RESUMO
The presence of renal dysfunction is not unusual in patients with pulmonary or cardiac dysfunction who require rescue with extracorporeal membrane oxygenation (ECMO). The complexity, implicit in the implementation of both techniques, can be overwhelming. This review aims to explain the most important aspects of continuous renal replacement therapy in a patient with extracorporeal support.
Assuntos
Injúria Renal Aguda/terapia , Terapia Combinada/métodos , Oxigenação por Membrana Extracorpórea/métodos , Terapia de Substituição Renal/instrumentação , Injúria Renal Aguda/diagnóstico , Injúria Renal Aguda/mortalidade , Chile/epidemiologia , Oxigenação por Membrana Extracorpórea/classificação , Humanos , Terapia de Substituição Renal/métodos , Fatores de Risco , Taxa de SobrevidaRESUMO
The presence of renal dysfunction is not unusual in patients with pulmonary or cardiac dysfunction who require rescue with extracorporeal membrane oxygenation (ECMO). The complexity, implicit in the implementation of both techniques, can be overwhelming. This review aims to explain the most important aspects of continuous renal replacement therapy in a patient with extracorporeal support.
Assuntos
Humanos , Oxigenação por Membrana Extracorpórea/métodos , Terapia de Substituição Renal/instrumentação , Terapia Combinada/métodos , Injúria Renal Aguda/terapia , Oxigenação por Membrana Extracorpórea/classificação , Chile/epidemiologia , Taxa de Sobrevida , Fatores de Risco , Terapia de Substituição Renal/métodos , Injúria Renal Aguda/diagnóstico , Injúria Renal Aguda/mortalidadeRESUMO
BACKGROUND: Epicardial adipose tissue (EAT) is a visceral adipose tissue (AT) surrounding and infiltrating myocardium and coronary arteries. Increased EAT may represent a chronic inflammatory injury and a link with coronary artery disease (CAD). Metalloproteinases (MMPs) are involved in expansion of AT. OBJECTIVE: To evaluate MMP-2 and -9 behaviour in EAT from CAD patients. METHODS: In EAT and subcutaneous AT (SAT) from patients undergoing coronary artery bypass graft (CABG, n=26) or valve replacement (No CABG, n=18), MMP-2 and -9 activity and localization, inflammatory cells and vascular endothelial growth factor (VEGF) levels were determined. RESULTS: In EAT from CABG, MMP-2 and -9 activity was increased compared with No CABG (p=0.041 and p=0.027, respectively) and compared with SAT (p=0.005 and p=0.048, respectively). In CABG patients EAT showed higher infiltration of macrophages and T lymphocytes than SAT (p=0.01 and p=0.002, respectively). In No CABG patients no sign of cellular retention was observed in EAT or SAT. Vascular density was higher in EAT from CABG than No CABG (p=0.015) and it was directly correlated with MMP-2 (p=0.006) and MMP-9 (p=0.02). VEGF levels in EAT were directly associated with MMP-2 (p=0.016). CONCLUSION: In EAT from CABG patients the increase of MMP-2 and -9 activity and the presence of inflammatory cells would be partially responsible for extracellular matrix (ECM) remodeling and major vascular density necessary for EAT expansion. Improved knowledge of EAT behaviour may allow to identify new therapeutic targets for the treatment of CAD.
Assuntos
Tecido Adiposo/enzimologia , Doença da Artéria Coronariana/enzimologia , Metaloproteinase 2 da Matriz/análise , Metaloproteinase 9 da Matriz/análise , Idoso , Idoso de 80 Anos ou mais , Biomarcadores/análise , Estudos de Casos e Controles , Ponte de Artéria Coronária , Doença da Artéria Coronariana/diagnóstico por imagem , Doença da Artéria Coronariana/cirurgia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Pericárdio , Gordura Subcutânea/enzimologia , Regulação para Cima , Fator A de Crescimento do Endotélio Vascular/análiseRESUMO
La artritis reumatoidea es una enfermedad inflamatoria que compromete las articulaciones periféricas y menos frecuentemente, otras partes del cuerpo. Dentro del curso de las investigaciones se ha determinado que existen asociaciones entre determinadas moléculas del complejo mayor de histocompatibilidad y la artritis reumatoidea, lo que supone que existe un trasfondo genético que favorece el desarrollo de la enfermedad. Las alteraciones en el proceso de maduración de las células del sistema inmune son también factibles. Algunos estudios apoyan la tesis de la existencia de un disbalance hormonal durante determinados periódos de la vida o secundaria a la expresión inapropiada de genes. Se sugiere además, la posible responsabilidad de la disregulación metabólica por defectos enzimáticos o por la presencia de anticuerpos en el origen de la artritis reumatoidea; como factores precipitantes actuarían las reacciones cruzadas inmunológicas después del ingreso al organismo de ciertas bacterias y virus que comparten secuencias de aminoácidos con moléculas humanas. La fisiopatología de la inflamación en los lugares afectados no difiere de la que subyace a una inflamación por otra causa, pero si existen otros mediadores diferentes a los habitualmente encontrados. Las interleucinas 1, 6 y 8, el factor de necrosis tumoral, el factor de crecimiento de los hepatocitos y las integrinas participan activamente en este proceso
