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A women problem?" 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"tieneTextoCompleto" => 0 "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "710" "paginaFinal" => "715" ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "M. Wagrowska-Danilewicz, M. Danilewicz" "autores" => array:1 [ 0 => array:1 [ "nombre" => "M. Wagrowska-Danilewicz, M. Danilewicz" ] ] ] ] "tienePdf" => false "PalabrasClave" => array:2 [ "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec436123" "palabras" => array:1 [ 0 => "synaptopodin, minimal change disease, focal segmental glomerulosclerosis" ] ] ] "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec436124" "palabras" => array:1 [ 0 => "synaptopodin, minimal change disease, focal segmental glomerulosclerosis" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:1 [ "resumen" => "Background and objectives: Synaptopodin is protein of podocytes, and a part of the actin-based contractile apparatus of foot-processes. Recently, proteins expressed by the podocyte were found to be important for the integrity of the glomerular filtration barrier. Podocytes are injured in many forms of glomerulopathies, including minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS). The study was undertaken to determinate if synaptopodin immunoexpression in renal tissue specimens differs between patients with steroid-responsive MCD, steroid-resistant MCD, and FSGS. Methods: Synaptopodin immunoexpression was evaluated by immunoperioxidase staining with a mouse anti-human monoclonal antibody in 12 renal biopsy specimens in patients with steroid-responsive MCD, 10 renal tissues in steroid-resistant MCD, and in 14 renal biopsy specimens in patients with FSGS. As a control 10 tissue specimens of the kidneys removed because of trauma were used. Synaptopodin expression was quantified as a percentage of glomerular tuft by computerized image analysis system. Results: In normal controls synaptopodin immunoexpression was seen in podocytes along the glomerular basement membrane in a finely linear pattern. No changes were found in synaptopodin immunoexpression in steroid-responsive MCD versus controls. In patients with steroid-resistant MCD and FSGS a granular pattern of synaptopodin immunoexpression was seen. Areas of sclerosis in patients with FSGS did not demonstrate synaptopodin expression. Statistical analysis showed significantly diminished synaptopodin immunoexpresion in glomeruli in patients with steroid-resistant MCD and FSGS as compared with steroid-responsive MCD group and controls. Moreover, in renal tissues in patients with FSGS the immunoexpression of synaptopodin was decreased in comparison with renal biopsies in patients with steroid-resistant MCD. In conclusions, our results suggest that abnormal distribution and reduced expression of synaptopodin may be associated with poor response to steroid therapy in MCD and FSGS. " ] "es" => array:1 [ "resumen" => "Antecedentes y objetivos: la sinaptopodina es una proteína de los podocitos y una parte del aparato contráctil basado en la actina de los procesos pediculados. Recientemente, se encontró que las proteínas expresadas por los podocitos son importantes para la integridad de la barrera de filtración glomerular. Los podocitos pueden verse dañados en muchas formas de glomerulopatías, incluyendo la enfermedad de cambios mínimos (ECM) y la glomerulosclerosis focal y segmentaria (GEFS). Este estudio se realizó para determinar si la inmunoexpresión de sinaptopodina en muestras de tejido renal difiere entre los pacientes con ECM respondedora a esteroides, ECM resistente a esteroides, y la GEFS. Métodos: la inmunoexpresión de sinaptopodina se evaluó mediante tinción de inmunoperoxidasa con un anticuerpo monoclonal anti-humano de ratón en 12 muestras de biopsia renal de pacientes con ECM respondedora a esteroides, 10 muestras renales de ECM resistente a esteroides, y en 14 muestras de biopsia renal de pacientes con GEFS. Se tomaron como controles 10 muestras tisulares de riñones extirpados por traumatismo. La expresión de sinaptopodina se cuantificó como el porcentaje de penacho glomerular mediante un sistema de análisi de la imagen computerizada. Resultados: en los contorles normales, la inmunoexpresión de sinaptopodina se vio en los podocitos a lo largo de la membrana basal glomerular en un patrón finalmente granular. No se observaron cambios en la inmunoexpresión de sinaptopodina en la ECM respondedora a esteroides frente a los controles. En pacientes con ECM resistente a esteroides y GEFS, se vio un patrón granular de inmunoexpresión de sinaptopodina. Las áreas de esclerosis en los pacientes con GEFS no mostraron expresión de sinaptopodina. El análisis estadístico mostró una inmunoexpresión de sinaptopodina significativamente disminuida en los glomerulos de pacientes con ECM resistente a esteroides y con GEFS en comparación con los grupos de ECM respondedora a esteroides y control. Además, en los tejidos renales de pacientes con GEFS, la inmunoexpresión de sinaptopodina estaba disminuida en comparación con las biopsias renales de pacientes con ECM resistente a esteroides. En conclusión, nuestros resultados sugieren que la distribución anormal y la expresión reducida de sinaptopodina podrían estar asociadas con una respuesta escasa al tratamiento con corticoides en la ECM y la GEFS." ] ] ] "idiomaDefecto" => "en" "url" => "/20132514/0000002700000006/v0_201502091551/X2013251407022008/v0_201502091551/en/main.assets" "Apartado" => null "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/X2013251407022008?idApp=UINPBA000064" ]
Original language: English
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