Dear Editor, 

Guillain-Barré syndrome (GBS) is the most frequent cause of acute polyneuropathy in adults. It manifests with progressive symmetrical motor weakness in the limbs and areflexia. Its most severe complication is acute respiratory failure, which has a mortality rate of 15 to 30% if it requires mechanical ventilation. It may be associated with respiratory or gastrointestinal infection (cytomegalovirus [CMV], Campylobacter yeyuni) in two thirds of all cases.1,2 It has been described in bone marrow transplants, but it is very rare in solid organ transplants.3 It has also been associated with neurotoxicity caused by calcineurin inhibitors.4We present two cases of GBS in patients undergoing kidney transplants. The first case is that of a woman who underwent a kidney transplant at age 22 with chronic renal failure (CRF) secondary to neurogenic bladder. She received steroids, tacrolimus and mycophenolate mofetil in addition to a prophylactic treatment against CMV, hyperimmune gamma-globulin (recipient IgG negative/donor IgG positive). Evolution of renal function was excellent. Five weeks after the transplant, the patient became ill with CMV (severe leucopoenia, hypertransaminasaemia, gastritis, AgP65 positive). She received intravenous gancyclovir during 15 days and made satisfactory progress. She was readmitted three weeks later due to progressive, symmetrical weakness of the lower limbs, paraesthesia and dysphagia, and in the next few hours she developed acute respiratory failure requiring mechanical ventilation. The second case is that of a 62 year old man with unexplained chronic renal failure who underwent renal transplantation. He was treated with steroids, tacrolimus and mycophenolate mofetil. His renal function progressed very well. However, 2.5 months after the transplant he was admitted for severe paralysis of the lower limbs which quickly progressed to tetraparesis. His AgP65 was checked and found positive, and he was treated with IV gancyclovir during 18 days. He did not require mechanical ventilation, but did need prolonged physical therapy. In both patients, the cerebrospinal fluid (CSF) and the electromyography offered a diagnosis of GBS (demyelinising sensory-motor polyneuropathy; CSF at normal pressure, proteins elevated, without pleocytosis). The first patient received four cycles of plasmapheresis and five doses of hyperimmune gammaglobulin (0.4g/kg/day) and the second, five doses of hyperimmune gamma-globulin (0.4g/kg/day). The first transplant patient underwent a full recovery and was extubated after seven days. After eight years of follow-up, she remains asymptomatic and has no neurological consequences. Six months after the event, the second patient has experienced neurological improvements, but he continues to have lower limb paresis and is still in physical therapy. Tacrolimus levels were normal at all times in both cases. Tacrolimus was replaced with everolimus in the second patient, but there were no changes in his slow neurological progress. GBS in solid organ transplants is a very rare condition, despite the fact that CMV infections are common, and it may put the patient’s life at risk. Very few cases have been described in the literature, and most are in men.5 In our patients, the CMV infection was the probable main trigger for the condition, considering its proximity in time. Early diagnosis is important so as to begin common neurological treatment for all forms of GBS, and treat the cause where applicable, as soon as possible.