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Acute renal failure following reintroduction of rifampicin after a prolonged interval
Br. J. Dis. Chest (1981) 75, 103
ACUTE RENAL FAILURE FOLLOWING R E I N T R O D U C T I O N OF R I F A M P I C I N A F T E R A PROLONGED INTERVAL A. G. DAVISON AND D. W . EMPEY
The London Hospital ( Whitechapel), London
INTRODUCTION
Acute renal failure has b e e n occasionally r e p o r t e d following t h e r e i n t r o d u c t i o n of r i f a m picin treatment ( K l e i n k n e c h t et al. 1972). A l t h o u g h a l o n g g a p b e t w e e n t r e a t m e n t s has been described ( L o r n o y 1976), this c o m p l i c a t i o n has u s u a l l y o c c u r r e d w h e n t h e t r e a t ment gap is short (Nessi et al. 1976) or d u r i n g i n t e r m i t t e n t t h e r a p y (Poole et al. 1971). We report a p a t i e n t w h o d e v e l o p e d a c u t e r e n a l failure w i t h t h e r e i n t r o d u c t i o n of r i f a m picin after a t r e a t m e n t g a p of 25 m o n t h s .
Case Report A 30-year-old Indian woman first presented with cervical lymphadenopathy at the age of 13 years. A clinical diagnosis of tuberculous lymphadenitis was made and she was treated with streptomycin, calcium benzamide salicyclate and isoniazid. She had further cervical lymphadenopathy when aged 15 and excision biopsy showed tuberculosis histologicaUy and acid-fast bacilli were identified. She was treated, with very poor compliance, with the same antituberculous chemotherapy for most of the next six years. When aged 27 she again presented with cervical lymphadenopathy and was treated with ethambutol, isoniazid and rifampicin daily. Rifampicin was stopped after six months. After eight months of chemotherapy she developed dysphagia and thoraeotomy revealed enlarged mediastinal and hilar glands and a necrotic posterior mediastinal mass compressing the oesophagus. Histology showed tuberculosis but culture for mycobacteria was negative. Postoperatively she was treated daily with rifampicin 450 rag, ethambutol 600 mg and isoniazid 300 mg for ten months and then with ethambutol and isoniazid for a further ten months. Fifteen months later she again had cervical lympbadenopathy; biopsy showed active tuberculosis histologically, but culture for mycobacteria was negative. Treatment was started with ethambutol 700 mg, isoniazid 300 mg and rifampicin 450 mg daily. Seven days later she developed 'flu-like' symptoms with fever, anorexia, arthralgia, headaches and nausea one hour after taking her tablets. She presented to hospital after four days, having herself noted a reduced urinary output. All drugs were stopped on admission. Plasma urea was 14.6 mmol/litre, haemoglobin 11.2 g/dl, platelets 230 x 109/litre and blood film was normal. She had heavy proteinuria and urinary casts. She was oliguric over the next four days. Plasma urea rose to 25 mmol/litre and plasma creatinine to 1380/~mol/litre. She underwent peritoneal dialysis for four days. Intravenous urography showed poor excretion with normal renal outlines and no evidence of obstruction. Rifampicin-dependent antibodies were detected (using rifampicin in a concentration of 400 mg/dl) in a titre of 256. She developed a fever and further cervical lymphadenopathy six weeks after renal function had returned to normal. Isoniazid and ethambutol were reintroduced singly and renal function remained normal.
104
A. G. Davison and D. W. Empev
DISCUSSION Thrombocytopenia, acute haemolytic anaemia, the 'flu' syndrome and acute renal failure have all been associated with rifampicin. These unwanted effects are usually seen during intermittent therapy (Poole et al. 1971) or following the early reintroduction of rifampicin after completion of a course (Nessi et al. 1976). Rifampicin antibodies are more commonly detected in patients who develop unwanted effects and titres fall at the end of treatment, although weak levels have been detected 16 months afterwards (Poole et al. 1971). This case demonstrates that acute renal failure may occur after a treatment gap of more than two years. The reintroduction of rifampicin is contraindicated in patients who have previously developed major side effects. If a second course of antituberculous chemotherapy is required, serious consideration should be given to using alternative agents if rifampicin has been given in the past. A complete drug history is essential in all patients but may be difficult to obtain because of the high mobility of patients between hospitals and countries. This patient attended five hospitals during treatment. If a second course of rifampicin is essential it would seem desirable to re-introduce the drug in small, gradually increasing doses under close daily observation (Girling 1977).
ACKNOWLEDGEMENTS We are grateful to the late Dr Sheila Worlledge for measurement of the rifampicin antibody levels.
REFERENCES GIRLING, D. J. (1977) Adverse reactions to rifampicin in anti-tuberculous regimens. J. antimicrob. Chemother. 3, 115. KLEINKNECHT,D., HOMBERG,J. C. ~ DECROIX,e . (1972) Acute renal failure after rifampicin. Lancet 1, 1238. LORNOY, W. (1976) Potentially serious side effects of intermittent treatment or repeated therapy with rifampicin--danger of acute renal failure. Acta din. belgica 31, 89. POOLE, G., STRADLING,P. & WOt/LLDEGE,S. (1971) Potentially serious side effects of high dose, twice weekly rifampicin. Br. reed. J. 3, 343. NESSI, R., BONOLDI, G. g., DEDAELLI, B. & DIFILIPPO, G. (1976) Acute renal failure after rifampicin: a case report and survey of the literature. Nephron 16, 148.
