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OBJECTIVES: To evaluate the complications and 30-day mortality rates following open radical nephrectomy and laparoscopic radical nephrectomy using the Clavien-Dindo classification system in a low-volume hospital. METHODS: We conducted a retrospective analysis of 263 patients who underwent open or laparoscopic radical nephrectomy (1996-2016) in our local district general hospital. Postoperative complications and 30- day mortalities were evaluated using the Clavien-Dindo classification. The predictors of postoperative complications were assessed using multivariate logistic regression analysis. RESULTS: We found that, compared to open radical nephrectomy, laparoscopic resulted in a significantly longer operative time (112.6±41 vs 199.3±61 minutes, p <  0.01) and a shorter hospital stay (8.5±2.4 vs 5.7±3 days, p < 0.001). The most common complications were bleeding or hematoma (4.9%) and problems associated with the wound (4.5%). There were no significant differences between the ORN and LRN groups in terms of complications based on the Clavien-Dindo classification. On multivariate analysis, a longer operative time (Odds Ratio, 1.009; 95% confidence interval, 1.002- 1.015; p = 0.010) and higher body mass index (Odds Ratio, 0.898; 95% confidence interval, 0.822-0.981; p = 0.017) were found to be significant predictors of complications after nephrectomy. CONCLUSIONS: Our study demonstrated that complication and 30-day mortality rates were low. There was a greater number of low-grade complications, and there were no significant differences in these rates between open and laparoscopic radical nephrectomy. A longer operative time and a higher BMI were predictors of possible complications. We provide additional evidence to support the feasibility of performing open or laparoscopic radical nephrectomy in low-volume hospitals.

OBJETIVOS: Evaluar la tasa de complicaciónes y mortalidad a 30 días después de nefrectomía radical abierta o laparoscópica utilizando el sistema de clasificación Clavien-Dindo en un hospital de bajo volumen quirúrgico.MÉTODOS: Realizamos un análisis retrospectivo de 263 pacientes a los que se les practicó nefrectomía radical laparoscópica o abierta (1996-2016). Las complicaciones postoperatorias y la mortalidad a 30 días fueron evaluadas utilizando la clasificación de Clavien-Dindo. Analizamos los factores predictores de complicaciones postoperatorias mediante análisis multivariado con regresión logística. RESULTADOS: Comparado a la nefrectomía abierta, la nefrectomía radical laparoscópica resultó en un mayor tiempo quirúrgico (112,6±41 vs 199,3±61 minutos, p < 0,01) y una menor estancia hospitalaria (8,5±2,4 vs 5,7±3 días, p <  0,001). Las complicaciones más frecuentes fueron sangrado o hematoma (4,9%) y problemas asociados a la herida (4,5%). No hubo diferencias significativas entre cirugía abierta o laparoscópica evaluando las complicaciones mediante la clasificación de Clavien-Dindo. En el análisis multivariado, un tiempo quirúrgico prolongado (Odds Ratio, 1.009; 95% intervalo de confianza, 1.002-1.015; p = 0,010) y un mayor índice de masa corporal (Odds Ratio, 0,898; 95% intervalo de confianza, 0,822-0,981; p = 0,017) fueron predictores significativos de complicaciones. CONCLUSIONES: Nuestro estudio muestra que la tasa de complicaciones y mortalidad a 30 días fueron bajas, con un mayor número de complicaciones de bajo grado y sin diferencias significativas entre cirugía abierta o laparoscópica. Un tiempo quirúrgico prolongado y mayor índice de masa corporal fueron predictores de posibles complicaciones. Aportamos evidencia adicional apoyando la realización de nefrectomía radical laparoscópica o abierta en hospitales de bajo volumen quirúrgico.

