Dobutamine-induced myoclonia in severe renal failure.

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, 71.6mg/dl (25.5mmol/l); creatinine, 5.2mg/dl (459mmol/l); albumin, 4.0 g/dl (40 g/l); total bilirubin, 14.0mg/dl (238mmol/l); direct bilirubin, 9.8mg/dl (166mmol/l); aspartate aminotransferase, 170 IU/l; alanine aminotransferase, 28 IU/l; urine pH 7.0, specific gravity 1.010, proteinuria 3þ; 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 8.6mg/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. 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.