Ethambutol-induced acute renal failure

Sir,

Ethambutol can cause ocular toxicity and hyperuricaemia, but ethambutol-associated acute renal failure during treatment of pulmonary tuberculosis is extremely rare [1,2]. Here we report the case of a man who manifested with oliguric acute renal failure and jaundice associated with ethambutol.

Case. A 33-year-old man was referred to our university hospital from a local clinic because of oliguria for the previous 2 days. Five years previously he had been treated for pulmonary tuberculosis with the antituberculosis medications rifampicin, pyrazinamide, isoniazid and ethambutol. Three days prior to admission, he was diagnosed as having a recurrence of pulmonary tuberculosis and was started on the same four medications at a local clinic. One day after the initiation of this treatment, he noted jaundice, abdominal pain and oliguria. Admission laboratory data were as follows: blood urea nitrogen, 71.6 mg/dl (25.5 mmol/l); creatinine, 5.2 mg/dl (459 µmol/l); albumin, 4.0 g/dl (40 g/l); total bilirubin, 14.0 mg/dl (238 mmol/l); direct bilirubin, 9.8 mg/dl (166 mmol/l); aspartate aminotransferase, 170 IU/l; alanine aminotransferase, 28 IU/l; urine pH 7.0, specific gravity 1.010, proteinuria 3+; and the urine sediment contained many red cells and 3–5 white cells per high-power field. Sputum stained positive for acid-fast bacilli. All four antituberculosis medications were stopped on the day of admission.

Anuria persisted for 4 days. On the 8th and 15th day after initiation of antituberculosis medication, isoniazid and rifampicin were reintroduced without development of anuria or other intolerance reactions. On the 24th day after initiation of antituberculosis medication, ethambutol was reintroduced, and abdominal pain, fever and general weakness occurred on the same evening. The serum creatinine level increased to 8.6 mg/dl and urine output decreased; therefore, haemodialysis was initiated (Figure 1). A renal biopsy performed on the 39th day after initiation of antituberculosis medication showed features characteristic of acute tubular necrosis that were more prominent than interstitial infiltration. The patient completely recovered his renal function after receiving isoniazid, rifampicin, pyrazinamide and cycloserine.



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Fig. 1. The time course of changes in serum creatinine and urine output. Haemodialysis is indicated by the arrowhead.

 
Comment. Ethambutol-induced acute renal failure is very rare; we know of only three reported cases of tubulointerstitial nephritis due to ethambutol administration [1,2]. In those cases, the renal function deteriorated only after administration of antituberculosis medication over several months, and liver function tests were normal. The clinical characteristic findings of ethambutol-induced acute renal failure in the present case were sudden onset of oliguria and renal failure, association with hepatotoxicity, and development after re-exposure to ethambutol. On the basis of the histological appearance and the time course of the disease, we suggest that the renal damage in our patient was due to a toxic rather than an allergic effect producing a tubular lesion and interstitial nephritis.

Conflict of interest statement. None declared.

Soon Hyo Kwon, Jung Hoon Kim, Jong Oh Yang, Eun-Young Lee and Sae Young Hong

Department of Internal Medicine Soonchunhyang University Cheonan Hospital 23–20 Bongmyung-dong Cheonan Korea Email: eylee{at}sch.ac.kr

References

  1. Garcia-Martin F, Mampaso F, de Arriba G et al. Acute interstitial nephritis induced by ethambutol. Nephron 1991; 59: 679–680[ISI][Medline]
  2. Collier J, Joekes AM, Philalithis PE, Thompson FD. Two cases of ethambutol nephrotoxicity. Br Med J 1976; 2: 1105–1106




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