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논문분류	춘계학술대회 초록집
제목	Rifampin-associated Tubulointersititial Nephritis and Fanconi Syndrome Presenting as Hypokalemic Paralysis
저자	Kyung Jin Yun1, Jung Eun Lee1, Hong Ki Min1, Sang Ju Lee1, Yoon Kyung Chang1,Kwang Sun Suh2, Chul Woo Yang1, Suk Young Kim1, Hyeon Seok Hwang1
출판정보	2013; 2013(1):
키워드	Rifampin, Fanconi증후군, 세뇨관간질신염/Rifampin, Fanconi syndrome, Tubulointerstitial nephritis
초록	Background: Rifampin is one of the most important drugs in first-line therapies for tuberculosis. The renal toxicity of rifampin has been reported sporadically and acute tubulointerstitial nephritis (ATIN) is a frequent histological finding. We describe for the first time a case of ATIN and Fanconi syndrome presenting as hypokalemic paralysis, associated with the use of rifampin. Case presentation: A 42-year-old man was admitted with sudden-onset lower extremity paralysis and mild renal insufficiency. He had been treated for pulmonary tuberculosis with isoniazid, rifampin, and ethambutol for 2 months. Laboratory tests revealed proteinuria, profound hypokalemia, hyperchloremic metabolic acidosis with a normal anion gap, positive urine anion gap, hypophosphatemia with hyperphosphaturia, hypouricemia with hyperuricosuria, glycosuria with normal serum glucose level, generalized aminoaciduria, and β2-microglobulinuria. A kidney biopsy revealed findings typical of ATIN and focal granular deposits of immunoglubulin A and complement 3 in the glomeruli and tubules. Electron microscopy showed epithelial foot process effacement and electron-dense deposits in the subendothelial and mesangial spaces. Cessation of rifampin resolved the patient’s clinical presentation of Fanconi syndrome, and improved his renal function and proteinuria. Conclusion: This case demonstrates that rifampin therapy can be associated with Fanconi syndrome presenting as hypokalemic paralysis, which is a manifestation of ATIN. Kidney function and the markers of proximal tubular injury should be carefully monitored in patients receiving rifampin.
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