Guillan-Barre Syndrome (GBS), also known as acute inflammatory demyelinating polyradiculoneuropathy, is characterized by rapid-onset weakness, hyporeflexia or areflexia , and elevated levels of protein in the CSF without pleocytosis. Case report: A 27 years-old Asian-male with end -stage renal disease as a result of reflux nephropathy underwent living-unrelated donor renal transplantation. Maintenance therapy included Cyclosporin, prednisolone and Mycophenolate mofetile. The patient was discharged with a serum creatinine levels 1.5mg/dl .Four months late, the patient was admitted again with fever, malaise, and weakness, all of which had started three days after upper respiratory tract infection. Two days after hospitalization, he developed bilateral lower extremities weakness, then it rapidly progressed to upper extremities. The patient had normal mental status, and cranial nerves were intact .Absence of tendon reflexes was noted. No disturbances of autonomic function was noted. Decreased force of lower extremities and gait disorder was determined. Laboratory findings were as following: WBC=7000, Hb=8.3, BUN=28, Cr 1.8, Ca=8.4, P=3.5, Na=141, K=4.2, LDH=245, CPK=8.1, urinalysis: PH=6, Pro=1+, sugar= -, blood=3+, RBC=many, WBC=14-16, CMV Ag (PP 65) was positive (20/50000). Nerve conduction velocity result showed: Acute demyelinating polyneuropathy compatible with GBS. CSF analysis was not done. Intravenous gancyclovir was started and during therapy muscle weakness was improved, but didn’t respond completely .According to neurologic consultation plasmapheresis was started due to gait difficulty, although the patient did not have swollowing difficulty or respiratory problems. After four sessions of plasmapheresis his symptoms dramatically improved, and he was discharged from hospital. The Guillain-Barre syndrome associated with CMV infection is a recognized entity of unknown pathogenesis. In two-third of such cases, the syndrome follows an episode of upper respiratory tract infection. Based on literature review, only11cases of GBS have been reported. In 9 patients GBS was attributed to CMV infection and in the tenth patient to cyclosporin A neurotoxicity and in eleventh patients attributed to C jejuni. GBS is believed to be caused by autoimmune mechanisms that are predominantly T-cell mediated. This case suggests that the onset of the GBS after renal transplantation could be related to cytomegalovirus infection. Therefore early diagnosis and treatment of CMV infection and also considering plasmapheresis in especial cases are strongly suggested.