Rifampin-associated tubulointersititial nephritis and Fanconi syndrome presenting as hypokalemic paralysis

BMC Nephrology

Hyeon Seok Hwang¹  Suk Young Kim¹  Chul Woo Yang¹  Kwang Sun Suh²  Yoon Kyung Chang¹  Sang Ju Lee¹  Eun Oh Kim¹  Hong Ki Min¹ 

[1] Division of Nephrology, Department of Internal Medicine, The Catholic University of Korea, Seoul, Korea;Department of Pathology, Chungnam National University College of Medicine, Daejeon, Korea

关键词: Hypokalemic paralysis;    Tubulointerstitial nephritis;    Fanconi syndrome;    Rifampin;   

Others  :  1083025
DOI  :  10.1186/1471-2369-14-13

 received in 2012-11-13, accepted in 2013-01-14,  发布年份 2013

【 摘 要 】

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.

【 授权许可】

   
2013 Min et al.; licensee BioMed Central Ltd.

【 图 表 】

Figure 1.

【 参考文献 】

• [1]Muthukumar T, Jayakumar M, Fernando EM, Muthusethupathi MA: Acute renal failure due to rifampicin: a study of 25 patients. Am J Kidney Dis 2002, 40(4):690-696.
• [2]Nessi R, Bonoldi GL, Redaelli B, di Fillippo G: Acute renal failure after rifampicin: a case report and survey of the literature. Nephron 1976, 16:148-159.
• [3]Schubert C, Bates WD, Moosa MR: Acute tubulointerstitial nephritis related to antituberculous drug therapy. Clin Nephrol 2010, 73(6):413-419.
• [4]Izzedine H, Launay-Vacher V, Isnard-Bagnis C, Deray G: Drug-induced Fanconi's syndrome. Am J Kidney Dis 2003, 41(2):292-309.
• [5]Lino M, Binaut R, Noël LH, Patey N, Rustin P, Daniel L, Serpaggi J, Varaut A, Vanhille P, Knebelmann B, Grünfeld JP, Fakhouri F: Tubulointerstitial nephritis and Fanconi syndrome in primary biliary cirrhosis. Am J Kidney Dis 2005, 46(3):e41-e46.
• [6]Buysschaert M, Cosyns JP, Barreto L, Jadoul M: Pamidronate-induced tubulointerstitial nephritis with Fanconi syndrome in a patient with primary hyperparathyroidism. Nephrol Dial Transplant 2003, 18(4):826-829.
• [7]Hong YT, Fu LS, Chung LH, Hung SC, Huang YT, Chi CS: Fanconi’s syndrome, interstitial fibrosis and renal failure by aristolochic acid in Chinese herbs. Pediatr Nephrol 2006, 21(4):577-579.
• [8]Neelakantappa K, Gallo GR, Lowenstein J: Ranitidine-associated interstitial nephritis and Fanconi syndrome. Am J Kidney Dis 1993, 22(2):333-336.
• [9]De Vriese AS, Robbrecht DL, Vanholder RC, Vogelaers DP, Lameire NH: Rifampicin-associated acute renal failure: pathophysiologic, immunologic, and clinical features. Am J Kidney Dis 1998, 31(1):108-115.
• [10]Racusen LC, Solez K: Nephrotoxic tubular and interstitial lesions: morphology and classification. Toxicol Pathol 1986, 14(1):45-57.
• [11]Gabow PA, Lacher JW, Neff TA: Tubulointerstitial and glomerular nephritis associated with rifampin. Report of a case. JAMA 1976, 235(23k0):2517-2518.
• [12]Praga M, González E: Acute interstitial nephritis. Kidney Int 2010, 77(11):956-961.
• [13]Rossert J: Drug-induced acute interstitial nephritis. Kidney Int 2001, 60(2):804-817.
• [14]Sugisaki T, Klassen J, Milgrom F, Andres GA, McCluskey RT: Immunopathologic study of an autoimmune tubular and interstitial renal disease in brown Norway rats. Lab Invest 1973, 28(6):658-671.
• [15]Neugarten J, Gallo GR, Baldwin DS: Rifampin-induced nephrotic syndrome and acute interstitial nephritis. Am J Nephrol 1983, 3(1):38-42.
• [16]Kohno K, Mizuta Y, Yoshida T, Watanabe H, Nishida H, Fukami K, Iida S, Haramaki R, Wada Y, Tamai O, Tamaki K, Kato S, Morimatsu M, Okuda S: Minimal change nephrotic syndrome associated with rifampicin treatment. Nephrol Dial Transplant 2000, 15(7):1056-1059.
• [17]Yong JL, Killingsworth M: Diffuse glomerulonephritis associated with rifampicin treatment for tuberculosis. Pathology 2002, 34(3):295-297.
• [18]Sebastian A, McSherry E, Morris RC Jr: Renal potassium wasting in renal tubular acidosis (RTA): Its occurrence in types 1 and 2 RTA despite sustained correction of systemic acidosis. J Clin Invest 1971, 50(3):667-678.
• [19]Sebastian A, McSherry E, Morris RC Jr: On the mechanism of renal potassium wasting in renal tubular acidosis associated with the Fanconi syndrome (type 2 RTA). J Clin Invest 1971, 50(1):231-243.
• [20]Rose BD, Post TW: Clinical Physiology of Acid–base and Electrolyte Disorder. 5th edition. New York: McGraw-Hill; 2001:612-627.
• [21]Feinfeld DA, Ansari N, Nuovo M, Hussain A, Mir R: Tubulointerstitial nephritis associated with minimal self reexposure to rifampin. Am J Kidney Dis 1999, 33(5):e3.
• [22]Yoshioka K, Satake N, Kasamatsu Y, Nakamura Y, Shikata N: Rapidly progressive glomerulonephritis due to rifampicin therapy. Nephron 2002, 90(1):116-118.