Varicella Zoster Virus Vasculopathy After Kidney Transplantation

Vasculopathy caused by varicella zoster virus (VZV) reactivation is a rare but clinically relevant complication in kidney transplant recipients,1,2 as demonstrated by the following cases. CASE 1 A 64-year-old woman developed left lower limb paresis with sciatica 3 weeks after kidney transplantation, complicated by confusion, fever, and generalized zoster rash 2 weeks later. Her immunosuppression consisted of tacrolimus, mycophenolate mofetil (MMF), and prednisone without any antiviral prophylaxis (pretransplant serostatus positive for cytomegalovirus IgG, herpes simplex virus 1 IgG, Epstein-Barr virus nuclear antigen IgG, and VZV IgG). She had received an induction with basilixumab, and she never experienced acute rejection. On admission, cerebrospinal fluid (CSF) analysis showed mild pleocytosis with positive VZV using polymerase chain reaction. Brain magnetic resonance imaging (MRI) was normal. The MRI of the lumbar spine showed changes consistent with arachnoiditis. The MMF was discontinued and intravenous acyclovir (10 mg/kg 3 times daily) was started. Twelve days later, confusion worsened. Brain CT demonstrated subarachnoid hemorrhage within bilateral Sylvian fissures (Figure 1A), owing to presumed vessel damage by VZV. However, digital subtraction angiography revealed no vascular lesions. Brain MRI performed 17 days later revealed no infarct, hydrocephalus, or evidence of encephalitis. Acyclovir was discontinued after 21 days. The neurological status improved over the next 2 months but monoparesis remained.FIGURE 1: Axial unenhanced CTs revealing (A) bilateral Sylvian fissure subarachnoid hemorrhage (arrows) in case 1 and (B) right frontal and basal ganglia infarcts (arrows) in case 2.CASE 2 A 32-year-old man returned to dialysis after transplant failure, and some days later, he presented with right-sided zoster ophthalmicus with keratouveitis. Shingles responded to tacrolimus and MMF dose reduction and intravenous acyclovir (10 mg/kg every 8 hours adjusted to creatinine clearance) for 7 days followed by valacyclovir for 10 days. Five weeks later, he developed right third and sixth cranial nerve palsy. Brain MRI revealed inflammation of the right orbital apex and a right lenticulostriate infarct. Intravenous acyclovir was resumed. The MMF was withdrawn and tacrolimus through level was decreased to 3 ng/mL. One week later, the patient developed an acute left-sided sensorimotor stroke. Brain imaging indicated additional acute infarcts (Figure 1B). Digital subtraction angiography revealed multifocal arterial stenosis consistent with arteritis. The CSF analysis identified pleocytosis, increased protein levels, but negative VZV PCR (intrathecal anti-VZV antibodies were not checked). Within the next 2 weeks, the vasculopathy continued to progress with occurrence of new asymptomatic brain infarcts and disseminated to arteries of different sizes bilaterally. The condition finally stabilized with the discontinuation of immunosuppression and the allograft nephrectomy, aimed at restoring VZV immunity without precipitating graft rejection. Acyclovir was discontinued after 1 month. Eight years later, the patient remains with a right-eye keratitis and left-sided deficit. These 2 cases emphasize the protean CNS manifestations of VZV vasculopathy.3,4 Intracranial arteries of any size can be affected by this condition, with progressive multifocal stenoses, ectasia, and pseudoaneurysm, causing combinations of craniofacial pain, intracerebral or subarachnoid hemorrhage, and brain or cranial nerve ischemia. The spinal cord and nerve roots can also be affected. Neurological manifestations and CNS imaging findings are therefore variable and relatively nonspecific.3,4 Angiographic studies may even be normal, especially in cases only involving small vessels.3 Rapid viral diagnosis is important: mortality is high without treatment, and sequelae are frequent, especially in immunocompromised individuals.1,3,4 A temporal association of shingles with neurological symptoms suggests VZV-induced vasculopathy, which may be overlooked due to prolonged prodrome or absence of rash.1-4 Documentation of anti-VZV antibodies or VZV DNA in the CSF confirms the diagnosis. Both tests are recommended: VZV PCR may be positive during a short period.3,4 The VZV vasculitis is unlikely if both results are negative. Early virologic confirmation and prompt initiation of intravenous acyclovir (10–15 mg/kg every 8 hours for a minimum of 14 days) combined with tapering of immunosuppression are essential.2,3 Monitoring of VZV DNA in the CSF and of intrathecal antibody production was suggested to guide the duration of antiviral treatment.5 Regarding prophylaxis, there are no definitive recommendations in kidney transplantation.2

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