ACUTE RENAL FAILURE FOLLOWING R E I N T R O D U C T I O N OF R I F A M P I C I N A F T E R A PROLONGED INTERVAL A. G. DAVISON AND D. W . EMPEY
The London Hospital ( Whitechapel), London
INTRODUCTION
Acute renal failure has b e e n occasionally r e p o r t e d following t h e r e i n t r o d u c t i o n of r i f a m picin treatment ( K l e i n k n e c h t et al. 1972). A l t h o u g h a l o n g g a p b e t w e e n t r e a t m e n t s has been described ( L o r n o y 1976), this c o m p l i c a t i o n has u s u a l l y o c c u r r e d w h e n t h e t r e a t ment gap is short (Nessi et al. 1976) or d u r i n g i n t e r m i t t e n t t h e r a p y (Poole et al. 1971). We report a p a t i e n t w h o d e v e l o p e d a c u t e r e n a l failure w i t h t h e r e i n t r o d u c t i o n of r i f a m picin after a t r e a t m e n t g a p of 25 m o n t h s .
Case Report A 30-year-old Indian woman first presented with cervical lymphadenopathy at the age of 13 years. A clinical diagnosis of tuberculous lymphadenitis was made and she was treated with streptomycin, calcium benzamide salicyclate and isoniazid. She had further cervical lymphadenopathy when aged 15 and excision biopsy showed tuberculosis histologicaUy and acid-fast bacilli were identified. She was treated, with very poor compliance, with the same antituberculous chemotherapy for most of the next six years. When aged 27 she again presented with cervical lymphadenopathy and was treated with ethambutol, isoniazid and rifampicin daily. Rifampicin was stopped after six months. After eight months of chemotherapy she developed dysphagia and thoraeotomy revealed enlarged mediastinal and hilar glands and a necrotic posterior mediastinal mass compressing the oesophagus. Histology showed tuberculosis but culture for mycobacteria was negative. Postoperatively she was treated daily with rifampicin 450 rag, ethambutol 600 mg and isoniazid 300 mg for ten months and then with ethambutol and isoniazid for a further ten months. Fifteen months later she again had cervical lympbadenopathy; biopsy showed active tuberculosis histologically, but culture for mycobacteria was negative. Treatment was started with ethambutol 700 mg, isoniazid 300 mg and rifampicin 450 mg daily. Seven days later she developed 'flu-like' symptoms with fever, anorexia, arthralgia, headaches and nausea one hour after taking her tablets. She presented to hospital after four days, having herself noted a reduced urinary output. All drugs were stopped on admission. Plasma urea was 14.6 mmol/litre, haemoglobin 11.2 g/dl, platelets 230 x 109/litre and blood film was normal. She had heavy proteinuria and urinary casts. She was oliguric over the next four days. Plasma urea rose to 25 mmol/litre and plasma creatinine to 1380/~mol/litre. She underwent peritoneal dialysis for four days. Intravenous urography showed poor excretion with normal renal outlines and no evidence of obstruction. Rifampicin-dependent antibodies were detected (using rifampicin in a concentration of 400 mg/dl) in a titre of 256. She developed a fever and further cervical lymphadenopathy six weeks after renal function had returned to normal. Isoniazid and ethambutol were reintroduced singly and renal function remained normal.
104
A. G. Davison and D. W. Empev
DISCUSSION Thrombocytopenia, acute haemolytic anaemia, the 'flu' syndrome and acute renal failure have all been associated with rifampicin. These unwanted effects are usually seen during intermittent therapy (Poole et al. 1971) or following the early reintroduction of rifampicin after completion of a course (Nessi et al. 1976). Rifampicin antibodies are more commonly detected in patients who develop unwanted effects and titres fall at the end of treatment, although weak levels have been detected 16 months afterwards (Poole et al. 1971). This case demonstrates that acute renal failure may occur after a treatment gap of more than two years. The reintroduction of rifampicin is contraindicated in patients who have previously developed major side effects. If a second course of antituberculous chemotherapy is required, serious consideration should be given to using alternative agents if rifampicin has been given in the past. A complete drug history is essential in all patients but may be difficult to obtain because of the high mobility of patients between hospitals and countries. This patient attended five hospitals during treatment. If a second course of rifampicin is essential it would seem desirable to re-introduce the drug in small, gradually increasing doses under close daily observation (Girling 1977).
ACKNOWLEDGEMENTS We are grateful to the late Dr Sheila Worlledge for measurement of the rifampicin antibody levels.
REFERENCES GIRLING, D. J. (1977) Adverse reactions to rifampicin in anti-tuberculous regimens. J. antimicrob. Chemother. 3, 115. KLEINKNECHT,D., HOMBERG,J. C. ~ DECROIX,e . (1972) Acute renal failure after rifampicin. Lancet 1, 1238. LORNOY, W. (1976) Potentially serious side effects of intermittent treatment or repeated therapy with rifampicin--danger of acute renal failure. Acta din. belgica 31, 89. POOLE, G., STRADLING,P. & WOt/LLDEGE,S. (1971) Potentially serious side effects of high dose, twice weekly rifampicin. Br. reed. J. 3, 343. NESSI, R., BONOLDI, G. g., DEDAELLI, B. & DIFILIPPO, G. (1976) Acute renal failure after rifampicin: a case report and survey of the literature. Nephron 16, 148.