Posterior Reversible Encephalopathy Syndrome After Renal Transplant: A Simple Solution for a Complicated Patient

BACKGROUND Posterior reversible leukoencephalopathy syndrome (PRES) is characterized by an acute neurologic dysfunction coupled with characteristic findings on brain imaging. PRES occurs in the setting of hypertensive emergencies, eclampsia and as a neurotoxic effect of immunosuppressive agents. While overwhelmingly reversible without residual deficits when promptly recognized, vague symptomatology may delay the diagnosis of PRES. RESULTS/SUMMARY A 50-year-old man who had undergone a recent kidney transplant was admitted to our clinic due to multiple episodes of seizure. He had no prior history of seizures or alcoholism. His transplantation had been without complication; he was discharged and given prednisone, tacrolimus, mycophenolate, acyclovir, trimethoprim-sulfamethoxazole, atenolol and enalapril. On the day of presentation, he experienced a severe headache, blurred vision and tonic-clonic seizure-like activity. His neurologic examination was limited by sedation, although no focal deficits were evident. Laboratory studies were unremarkable. A lumbar puncture revealed normal opening pressure, negative Gram stain, benign CSF analysis and India ink preparation. An MRI of the brain revealed bilateral enhancing parietal-occipital lesions, seen prominently on FLAIR sequence. Tacrolimus and all other medications were continued. The patient remained afebrile and normotensive and was extubated on the second hospital day. The patient reported no neurologic symptoms and was discharged on the third hospital day after a full recovery. CONCLUSIONS While the outcome of PRES is typically benign, a delay in diagnosis may lead to permanent neurologic deficits, and misdiagnosis can be lethal. The cornerstone of treatment is removal of the offending agent or treatment of the underlying etiology. A clinical picture of headache, visual abnormalities, altered mentation and seizures is sufficient to prompt an empiric discontinuation of agents known to cause PRES. Calcineurin inhibitors such as tacrolimus are known to cause PRES, and in our patient, discontinuation led to a complete clinical resolution.