Guillan-Barre Syndrome is characterized by rapid-onset weakness, hyporeflexia or areflexia, and elevation of protein levels in CSF without pleocytosis. A 45 years-old male with end -stage renal disease due to gout nephropathy underwent renal transplantation. Maintenance therapy included Cyclosporine 225mg/d, Prednisolone and ceLlcept. The patient was discharged with a serum creatinine level 1.5mg/dl. Three months later, he was admitted with lower extremity weakness started one week before admission followed by fever and malaise. Two days after hospitalization, weakness progressed to upper extremities. On physical examination, his vital signs were normal, Lung, Heart, abdomen were unremarkable. Mental status and cranial nerves were intact. Tendon reflexes, autonomic function and sensory nerves were normal. Decreased force of lower and upper extremities and gait disorder were noted. Laboratory findings were: Normal CBC, Cr= 2.5, Ca=8.4, P=3.5, Na=135, K=3.3 .CMV Ag (PP 65) was negative, CMV IgM=1.8, IgG=4.8. Nerve conduction velocity showed: Acute axonal polyneuropathy compatible with a kind of Guillan-Barre Syndrome. CSF analysis was not done. Plasmapheresis and IV Ig (4mg/kg/qid for 5 days) was started, as treatment and cyclosporine dose was reduced to 200 mg/d. After four sessions of plasmapheresis, symptoms improved but didn’t completely resolve. Based on previous literature, only 11cases of post renal transplant GBS have been reported. In 9 patients GBS was attributed to CMV infection and in one to cyclosporin A neurotoxicity and one to C jjejuni. This case suggests that the onset of the GBS after renal transplantation could be related to cytomegalovirus infection or cyclosporin neurotoxicity. Early diagnosis and treatment of CMV infection, cyclosporin dose reduction and considering plasmapheresis in especial cases are strongly suggested.