Fluindione-induced immuno-allergic interstitial nephritis

نویسندگان

  • Rania Kheder-Elfekih
  • Caroline Poitou
  • Isabelle Brocheriou
  • Helene Depreneuf
  • Hassane Izzedine
چکیده

Drug-induced acute interstitial nephritis (AIN) is an established cause of acute kidney injury (AKI). Antibiotics and non-steroidal anti-inflammatory drugs (NSAIDs) are the most frequent offending drugs [1]. Only a few vitamin K antagonist-induced AIN cases have been reported. Some publications describe AIN associated with fluindione (Previscan R ©), an anticoagulant of the antivitamin K family, derived from indanedione, exclusively marketed in France. We present an additional case of AIN secondary to fluindione and review the available literature. A 70-year-old woman was hospitalized for AKI. Her treatment list included amlodipine and atenolol. In December 2007, the serum creatinine (SCr) level was 70 μmol/L and an asymptomatic atrial fibrillation was detected. Fluindione was hence initiated. SCr rose to 220 μmol/L (04/08). On admission, her SCr level had reached 3.4 mg/dL and fluindione was stopped. Blood pressure was 110/ 80 mmHg, and neither cutaneous rash nor peripheral lymphadenopathy was found. Laboratory tests showed SCr 299.2 μmol/L, proteinuria 2 g/24 h (1 g albumin and lowmolecular-weight proteins, each) and negative urine sediment. A renal ultrasound revealed reduced-sized (10 cm) kidneys without obstructive uropathy. Immunological analyses were negative. A transjugular renal biopsy was performed. The renal biopsy included 11 glomeruli; 5 were sclerotic and 6 were normal. A diffuse infiltrate of lymphocytes, eosinophils and monocytes was found in the interstitium associated with severe tubulitis (Figure 1). Immunostains demonstrated CD3-positive lymphoid cells in the interstitium (Figure 2) compared to CD20 immunohistochemical staining (Figure 3). Immunofluorescence was negative. Electron microscopy was not performed. The

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عنوان ژورنال:

دوره 2  شماره 

صفحات  -

تاریخ انتشار 2009