[A case of Bufferin induced acute interstitial nephritis--analysis of immune cells and cytokine]
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Updated: Jul 28, 2026

Identification of the Source of Secreted Proteins in the Kidney by Brefeldin A Injection
Published on: November 10, 2021
M Okada1, K Yoshioka, S Isokawa
1Department of Pediatrics, Kinki University School of Medicine.
Insights
This case report details acute interstitial nephritis in a teenager caused by Bufferin. The findings suggest cell-mediated immune responses contribute to drug-induced kidney injury.
Area of Science:
- Nephrology
- Immunology
- Pharmacology
Background:
- Acute interstitial nephritis (AIN) is a kidney disease often caused by medications.
- Identifying the causative agent is crucial for effective treatment and management.
Observation:
- A 15-year-old female presented with fever and impaired renal function, including elevated BUN and creatinine.
- Renal biopsy revealed interstitial edema, inflammatory cell infiltration (T cells, monocytes/macrophages), and minor glomerular changes.
- Interstitial cells expressed interleukin-1 (IL-1) and tumor necrosis factor (TNF).
Findings:
- Bufferin tested positive in a lymphocyte stimulation test, indicating a potential drug hypersensitivity.
- The patient's presentation and biopsy results were consistent with drug-induced AIN.
- Evidence suggests a cell-mediated immune mechanism underlying the observed kidney injury.
Implications:
- This case highlights Bufferin as a potential cause of AIN.
- The findings support the role of T-cell mediated immunity in drug-induced AIN.
- Further research into immune mechanisms of drug-induced kidney injury is warranted.
Abstract:
This paper describes a case report of acute interstitial nephritis associated with Bufferin. A 15-year-old girl were referred to our hospital due to fever and renal dysfunction. Laboratory findings showed elevation of serum BUN and creatinine, and increased urinary beta 2-MG excreation. Light microscopic findings of her renal biopsy specimen revealed edema and numerous inflammatory cells in the interstitium, and minor alterations in glomeruli. The interstitial infiltrates consisted mainly of T cells and also monocytes/macrophages. Interstitial cells were labelled with antibodies to interleukin (IL)-1 and tumor necrose factor (TNF). Bufferin was positive by lymphocyte stimulation test. Thus, we considered that this drug was causative in this case. This observation suggests the participation of cell-mediated immune injury in drug induced acute interstitial nephritis.
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