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Objetivos: Evaluar la tasa de complicaciónes y mortalidad a 30 días después de nefrectomía radical abierta o laparoscópica utilizando el sistema de clasificación Clavien-Dindo en un hospital de bajo volumen quirúrgico. Métodos: Realizamos un análisis retrospectivo de 263 pacientes a los que se les practicó nefrectomía radical laparoscópica o abierta (1996-2016). Las complicaciones postoperatorias y la mortalidad a 30 días fueron evaluadas utilizando la clasificación de Clavien-Dindo. Analizamos los factores predictores de complicaciones postoperatorias mediante análisis multivariado con regresión logística. Resultados: Comparado a la nefrectomía abierta, la nefrectomía radical laparoscópica resultó en un mayor tiempo quirúrgico (112,6 ± 41 vs 199,3 ± 61 minutos, p < 0,01) y una menor estancia hospitalaria (8,5 ± 2,4 vs 5,7 ± 3 días, p < 0,001). Las complicaciones más frecuentes fueron sangrado o hematoma (4,9%) y problemas asociados a la herida (4,5%). No hubo diferencias significativas entre cirugía abierta o laparoscópica evaluando las complicaciones mediante la clasificación de Clavien-Dindo. En el análisis multivariado, un tiempo quirúrgico prolongado (Odds Ratio, 1.009; 95% intervalo de confianza, 1.002-1.015; p = 0,010) y un mayor índice de masa corporal (Odds Ratio, 0,898; 95% intervalo de confianza, 0,822-0,981; p = 0,017) fueron predictores significativos de complicaciones. Conclusiones: Nuestro estudio muestra que la tasa de complicaciones y mortalidad a 30 días fueron bajas, con un mayor número de complicaciones de bajo grado y sin diferencias significativas entre cirugía abierta o laparoscópica. Un tiempo quirúrgico prolongado y mayor índice de masa corporal fueron predictores de posibles complicaciones. Aportamos evidencia adicional apoyando la realización de nefrectomía radical laparoscópica o abierta en hospitales de bajo volumen quirúrgico

Objectives: To evaluate the complications and 30-day mortality rates following open radical nephrectomy and laparoscopic radical nephrectomy using the Clavien-Dindo classification system in a low-volume hospital. Methods: We conducted a retrospective analysis of 263 patients who underwent open or laparoscopic radical nephrectomy (1996-2016) in our local district general hospital. Postoperative complications and 30-day mortalities were evaluated using the Clavien-Dindo classification. The predictors of postoperative complications were assessed using multivariate logistic regression analysis. Results: We found that, compared to open radical nephrectomy, laparoscopic resulted in a significantly longer operative time (112.6 ± 41 vs 199.3 ± 61 minutes, p < 0.01) and a shorter hospital stay (8.5 ± 2.4 vs 5.7 ± 3 days, p < 0.001). The most common complications were bleeding or hematoma (4.9%) and problems associated with the wound (4.5%). There were no significant differences between the ORN and LRN groups in terms of complications based on the Clavien-Dindo classification. On multivariate analysis, a longer operative time (Odds Ratio, 1.009; 95% confidence interval, 1.002-1.015; p = 0.010) and higher body mass index (Odds Ratio, 0.898; 95% confidence interval, 0.822-0.981; p = 0.017) were found to be significant predictors of complications after nephrectomy. Conclusions: Our study demonstrated that complication and 30-day mortality rates were low. There was a greater number of low-grade complications, and there were no significant differences in these rates between open and laparoscopic radical nephrectomy. A longer operative time and a higher BMI were predictors of possible complications. We provide additional evidence to support the feasibility of performing open or laparoscopic radical nephrectomy in low-Volume hospitals

