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Resumen: La encefalopatía por contraste es una complicación neurológica relacionada con el contraste utilizado en procedimientos endovasculares o tomografía computarizada (TC). Los principales factores de riesgo son la hipertensión arterial, la diabetes mellitus, la enfermedad renal crónica (ERC), contrastes hiperosmolares, cantidad de contraste infundida y su infusión directa en el territorio cerebral posterior, o patologías que cursen con daño de barrera hematoencefálica. La sintomatología es inespecífica y puede presentarse como alteración del nivel de conciencia, focalidad neurológica o crisis comiciales. El diagnóstico es de exclusión tras haber descartado los accidentes cerebrovasculares (ACV) isquémicos o hemorrágicos; el TC o la resonancia magnética (RM) son de utilidad para su diferenciación. Generalmente aparece poco tiempo tras la exposición y la sintomatología dura 48-72 h con recuperación completa, aunque se han descrito casos con persistencia de los síntomas o mayor duración. El tratamiento es la monitorización con medidas de soporte y la terapia de sustitución renal con hemodiálisis (HD) en aquellos pacientes en programa crónico. Es importante que el nefrólogo conozca esta entidad, dada la susceptibilidad del paciente en HD, así como su potencial papel terapéutico en estos pacientes. Abstract: Contrast-induced encephalopathy is a neurological complication related to contrast used in endovascular procedures or computed tomography (CT). The main risk factors are arterial hypertension, diabetes mellitus, chronic kidney disease (CKD), hyperosmolar contrasts, the amount of infused contrast and its direct infusion in the posterior cerebral territory, or pathologies with blood–brain barrier damage. Symptomatology is non-specific and may present as altered level of consciousness, neurological focality or seizures. Diagnosis is done by exclusion after ischemic or hemorrhagic stroke has been ruled out; CT or MRI are useful for differentiation. Generally, it appears shortly after exposure and the symptoms lasts 48–72 h with complete recovery, although cases with persistence of symptoms or longer duration have been described. Treatment consists of monitoring, supportive measures and renal replacement therapy (RRT) with hemodialysis (HD) in patients in chronic RRT program. It is important for the nephrologist to be aware of this entity given the susceptibility of the patient on HD as well as its potential therapeutic role in these patients.

Contrast-induced encephalopathy is a neurological complication related to contrast used in endovascular procedures or computed tomography (CT). The main risk factors are arterial hypertension, diabetes mellitus, chronic kidney disease (CKD), hyperosmolar contrasts, the amount of infused contrast and its direct infusion in the posterior cerebral territory, or pathologies with blood-brain barrier damage. Symptomatology is non-specific and may present as altered level of consciousness, neurological focality or seizures. Diagnosis is done by exclusion after ischemic or hemorrhagic stroke has been ruled out; CT or MRI are useful for differentiation. Generally, it appears shortly after exposure and the symptoms lasts 48−72h with complete recovery, although cases with persistence of symptoms or longer duration have been described. Treatment consists of monitoring, supportive measures and kidney replacement therapy (KRT) with hemodialysis (HD) in patients in chronic KRT program. It is important for the nephrologist to be aware of this entity given the susceptibility of the patient on HD as well as its potential therapeutic role in these patients. Resumen: La encefalopatía por contraste es una complicación neurológica relacionada con el contraste utilizado en procedimientos endovasculares o tomografía computarizada (TC). Los principales factores de riesgo son la hipertensión arterial, la diabetes mellitus, la enfermedad renal crónica (ERC), contrastes hiperosmolares, cantidad de contraste infundida y su infusión directa en el territorio cerebral posterior, o patologías que cursen con daño de barrera hematoencefálica. La sintomatología es inespecífica y puede presentarse como alteración del nivel de conciencia, focalidad neurológica o crisis comiciales. El diagnóstico es de exclusión tras haber descartado los accidentes cerebro-vasculares isquémicos o hemorrágicos, el TC o la resonancia magnética son de utilidad para su diferenciación. Generalmente, aparece poco tiempo tras la exposición y la sintomatología dura 48−72h con recuperación completa, aunque se han descrito casos con persistencia de los síntomas o mayor duración. El tratamiento es la monitorización con medidas de soporte y la terapia de sustitución renal con hemodiálisis (HD) en aquellos pacientes en programa crónico. Es importante que el nefrólogo conozca esta entidad dada la susceptibilidad del paciente en HD así como su potencial papel terapéutico en estos pacientes.

Background. In kidney transplant recipients, there is discordance between the development of cellular and humoral response after vaccination against SARS-CoV-2. We sought to determine the interplay between the 2 arms of adaptive immunity in a 3-dose course of mRNA-1273 100 μg vaccine. Methods. Humoral (IgG/IgM) and cellular (N- and S-ELISpot) responses were studied in 117 kidney and 12 kidney-pancreas transplant recipients at the following time points: before the first dose, 14 d after the second dose‚ and before and after the third dose, with a median of 203 and 232 d after the start of the vaccination cycle, respectively. Results. After the second dose, 26.7% of naive cases experienced seroconversion. Before the third dose and in the absence of COVID-19, this percentage increased to 61.9%. After the third dose, seroconversion occurred in 80.0% of patients. Naive patients who had at any time point a detectable positivity for S-ELISpot were 75.2% of the population, whereas patients who maintained S-ELISpot positivity throughout the study were 34.3%. S-ELISpot positivity at 42 d was associated with final seroconversion (odds ratio‚ 3.14; 95% confidence interval‚ 1.10-8.96; P = 0.032). Final IgG titer was significantly higher in patients with constant S-ELISpot positivity (P