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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">To the Editor&#58;</span></p><p class="elsevierStylePara">Posterior reversible encephalopathy syndrome &#40;PRES&#41; can occur in recipients of solid organ transplants associated with calcineurin inhibitors&#46; The incidence of this syndrome in kidney transplant recipients is low&#44; approximately 0&#46;34&#37;&#44;<span class="elsevierStyleSup">1&#44;2</span> and should be suspected when neurological symptoms arise in association with characteristic lesions found in cerebral magnetic resonance &#40;CMR&#41; images&#44; which revert after reducing or suspending the dose of tacrolimus&#46; In order to resolve this condition and avoid neurological sequelae&#44; an early diagnosis and suspension of the causal calcineurin inhibitor is needed&#46;<span class="elsevierStyleSup">3</span></p><p class="elsevierStylePara">Here we present the case of a kidney transplant recipient who developed atypical PRES associated with tacrolimus&#46;</p><p class="elsevierStylePara">Ours was a 32-year old male patient with a personal history of arterial hypertension and stage 5 chronic kidney disease&#44; who had received a kidney transplant 2 years earlier with the prescription of sirolimus&#44; but who was switched to tacrolimus due to gastrointestinal intolerance to the first drug&#44; and had been taking tacrolimus for the past 5 months&#46;</p><p class="elsevierStylePara">The patient sought treatment at our hospital of IV level of complexity due to a first-onset generalised tonic-clonic seizure of 60 seconds in duration&#46; A physical examination showed that the patient was without fever&#44; had a blood pressure of 187&#47;133mm Hg&#44; and was sleepy in a postictal state&#44; with no other relevant findings&#46; A laboratory analysis revealed mild leukocytosis&#44; hyperlactaemic metabolic acidosis&#44; creatinine&#58; 5&#46;43mg&#47;dl &#40;baseline&#58; 3&#46;0mg&#47;dl&#41;&#44; and normal electrolyte levels&#46; We performed a simple cerebral computed axial tomography &#40;CAT&#41;&#44; which revealed several hyperdense lesions&#44; the largest of which was in the right frontal lobe&#59; we then administered a CMR &#40;Figure 1&#41;&#44; which revealed several lesions&#58;&#160; frontal lobe with mass effect and cortical&#47;subcortical without restrictions in the ADC sequence&#46; We performed several analyses to determine the extent of the lesions&#44; including&#58; cerebrospinal fluid analysis&#44; haemocultures and urine cultures &#40;negative&#41;&#44; and a stereotactic biopsy of the right frontal lobe lesion that revealed reactive gliosis and small foci of interstitial bleeding&#46; Given these findings&#44; we were able to rule out other possible diagnoses and settled on the probable diagnosis of neurotoxicity from tacrolimus&#46; We decided to suspend the medication and observe the patient&#8217;s evolution&#44; which was very favourable from a neurological standpoint&#46; The patient was discharged under a renal replacement therapy regimen&#44; since basal GFR were not recovered&#44; and no immunosuppressant medications were prescribed&#46; Three months later&#44; a follow-up simple cerebral tomography &#40;Figure 2&#41; showed that the supratentorial lesions had healed&#44; with only a small encephalomalacic area in the right frontal lobe at the site of the haematoma&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">DISCUSSION</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Calcineurin inhibitors have been described as potent immunosuppressants that are considered to be quite effective in the prevention of acute transplant rejection&#46; However&#44; these drugs are associated with several adverse side effects&#59; in the specific case of tacrolimus &#40;also known as FK-506 or Fujimycin&#41;&#44; reports have described increased incidence rates of diabetes and nephrotoxicity&#44; among others&#44; but nephrotoxicity in particular&#44; with even greater incidence rates than those produced by cyclosporine&#46;<span class="elsevierStyleSup">4 </span>The symptoms include headache&#44; trembling&#44; paraesthesia&#44; visual impairments&#44; convulsions&#44; and coma&#46;<span class="elsevierStyleSup">5</span> One form of presentation of this neurotoxicity is PRES&#44; a clinical&#47;radiological entity that is uncommon and was first described only recently &#40;1996&#41;&#46;<span class="elsevierStyleSup">6</span> A CMR has been considered as the gold standard<span class="elsevierStyleSup">7</span> for diagnosing this condition&#59; we typically see an increase in signal intensity for T2-weighted images in both posterior regions&#44; with compromised cortical tissue due to the lack of regulation of posterior circulation&#46;<span class="elsevierStyleSup">6</span> However&#44; these signals were then described in the frontal region due to vasogenic oedema of the subcortical white matter&#46;<span class="elsevierStyleSup">6&#44;8</span> The FLAIR sequence &#40;fluid-attenuated inversion recover&#41; increases the capacity for detecting minute lesions&#46; Diffusion weighted imaging sequences &#40;DWI&#41; and the apparent diffusion coefficient &#40;ADC&#41; are useful for differentiating vasogenic oedema with mild restriction from oedema with no restriction&#44; which indicates reversibility&#46;</p><p class="elsevierStylePara">Follow-up imaging controls are indispensable for supporting the diagnosis&#46;<span class="elsevierStyleSup">1&#44;6</span> There is no specific timeline established for these controls&#59; some authors recommend 4 weeks after resolution of clinical signs&#46; These controls can take place in the form of CMR or cerebral CAT scans&#46;<span class="elsevierStyleSup">6</span></p><p class="elsevierStylePara">In our patient&#44; we observed characteristics that can be considered atypical for this syndrome&#44; such as increased involvement of the right frontal lobe&#44; with cortical lesions and intra-lesion bleeding that surpassed the PRES lesions&#44; making these typically reversible lesions progress towards irreversible damage and encephalomalacia&#44; as observed in the follow-up cerebral imaging tests from this patient &#40;Figure 2&#41;&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The authors state that they have no potential conflicts of interest related to the content of this article&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><a href="grande&#47;11653&#95;108&#95;39913&#95;en&#95;f117&#46;jpg" class="elsevierStyleCrossRefs"><img src="11653_108_39913_en_f117.jpg" alt="Cerebral magnetic resonance&#44; FLAIR sequence"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Cerebral magnetic resonance&#44; FLAIR sequence</p><p class="elsevierStylePara"><a href="grande&#47;11653&#95;108&#95;39915&#95;en&#95;f217&#46;jpg" class="elsevierStyleCrossRefs"><img src="11653_108_39915_en_f217.jpg" alt="Simple cerebral computed axial tomography&#44; control"></img></a></p><p class="elsevierStylePara">Figure 2&#46; Simple cerebral computed axial tomography&#44; control</p>"
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