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La neuroplasticidad otorga al cerebro gran capacidad adaptativa frente a transformaciones del medio que acontecen en el envejecimiento. En los modelos animales aparecen alteraciones en la neurotransmisión y desequilibrios en la expresión del factor de crecimiento neural. A nivel morfométrico, los cambios no son constantes. La pérdida de volumen se relaciona con alteraciones de la neuroplasticidad y afectación del neuropilo cerebral. Aunque no hay datos concluyentes, el ejercicio físico mejora los cambios moleculares, biológicos, funcionales y conductuales-cognitivos asociados al envejecimiento cerebral. En el cerebro humano envejecido se describe pérdida de peso y volumen y aumento del tamaño ventricular. No obstante, la neuroimagen muestra una variabilidad importante y muchos ancianos sanos no presentan cambios macroscópicos significativos. Respecto al número de neuronas, en la mayoría de las regiones cerebrales permanece estable a lo largo de la vida. La neuroplasticidad no se pierde con el envejecimiento, los cambios en la arborización dendrítica, la densidad de espinas y las sinapsis están más relacionados con la actividad cerebral que con la edad. A nivel molecular, a pesar de que la presencia de proteínas alteradas tau y b-amiloide se emplea como biomarcador de enfermedad neurodegenerativa, los estudios posmortem muestran que estas proteínas anómalas son frecuentes en los cerebros de personas ancianas sin demencia. Por último, debido a la relación entre enfermedades neurodegenerativas y alteraciones metabólicas, se analiza la influencia del factor de crecimiento insulínico y el envejecimiento, tanto a nivel de modelos animales como en la especie humana, y el posible efecto neuroprotector de la insulina (AU)

Neuroplasticity lends the brain a strong ability to adapt to changes in the environment that occur during ageing. Animal models have shown alterations in neurotransmission and imbalances in the expression of neural growth factor. Changes at the morphometric level are not constant. Volume loss is related to alterations in neuroplasticity and involvement of the cerebral neuropil. Although there are no conclusive data, physical exercise improves the molecular, biological, functional and behavioural-cognitive changes associated with brain ageing. The aged human brain has been described as showing weight and volume loss and increased ventricular size. However, neuroimaging shows significant variation and many healthy elderly individuals show no significant macroscopic changes. In most brain regions, the number of neurons remains stable throughout life. Neuroplasticity does not disappear with ageing, and changes in dendritic arborization and the density of spines and synapses are more closely related to brain activity than to age. At the molecular level, although the presence of altered Tau and b-amyloid proteins is used as a biomarker of neurodegenerative disease, postmortem studies show that these abnormal proteins are common in the núbrains of elderly people without dementia. Finally, due to the relationship between neurodegenerative diseases and metabolic alterations, this article analyses the influence of insulin-like growth factor and ageing, both in animal models and in humans, and the possible neuroprotective effect of insulin (AU)

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Neuroplasticity lends the brain a strong ability to adapt to changes in the environment that occur during ageing. Animal models have shown alterations in neurotransmission and imbalances in the expression of neural growth factor. Changes at the morphometric level are not constant. Volume loss is related to alterations in neuroplasticity and involvement of the cerebral neuropil. Although there are no conclusive data, physical exercise improves the molecular, biological, functional and behavioural-cognitive changes associated with brain ageing. The aged human brain has been described as showing weight and volume loss and increased ventricular size. However, neuroimaging shows significant variation and many healthy elderly individuals show no significant macroscopic changes. In most brain regions, the number of neurons remains stable throughout life. Neuroplasticity does not disappear with ageing, and changes in dendritic arborization and the density of spines and synapses are more closely related to brain activity than to age. At the molecular level, although the presence of altered Tau and ß-amyloid proteins is used as a biomarker of neurodegenerative disease, postmortem studies show that these abnormal proteins are common in the brains of elderly people without dementia. Finally, due to the relationship between neurodegenerative diseases and metabolic alterations, this article analyses the influence of insulin-like growth factor and ageing, both in animal models and in humans, and the possible neuroprotective effect of insulin.

