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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">To the Editor&#44;</span></p><p class="elsevierStylePara">Reversible posterior leukoencephalopathy syndrome &#40;RPLS&#41; involves altered vision and state of consciousness and convulsions&#44; and is associated with several factors including uraemia&#44; arterial hypertension &#40;AHT&#41;&#44; immunosuppressant treatment&#44; and Goodpasture syndrome&#44; among others&#46; Here we present a case in which all of these conditions occurred simultaneously&#46;</p><p class="elsevierStylePara">Our patient was a 22-year-old female who had developed severe renal failure for 4 months&#46; Anti-MBG antibodies were positive&#44; and we performed a renal biopsy that led to the diagnosis of extracapillary glomerulonephritis type I secondary to Goodpasture syndrome&#46; She was treated with three 1g boluses of methylprednisolone&#44; followed by prednisone at 60mg&#47;day along with 9 sessions of plasmapheresis and oral cyclophosphamide &#40;CP&#41; at 1mg&#47;kg&#47;day&#46; The patient did not develop pulmonary haemorrhage&#46; She did not recover renal function and we decided to start haemodialysis therapy using a tunnelled central venous catheter&#46; The patient&#8217;s overall health was good&#44; although blood pressure remained high despite treatment with amlodipine&#44; captopril&#44; and atenolol&#46;</p><p class="elsevierStylePara">In the inter-dialytic period&#44; the patient had general discomfort&#44; temporary disorientation&#44; and a fluctuating level of consciousness&#46; She was referred to the emergency department&#44; where she experienced two tonic-clonic seizures that were relieved with benzodiazepines&#44; recovering consciousness between seizures&#46; A physical examination revealed no fever&#44; blood pressure &#40;BP&#41; of 151&#47;108&#44; spontaneous eye opening&#44; and normal verbal responses&#46; Pupils were isochoric and responded normally&#46; Cranial nerve responses were normal&#44; with preserved strength and sensitivity in all four limbs&#46; Meningeal signs were negative&#44; and no other findings of interest were observed&#46; We performed a thoracic x-ray and cranial computed tomography with no relevant findings&#46; With a third seizure and progressive worsening of general health&#44; the patient was admitted to the intensive care unit&#46; She needed sedation&#44; endotracheal intubation&#44; and induced mechanical ventilation &#40;IMV&#41;&#46; Laboratory analysis showed leukocytosis with a left shift&#44; severe lactic acidosis&#44; and negative anti-membrane antibodies&#44; anti-nuclear antibodies&#44; anti-neutrophil cytoplasmic antibodies&#44; immunocomplexes&#44; anti-DNA&#44; anti-SS-A&#44; anti-SS-B&#44; anti-RNP&#44; and anti-Scl-70&#44; with normal complement and immunoglobulin levels&#46; Blood and urine cultures were negative&#44; and ion levels were stable&#46; Fibrobronchoscopy and lumbar puncture showed no findings&#46; Cerebrospinal fluid cultures for bacteria&#44; fungus&#44; and viruses were negative&#46; An electroencephalogram revealed a slow basal rhythm in the delta range with theta wave activity predominantly in both temporal regions&#46; Two epileptiform discharges were observed in the right parietal region&#46; A cranial nuclear magnetic resonance revealed signal hyperintensity in T2-weighted images and FLAIR sequences&#44; suggesting vasogenic oedema&#44; in the cortico-subcortical region of the posterior portion of both parietal&#44; and occipital and right frontal lobes&#46; The diffusion-weighted images showed no significant restriction &#40;Figure&#41;&#46; Given these findings&#44; the patient was diagnosed with RPLS&#46; Treatment was started with phenytoin&#44; empirical antibiotic therapy&#44; and continuous venovenous haemodiafiltration&#46; The patient continued to experience severe AHT that required treatment with 6 different drugs &#40;captopril&#44; amlodipine&#44; doxazosin&#44; atenolol&#44; nitroglycerin&#44; and urapidil&#41;&#46; In the following days&#44; the patient improved considerably&#44; with no new seizures and controlled blood pressure&#44; which led to IMV withdrawal and discharge after 18 days of hospitalisation&#44; with maintenance therapy based on atenolol and captopril&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">DISCUSSION </span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">RPLS<span class="elsevierStyleSup">1-3</span> involves vasogenic cerebral oedema that is generally associated with AHT&#44; causing cerebral blood overflow and endothelial abnormalities and alters cerebral circulatory self-regulation&#46; This disease mainly affects white matter due to its tissue density and the posterior lobules due to their scarce sympathetic innervation&#44; making these regions more vulnerable to AHT&#46; Several different causes have been proposed for this phenomenon &#40;Table&#41;&#46; It involves headache&#44; altered state of consciousness&#44; visual abnormalities &#40;blurred vision&#44; scotoma&#44; cortical blindness&#41; and tonic-clonic seizures&#46; It is treated by controlling AHT&#44; preferably using nicardipine or labetalol &#40;precaution is recommended when using nitroprusside due to the possibility of triggering paradoxical cerebral vasodilation that would worsen the cerebral oedema&#41;&#44; and seizures are prevented with phenytoin or benzodiazepines&#46; The disease progresses in a relatively benign manner until recovery&#44; although renal failure &#40;uraemia and immunosuppression increase the neurotoxicity of hypertensive encephalopathy&#41; and NMR results suggesting hyperintensity or extensive cerebral damage that affect the brain stem are poor prognostic markers&#46;</p><p class="elsevierStylePara">In the medical literature&#44; only two cases have been described of RPLS coexisting with Goodpasture syndrome&#46; The first<span class="elsevierStyleSup">4</span> involved a 27-year-old male on treatment with CP and prednisone&#44; with renal and pulmonary symptoms that arose during a hypertensive crisis that was resolved after 48 hours by controlling blood pressure and substituting CP for rituximab&#46; The second<span class="elsevierStyleSup">5</span> was a 22-year-old female also with renal and pulmonary symptoms who was on haemodialysis and plasmapheresis treatment&#44; not with CP&#46; She needed IMV&#46; In all three cases&#44; symptoms were severe&#44; with visual abnormalities&#44; headache&#44; and seizures&#44; but were resolved in a maximum of 3 weeks with no sequelae or recurrences after controlling BP and&#44; in the first case&#44; after modifying the immunosuppressant treatment&#46; In our case&#44; the patient sought treatment 4 months after developing the disease&#44; when her anti-MBG antibodies were negative and she was not taking any immunosuppressant therapy&#46;</p><p class="elsevierStylePara">In this context&#44; it is especially important to control AHT in order to prevent a severe set of symptoms that&#44; although they generally progress benignly&#44; may cause potentially severe encephalopathy&#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 affirm that they have no conflicts of interest related to the content of this article&#46;</p><p class="elsevierStylePara"><a href="grande&#47;11427&#95;16025&#95;33355&#95;en&#95;f1&#95;611427&#46;jpg" class="elsevierStyleCrossRefs"><img src="11427_16025_33355_en_f1_611427.jpg" alt="Cranial nuclear magnetic resonance"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Cranial nuclear magnetic resonance</p><p class="elsevierStylePara"><a href="grande&#47;11427&#95;16025&#95;33356&#95;en&#95;t1&#95;6114272&#46;jpg" class="elsevierStyleCrossRefs"><img src="11427_16025_33356_en_t1_6114272.jpg" alt="Causes of reversible posterior leukoencephalopathy syndrome"></img></a></p><p class="elsevierStylePara">Table 1&#46; Causes of reversible posterior leukoencephalopathy syndrome</p>"
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