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제목	A Case of Acute Tubulointerstitial Nephritis with Infliximab
저자	Gang Jee Ko1, Yang Jae Yoo1, Mi Yeon Jung1, Yu Ah Hong1, Heui Jung Pyo,Young Joo Kwon1, Nam Hee Won2
출판정보	2013; 2013(1):
키워드	급성 간질성 신염, Infliximab, 약제유발 신부전/Acute tubulointerstitial nephritis, Infliximab, ARF
초록	Infliximab is a chimeric tumor necrosis factor-alpha (TNF-a) monoclonal antibody, which has been extensively used in patients with rheumatoid arthritis and inflammatory bowel disease. Infection was known as the major side effect of infliximab and renal complications have not been recognized. However, here we report a patient who presented acute tubulointerstitial nephritis (ATIN) after treatment of infliximab for Crohn’s disease. A 25-year-old woman was admitted with purpuric rash on both lower extremities and arthralgia. She was diagnosed with Crohn's disease 5 years ago and has been treated with mesalazine. Inflximab was combined 2 years ago. Upon the laboratory test, creatinine was elevated to 1.9 mg/dL from 0.6 mg/dL which was measured 1 year ago. Abnormal finding in urinalysis such as hematuria, pyuria and proteinuria was not observed. Renal image with ultrasonography and serologic examination did not show significant abnormalities, and 10 mg of oral prednisolone was given to control purpura and edema with the impression of Henoch-Schonlein purpura. After administration of prednisolone, purpura and edema was resolved, and creatinine was decreased to 1.46 mg/dL. Creatinine was increased again upto 2.6 mg/dL at 2 months after discontinuation of prednisolone. Renal biopsy showed acute tubulointerstitial nephritis with interstitial inflammation. Drug induced interstitial nephritis was suspected as significant infiltration of eosinophils, and chronic exposure of causative drugs was also suspected because chronic tubulointerstitial nephritis was superimposed. Infliximab was supposed as a causative agent because there was no other medications causing ATIN and creatinine was increased as stepladder pattern according to infliximab treatment schedule in every 2 months. Oral prednisolone was administered, and modality of treatment for Crohn’s disease was switched to humanized TNF-a antibody, adalimumab to minimize immunologic reaction. Serum creatinine level was partially recovered to 1.6 mg/dL after 2 weeks of steroid therapy. ATIN should be suspected as a cause of acute kidney injury during immunologic treatment.
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