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Brain ageing leads to a series of changes that reduce the processes of adaptation and response. These transformations can end in cognitive impairment and/or dementia. Although the cause of these changes is diverse, inflammation and oxidative stress explain some of the pathophysiological mechanisms of these anomalies of brain functioning. Neuroinflammation triggers neuronal injury through the presence of inflammatory cytokines and the activation of microglia through membrane receptors and nuclear activation factors. This neuroinflammatory phenomenon also affects neuron plasticity, altering the genesis and maintenance of long-term potentiation, leading to impairment of hippocampus-dependent memory. Oxidative stress and the production of free oxygen radicals also cause toxic effects in aged brains, largely due to lipid peroxidation and DNA damage. The identification of the molecular mechanisms involved in the pathogenesis of these events could shed new light on possible therapeutic targets and offer strategies for the prevention of diseases related to brain ageing, cognitive impairment and dementia.

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En el envejecimiento cerebral ocurren una serie de cambios que conllevan la disminución de los procesos de adaptación y respuesta. Estas transformaciones pueden finalizar en el padecimiento de deterioro cognitivo y/o demencia. Aunque el origen de estas modificaciones es diverso, la inflamación y el estrés oxidativo explican parte de los mecanismos fisiopatológicos de dichas anomalías del funcionamiento cerebral. La neuroinflamación desencadena daño a nivel neuronal mediante la presencia de citocinas inflamatorias y la activación de la microglía, a través de receptores de membrana y factores de activación nuclear. Este fenómeno neuroinflamatorio también afecta la plasticidad neuronal, alterando la génesis y el mantenimiento de la potenciación a largo plazo ocasionando deterioro en la memoria dependiente del hipocampo. El estrés oxidativo y la producción de radicales libres de oxígeno, también originan efectos tóxicos en los cerebros envejecidos, en gran parte debido a la peroxidación lipídica y daños en el ADN. La identificación de los mecanismos moleculares implicados en la patogénesis de estos sucesos puede arrojar nueva luz sobre posibles dianas terapéuticas y ofrecer estrategias para la prevención de las patologías relacionadas con el envejecimiento cerebral, el deterioro cognitivo y la demencia (AU)

Brain ageing leads to a series of changes that reduce the processes of adaptation and response. These transformations can end in cognitive impairment and/or dementia. Although the cause of these changes is diverse, inflammation and oxidative stress explain some of the pathophysiological mechanisms of these anomalies of brain functioning. Neuroinflammation triggers neuronal injury through the presence of inflammatory cytokines and the activation of microglia through membrane receptors and nuclear activation factors. This neuroinflammatory phenomenon also affects neuron plasticity, altering the genesis and maintenance of long-term potentiation, leading to impairment of hippocampus-dependent memory. Oxidative stress and the production of free oxygen radicals also cause toxic effects in aged brains, largely due to lipid peroxidation and DNA damage. The identification of the molecular mechanisms involved in the pathogenesis of these events could shed new light on possible therapeutic targets and offer strategies for the prevention of diseases related to brain ageing, cognitive impairment and dementia (AU)

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Introducción. La evaluación nutricional longitudinal, debido a sus frecuentes alteraciones, es especialmente relevante en al anciano con deterioro cognitivo. El objetivo del presente estudio es valorar a lo largo del tiempo el efecto y la posible interacción del deterioro cognitivo y del envejecimiento en los parámetros nutricionales. Material y métodos. Estudio longitudinal prospectivo de 2 años de seguimiento en 301 ancianos (233 mujeres y 68 varones) en el medio residencial, 51 de los cuales tienen criterios de demencia. Los parámetros antropométricos y bioquímicos se obtuvieron según técnicas normalizadas. Resultados. Los ancianos con demencia presentan, en todos los parámetros estudiados, valores inferiores respecto a los ancianos sin demencia. En los pacientes con deterioro cognitivo los valores medios de los parámetros nutricionales permanecen estables y sin diferencias significativas tras 2 años de seguimiento: índice de masa corporal 24,5 ± 4,9 vs 24,2 ± 4,1; pliegue tricipital 15,0 ± 6,0 vs 14,7 ± 6,9; circunferencia braquial 25,9 ± 3,3 vs 25,7 ± 3,5, y albúmina 3,7 ± 0,3 vs 3,7 ± 0,3. En los pacientes sin deterioro cognitivo los valores al final del estudio han descendido respecto a los valores basales, excepto el pliegue bicipital y los triglicéridos. Conclusiones. Tras 2 años de seguimiento no se observa descenso de los parámetros nutricionales estudiados en los ancianos con demencia; sin embargo, sí aparece un descenso en los ancianos sin deterioro cognitivo. Las causas de estas diferencias pueden ser múltiples. Son necesarios más estudios, con mayor número de ancianos y un mayor periodo de seguimiento, para validar estos hallazgos (AU)

