Introduction: Facial nerve palsy is a frequent clinical presentation in everyday practice. The first step in the clinical assessment is to differentiate between peripheral and central forms.
Peripheral facial palsy may be secondary to a variety of diseases, for instance, viral infections such as Herpes simplex infection, or may be idiopathic (Bell’s palsy) with the latter more common.
The use of various combinations of immunosuppressive drugs in kidney transplant recipients is responsible for latent viral infection and thus makes this population more prone to complications.
Methods: Herein, we describe two cases of kidney transplant recipients who were admitted to our department with peripheral facial nerve palsy and were treated according to our protocol.
Case series: Our first patient is a 29-year-old kidney transplant recipient from a deceased donor with a past medical history of end-stage kidney disease due to focal and segmental glomerulosclerosis who was admitted in our department for asymmetry of the face with no furrows on the left side of his forehead, a drooping eyelid with an inability to close the left eye and a droop of the left labial commissure. The rest of the clinical exam was normal. There was no history of vesicular eruptions development. Serological tests for viral infection came back negative. He was diagnosed with Bell’s palsy grade V and he was started on corticosteroids with a starting dose of 50 mg and a rapid taper over a total duration of 10 days in combination with oral antiviral therapy and physical therapy. The patient responded gradually to treatment and his paralysis was grade II at discharge.
Our second patient is a 42-year-old kidney transplant recipient from a deceased donor with a past medical history of acute pancreatitis of undetermined origin who was for a heavy feeling of the face affecting mostly the right lip commissure, an absence of the right nasolabial fold, a total inability to close the right eye with an incapacity to wrinkle the right part of his forehead with no furrows concordant with the diagnosis of peripheral facial nerve palsy grade V. He was started early on a 1-week course of  IV aciclovir association with 1 mg/kg of oral corticosteroid and slowly tapered over 15 days, physical therapy and artificial protection of the cornea pending the results of serological tests (of herpes virus) which came back negative. The evolution was marked with a spectacular improvement within 10 days of treatment and he was capable of complete occlusion of his right eye, no deviation of his right lip commissure and the capacity to wrinkle his forehead and grimace.  
Conclusion: Bell’s palsy is always a diagnosis of exclusion. A good clinical assessment and a thorough workup must be done in order to eliminate the differential diagnoses. Immunocompromised patients are vulnerable to such conditions and are at risk to develop severe forms. Thus, the treatment should be started early to prevent sequelae.