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A 33-year-old male renal transplant recipient was admitted to the renal unit with a rapid deterioration in his renal function. His previous medical history included insulin-dependent diabetes mellitus, diagnosed at the age of 11. He had suffered from several diabetic complications including proliferative diabetic retinopathy, presumed diabetic nephropathy, hypertension and hyperlipidaemia. At the age of 29, he reached end-stage renal failure and was commenced on haemodialysis. He remained on dialysis for 5 months before receiving a transplant kidney (0 : 0 : 0 mismatch with a cold ischaemic time of 13 h 44 min). The post-operative recovery was completely unremarkable with no episodes of rejection. He was discharged on the 10th post-operative day with a serum creatinine of 160 mmolul on an immunosuppressive regimen of cyclosporin A, azathioprine and prednisolone in combination with aspirin and a calcium channel antagonist. Subsequent progress was uneventful and he maintained good graft function with a serum creatinine in the range of 150 mmolul to 190 mmolul and cyclosporin A trough concentrations of 140 nguml to 220 nguml. Thirty-four months after the transplant, the patient was kicked in the right iliac fossa overlying the transplant kidney. His occupation involved caring for young adults with mental and behavioural difficulties. The kick delivered by one of these male adults, managed to propel our transplant patient about 5 m, giving an indication of the force involved. The patient began to develop symptoms of increasing tenderness of his graft followed by general malaise and nausea within 3 days of the event. He reported to his general practitioner who checked his electrolytes and found the serum creatinine concentration to be 571 mmolul, nine days after the event. The renal unit was contacted and he was admitted the next day. The serum creatinine on admission was 562 mmolul, with bicarbonate and potassium concentrations being 16.4 mmolul and 5.4 mmolul respectively. Serum trough cyclosporin A concentration was 150 nguml and the blood glucose was 12.8 mmolul. Full blood count was within normal range and urine analysis revealed 1q of glucose only. There were no red blood cells, casts or white blood cells on urine microscopy. Urine culture was negative. The urinary albuminu creatinine ratio was 5.4 mgummol. A renal ultrasound was performed which showed an enlarged allograft kidney measuring 13 cm but with no evidence of obstruction and normal doppler flows. The following morning the patient underwent graft biopsy, which was reported as follows: ‘Renal cortex contains at least 4 glomeruli which show no significant abnormality. There is a moderate diffuse lymphocytic tubulitis. No vasculitis is identified, however there is diffuse interstitial haemorrhage. The appearances are those of cellular rejection. Whilst the interstitial haemorrhage could be due to trauma, there is a very strong possibility that this is due to vascular rejection, not seen in this material.’ These changes are seen in Figure 1. The patient was treated with three intravenous pulsed doses of 500 mg of methylprednisolone. The dose of cyclosporin A was increased from 300 mg daily to 400 mg daily. He was discharged on an increased dose of oral prednisolone, in addition to the cyclosporin and azathioprine. The patient’s creatinine improved from a peak of 623 mmolul and eventually reached a plateau of 318 mmolul, 21 days post discharge. Unfortunately, the patient’s renal function slowly declined and eventually he commenced haemodialysis 3 months later. The course of events is demonstrated in Figure 2. Correspondence and offprint requests to: E. Mohammed, Wessex Renal Transplant Unit, St Mary’s Hospital, Portsmouth PO3 6AD, UK. Email: emilitoperez@hotmail.com Nephrol Dial Transplant (2002) 17: 283–284

Is trauma associated with acute rejection of a renal transplant?