Introduction. It is important to assess longitudinal nutritional parameters during the ageing process in order to determine body composition changes. This procedure is more relevant when dealing with institutionalised geriatric patients suffering from cognitive impairment. The aim of this study was to assess the interactions, if any, between mental status and several nutritional parameters in a cohort of elderly people. Material and methods. A longitudinal prospective two years follow-up evaluation was performed on 301 elderly residents (233 females and 68 males) in a nursing home, of whom 51 of them fulfilled the clinical criteria for dementia. Both anthropometric and biochemical parameters were obtained annually, according to standard procedures. Results. The dementia group had lower values when compared to the non-dementia group. Furthermore, nutritional values remained constant in the group with cognitive impairment (no significant differences were observed throughout the study period). BMI 24.5 ± 4.9 vs 24.2 ± 4.1; tricipital skinfold 15.0 ± 6.0 vs 14.7 ± 6.9; brachial circumference 25.9 ± 3.3 vs 25.7 ± 3.5, and albumin 3.7 ± 0.3 vs 3.7 ± 0.3. At the end of the study, the group without cognitive impairment showed lower values in all the parameters analysed when compared to the baseline ones, except for bicipital fold and plasma triglycerides. Conclusions. Our study shows that there are no variations in the elderly with cognitive impairment, as regards the nutritional, anthropometric and biochemist parameters analysed. On the contrary, the group with normal cognitive status showed a reduction in most of the parameters. Further studies analysing larger populations of elderly people and over longer periods of time will provide more information to improve our knowledge on this important issue (AU)

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INTRODUCTION: It is important to assess longitudinal nutritional parameters during the ageing process in order to determine body composition changes. This procedure is more relevant when dealing with institutionalised geriatric patients suffering from cognitive impairment. The aim of this study was to assess the interactions, if any, between mental status and several nutritional parameters in a cohort of elderly people. MATERIAL AND METHODS: A longitudinal prospective two years follow-up evaluation was performed on 301 elderly residents (233 females and 68 males) in a nursing home, of whom 51 of them fulfilled the clinical criteria for dementia. Both anthropometric and biochemical parameters were obtained annually, according to standard procedures. RESULTS: The dementia group had lower values when compared to the non-dementia group. Furthermore, nutritional values remained constant in the group with cognitive impairment (no significant differences were observed throughout the study period). BMI 24.5±4.9 vs 24.2±4.1; tricipital skinfold 15.0±6.0 vs 14.7±6.9; brachial circumference 25.9±3.3 vs 25.7±3.5, and albumin 3.7±0.3 vs 3.7±0.3. At the end of the study, the group without cognitive impairment showed lower values in all the parameters analysed when compared to the baseline ones, except for bicipital fold and plasma triglycerides. CONCLUSIONS: Our study shows that there are no variations in the elderly with cognitive impairment, as regards the nutritional, anthropometric and biochemist parameters analysed. On the contrary, the group with normal cognitive status showed a reduction in most of the parameters. Further studies analysing larger populations of elderly people and over longer periods of time will provide more information to improve our knowledge on this important issue.

