recovery (serum creatinine: ~1.1 mg/dL).

This report underscores the importance of suspecting DI-AIN in patients with AKI and a history of NSAID exposure. The pronounced elevation of urinary tubular markers, despite only mild proteinuria, was pivotal in raising clinical suspicion. The negative autoimmune serology further strengthened the diagnosis of a drug-induced etiology. Empirical steroid therapy, initiated due to compelling clinical evidence before histopathological confirmation, appeared to be an effective intervention. While this single case cannot establish a therapeutic standard, it illustrates a clinical scenario where early, empirically-guided treatment may be justified. Kidney biopsy remains indispensable for definitive diagnosis. The report also highlights the pressing need for enhanced patient education on appropriate NSAID utilization. Repeated use of common NSAIDs can precipitate DI-AIN. A diagnostic profile of elevated urinary tubular markers with only mild proteinuria can be a key indicator for suspecting this condition. Empirical steroid therapy, guided by strong clinical suspicion, can be an effective early intervention, with subsequent kidney biopsy providing definitive diagnostic validation. Enhanced patient education on appropriate NSAID use is essential.