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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Tosufloxacin (TFLX), a fluoroquinolone antibiotic approved for pediatric use in Japan, is primarily prescribed for macrolide-resistant Mycoplasma pneumoniae infections. While effective, TFLX-associated renal complications have been reported, particularly in infants. We present a rare case of TFLX-induced crystalline nephropathy that manifests transient nephrogenic diabetes insipidus (NDI).
A previously healthy 22-month-old boy with acute otitis media was administered TFLX at a dose of 12 mg/kg/day following unsuccessful treatment with ampicillin and cefditoren pivoxil. Within 48 hours, he developed severe polydipsia and polyuria, with a nocturnal urine output 470 mL in 9 hours, corresponding to an estimated daily volume of 104 mL/kg. Laboratory findings revealed a serum sodium level of 140 mEq/L, a serum osmolality 283 mOsm/kg, and an elevated plasma vasopressin of 9.8 pg/mL (reference range: <2.8 pg/mL). However, his urine was inappropriately dilute, with an of osmolality 273 mOsm/kg and specific gravity 1.009. Urinary aquaporin-2 (AQP2) was undetectable. Microscopic examination of the urine sediment revealed numerous needle-shaped and sea-urchin-like crystals, along with epithelial casts. Sternheimer staining demonstrated epithelial casts entangled with crystals, confirmed as TFLX by solubility testing. Round tubular epithelial progenitor cells indicated active tubular injury and regeneration. Tubular damage biomarkers remained normal. Brain MRI excluded central diabetes insipidus.
Following the discontinuation of TFLX, the patient’s clinical condition improved rapidly. His urine output decreased within 24 hours and returned to normal by day 4. On day 7, the serum osmolality was 281 mOsm/kg, plasma vasopressin was 4.2 pg/mL, and the spot urine specific gravity was 1.015. Urinary crystals and casts resolved completely, and urinary AQP2 became detectable (4.5 ng/mL).This case demonstrates TFLX-induced transient NDI characterized by: temporal association with TFLX administration, hypotonic urine despite elevated vasopressin, suppressed urinary AQP2, presence of TFLX crystals, and rapid resolution after discontinuation. The underlying pathophysiology is thought to involve the deposition of TFLX crystal in the collecting ducts, which causes mechanical obstruction and disrupts vasopressin-mediated AQP2 trafficking. TFLX-induced crystalluria occurs eight times more frequently in infants than in adults, suggesting age-related vulnerability.
We report a case of TFLX-induced crystalline nephropathy that resulted in transient NDI in an infant. This highlights the vulnerability of infants to fluoroquinolone-induced renal complications. When fluoroquinolones are deemed necessary for young children, careful monitoring of parameters such as urine output, specific gravity, and urinary sediment may facilitate the early detection of drug-induced NDI.
