A 57-year-old Caucasian man was diagnosed to have focal segmental glomerlosclerosis (FSGS) in 1995. He eventually underwent a cadaveric renal transplantation in February 2002 and because this was complicated by delayed graft function, his creatinine plateaued at a baseline of 266 mmol/l (creatinine clearance 34ml/min). In November 2002, he presented with a 4 week history of generalized malaise, dark urine, poor appetite, widespread muscle aches and difficulty in using his proximal muscles. The symptoms had begun about 1 week after he had received an inactivated influenza vaccine (split virion—Avantis Pasteur). His concurrent medications included cyclosporin A 125mg BD, prednisolone 10mg OD, azathioprine 150mg OD and simvastatin 20mg OD. He had taken the statin for at least 6 years without complications and the monitored creatine kinase (CK) had always been within the normal range. There was no family history of neurological or muscular disease. Neurological examination revealed flaccid weakness involving the proximal muscles of both upper and lower limbs, but no muscle fasciculation or tenderness. Abdominal examination revealed a non-tender renal transplant. His blood urea was 33.5mmol/l and creatinine 649 mmol/l (creatinine clearance 10ml/min). The creatinine kinase (CK) was markedly elevated at 17 000U/l. The urine dipstick revealed large quantities of protein and blood. The measured urinary myoglobin was 238 600 mg/l (normal less than 15 mg/l). Other admission laboratory data was normal except for potassium 6.3mmol/l, phosphate 2.36mmol/l and haemoglobin 88 g/l. Calcium was 2.47mmol/l and white cell count 4.6 10/l. Serum cyclosporin A level was 167 ng/ml. A full renal immunological screen was negative. A transplant ultrasound was normal. Transplant biopsy revealed moderate tubular atrophy with tubulitis and the presence of brown granular tubular casts consistent with myoglobin. A muscle biopsy revealed scattered regenerating and degenerating fibres with no significant inflammatory infiltrate, compatible with a toxic myositis. Further investigations ruled out the possibility of primary muscle disease or metabolic myopathy. Other causes of toxic myositis, like drugs and viral infections, were excluded. There had been no recent change in the patient’s medication. A neurological opinion agreed that the influenza vaccination was the most likely cause of the toxic myositis. The prednisolone was increased to 60mg per day and the renal function gradually improved with serum creatinine falling to 370 mmol/l. Although the CK value normalized on day 10, his muscleweaknessgradually improvedover severalweeks.
