BACKGROUND: Moxifloxacin is a fluoroquinolone antimicrobial agent with proven efficacy against community-acquired respiratory pathogens. Common adverse effects associated with its use include gastro-intestinal symptoms, but nephrotoxicity has not yet been reported to the manufacturer or in the literature (based on a MEDLINE search [key words: fluoroquinolone, moxifloxacin, kidney, interstitial, and nephritis; years: 1970-2005]). OBJECTIVE: The purpose of this article was to describe a case of nephrotoxicity associated with moxifloxacin use. METHODS: A 68-year-old woman weighing 65 kg was referred to our nephrology clinic by her general practitioner because of an acute increase in serum creatinine concentration (SCC). In this patient, biopsyproven acute tubulointerstitial nephritis (ATIN) developed approximately 10 days after the end of moxifloxacin therapy for a nonspecific bronchial infection. The patient initially presented with nonspecific clinical symptoms, foaming of her urine, elevated erythrocyte sedimentation rate, and the acute increase in SCC. Urinalysis revealed signs of tubulointerstitial damage, including leukocyturia and proteinuria with a high concentration of alpha(1)-microglobulin. Oral corticosteroid therapy with prednisolone was started approximately 14 days after symptom development, beginning at 1 mg/kg body weight QD. RESULTS: After the initiation of therapy, renal function was gradually restored over 6 months, but mild proteinuria persisted. Although the exact pathogenesis of drug-induced ATIN remains unclear, an immune-mediated hypersensitivity reaction is the assumed mechanism. CONCLUSIONS: Fluoroquinolones might have a nephrotoxic effect. In this patient, ATIN was likely associated with moxifloxacin use. Because the course of ATIN is unpredictable and might lead to long-term dialysis, considering ATIN as a possible diagnosis in the scenario of systemic symptoms after moxifloxacin treatment is essential.
BACKGROUND:Moxifloxacin is a fluoroquinolone antimicrobial agent with proven efficacy against community-acquired respiratory pathogens. Common adverse effects associated with its use include gastro-intestinal symptoms, but nephrotoxicity has not yet been reported to the manufacturer or in the literature (based on a MEDLINE search [key words: fluoroquinolone, moxifloxacin, kidney, interstitial, and nephritis; years: 1970-2005]). OBJECTIVE: The purpose of this article was to describe a case of nephrotoxicity associated with moxifloxacin use. METHODS: A 68-year-old woman weighing 65 kg was referred to our nephrology clinic by her general practitioner because of an acute increase in serum creatinine concentration (SCC). In this patient, biopsyproven acute tubulointerstitial nephritis (ATIN) developed approximately 10 days after the end of moxifloxacin therapy for a nonspecific bronchial infection. The patient initially presented with nonspecific clinical symptoms, foaming of her urine, elevated erythrocyte sedimentation rate, and the acute increase in SCC. Urinalysis revealed signs of tubulointerstitial damage, including leukocyturia and proteinuria with a high concentration of alpha(1)-microglobulin. Oral corticosteroid therapy with prednisolone was started approximately 14 days after symptom development, beginning at 1 mg/kg body weight QD. RESULTS: After the initiation of therapy, renal function was gradually restored over 6 months, but mild proteinuria persisted. Although the exact pathogenesis of drug-induced ATIN remains unclear, an immune-mediated hypersensitivity reaction is the assumed mechanism. CONCLUSIONS:Fluoroquinolones might have a nephrotoxic effect. In this patient, ATIN was likely associated with moxifloxacin use. Because the course of ATIN is unpredictable and might lead to long-term dialysis, considering ATIN as a possible diagnosis in the scenario of systemic symptoms after moxifloxacin treatment is essential.
Authors: J Daniel Kanofsky; Mary E Woesner; Alexander Z Harris; James P Kelleher; Karen Gittens; Elina Jerschow Journal: Prim Care Companion CNS Disord Date: 2011