A patient recently transplanted with a living donor kidney develops severe neurological symptoms

One week after receiving a kidney transplant donated by his father, a 20-year-old patient was transferred to our department. The history of his kidney problems started when he was 1 year old. He had obstructive nephropathy requiring repeat urological operations and resulting in end-stage renal failure necessitating chronic haemodialysis from the age of 8 until this recent transplantation. His post-transplantation immunosuppressive regimen consisted of ciclosporin, mycofenolate mofetil and prednisone. A few days after his transfer to our department, he developed a biopsy-proven borderline transplant rejection, which was treated with high doses of cortisone. His repeated complaints of headaches were attributed to the cortisone, and they resolved without any treatment. A few days later, he developed blurred vision in the right eye, and that was followed by a generalized seizure. On the very same day—the 15th day after his kidney transplantation—he had to be transferred to the intensive care unit for a status epilepticus. His blood pressure was normal—the highest ever being 150/80mmHg. His blood tests on the day of the onset of neurological symptoms showed the following: BUN 23mg/dl, creatinine 1.0mg/dl, Na 134mmol/l, K 3.8mmol/l, Ca 2.1mmol/l, erythrocytes 3.7 10/l, haematocrit 37%, haemoglobin 12.5 g/l, leucocytes 8200/l, thrombocytes 246 000/l, albumin 33 g/l, CRP 3mg/l. Apart from the time of borderline rejection, when his creatinine rose to a maximum of 1.6mg/dl, his blood tests were normal throughout his stay in the department. His ciclosporin trough levels had a mean value of around 250 ng/ml. Computed tomography (CT) showed hypodense areas mainly in the posterior white matter of his brain. Our radiologist suspected a posterior reversible encephalopathy syndrome (PRES). Magnetic resonance tomography (MRT) confirmed the diagnosis of PRES by showing the characteristic hyperintense parieto-occipital white matter lesions in the T2-weighted images (Figures 1 and 2). There was no involvement of the grey matter. Ciclosporin was discontinued immediately and replaced with rapamycin. Our patient recovered within days, showing no residual symptoms. A follow-up MRT was normal (Figure 3): all lesions had resolved. He has since been asymptomatic, with a serum creatinine of 0.9mg/dl, and on an immunosuppressive regimen consisting of rapamycin, mycofenolate mofetil and low dose prednisone.