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Acute interstitial nephritis associated with moxifloxacin use
Michael Argirov1, Gesa Ricken, Daniel Zecher
1Medizinische Poliklinik of Ludwigs-Maximilians-University, Munich, Germany. Michael.Argirov@med.uni-muenchen.de
Moxifloxacin, a fluoroquinolone antibiotic, may cause acute tubulointerstitial nephritis (ATIN). This case highlights the potential for nephrotoxicity, emphasizing the need to consider ATIN in patients with systemic symptoms post-moxifloxacin treatment.
Area of Science:
- Nephrology
- Pharmacology
- Internal Medicine
Background:
- Moxifloxacin is a widely used fluoroquinolone antibiotic for respiratory infections.
- While generally safe, its potential for adverse renal effects has not been extensively documented.
- Previous literature and manufacturer data did not report nephrotoxicity associated with moxifloxacin prior to this case.
Observation:
- A 68-year-old female developed acute tubulointerstitial nephritis (ATIN) approximately 10 days after completing moxifloxacin therapy.
- Clinical presentation included elevated serum creatinine, leukocyturia, proteinuria, and foaming urine.
- Kidney biopsy confirmed ATIN, suggesting an immune-mediated hypersensitivity reaction.
Findings:
- Treatment with oral corticosteroids (prednisolone) led to gradual restoration of renal function over six months.
- Mild proteinuria persisted despite treatment.
- The exact pathogenesis of drug-induced ATIN remains under investigation, but hypersensitivity is the suspected mechanism.
Implications:
- This case suggests that fluoroquinolones, including moxifloxacin, may possess nephrotoxic potential.
- ATIN is a serious adverse event that can lead to chronic kidney disease or dialysis.
- Clinicians should consider ATIN in the differential diagnosis for patients presenting with systemic symptoms following moxifloxacin treatment.
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