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La elevada prevalencia de la enfermedad de Alzheimer (EA), junto con la posibilidad de nuevas pautas en el diagnóstico mediante el empleo de los biomarcadores está cambiando el enfoque de los ancianos con demencia o en riesgo de padecerla. En este sentido parece importante revisar los aspectos genéticos de los ancianos con EA familiar, así como los ancianos con riesgo de padecer EA. La amplia difusión de los estudios genéticos asociados a esta afección también puede ser de gran ayuda. Además de los genes del amiloide, las presenilinas y la apolipoproteína E, implicados en la patogenia de la EA, debemos añadir otros genes recientemente relacionados con la enfermedad entre los que destacan el gen de la clusterina y los de fosfatidil-inositol de unión a clatrina y el del receptor de la proteína del complemento C3b(AU)

The high prevalence of Alzheimer's disease, along with the possibility of new approaches in diagnosis through the use of biomarkers of cerebrospinal fluid is shifting the focus to the elderly with dementia or at risk. In this sense it seems important to review the genetic aspects of the elderly with familial Alzheimer's disease as well as those at risk. The wide distribution of genetic studies associated with this condition may also be helpful. To the classical findings of the genes for amyloid, the presenilins and apolipoprotein E, we must add other genes recently implicated in the pathogenesis of the disease, among which are found the clusterin gene, encoding the phosphatidyl-inositol-binding clathrin assembly protein gene, and the receptor for the complement C3b protein(AU)

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The high prevalence of Alzheimer's disease, along with the possibility of new approaches in diagnosis through the use of biomarkers of cerebrospinal fluid is shifting the focus to the elderly with dementia or at risk. In this sense it seems important to review the genetic aspects of the elderly with familial Alzheimer's disease as well as those at risk. The wide distribution of genetic studies associated with this condition may also be helpful. To the classical findings of the genes for amyloid, the presenilins and apolipoprotein E, we must add other genes recently implicated in the pathogenesis of the disease, among which are found the clusterin gene, encoding the phosphatidyl-inositol-binding clathrin assembly protein gene, and the receptor for the complement C3b protein.

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El síndrome de Hutchinson-Gilford es un síndrome progeroide que se caracteriza por un envejecimiento acelerado que comienza tempranamente en la infancia. El estudio de células de pacientes y el desarrollo de modelos animales (Zmpste24­/­, Zmpste24­/­Lmna+/­, LmnaLCO/LCO) que reproducen esta dolencia ha aportado nuevos conocimientos para entender las bases genéticas de esta enfermedad y así también profundizar en las del envejecimiento fisiológico. El fenotipo característico de este síndrome se debe a alteraciones en la lamina nuclear, estructura formada por un conjunto de filamentos intermedios (laminas A, B y C) que permiten mantener la organización de la envoltura nuclear. Se ha demostrado que una mutación del gen LMNA, que sintetiza la lamina A, es la del depósito de lamina A farnesilada (progerina) que es la causante de las alteraciones en la envoltura nuclear y del fenotipo de este raro síndrome. El empleo de moléculas que actúan sobre diferentes pasos en la síntesis de progerina se está revelando como un futuro terapéutico prometedor para revertir los efectos nocivos de su síntesis

Hutchinson-Gilford disease is a progeroid syndrome characterized by accelerated ageing beginning in early childhood. Study of several types of cells from patients with this syndrome and the development of animal models (Zmpste24­/­, Zmpste24­/­Lmna+/­, LmnaLCO/LCO) that mimic this disease have increased knowledge of the genetic foundations of this rare entity and those of normal ageing. The phenotypic features of this syndrome are caused by alterations in the fibrillar components of the nuclear lamina (lamins A, B, and C), which maintain the structure of the nuclear envelope. A point mutation in the gene for lamin A (LMNA) induces deposit of a farnesylated lamin A (progerin), which causes the nuclear alterations observed in the affected cells. The use of several molecules that interfere with progerin synthesis has been proposed as a promising potential therapeutic approach to reverse the adverse effects of progerin synthesis

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