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"documento" => "simple-article" "crossmark" => 1 "subdocumento" => "crp" "cita" => "Gastroenterol Hepatol. 2024;47:381-3" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "es" => array:11 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Carta científica</span>" "titulo" => "Glomerulonefritis fibrilar extrarrenal como nueva etiología de enfermedad hepática avanzada" "tienePdf" => "es" "tieneTextoCompleto" => "es" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "381" "paginaFinal" => "383" ] ] "titulosAlternativos" => array:1 [ "en" => array:1 [ "titulo" => "Extrarenal fibrillary glomerulonephritis as an unknown etiology of advanced liver disease" ] ] "contieneTextoCompleto" => array:1 [ "es" => true ] "contienePdf" => array:1 [ "es" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figura 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1220 "Ancho" => 1867 "Tamanyo" => 585821 ] ] "descripcion" => array:1 [ "es" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Imágenes histopatológicas de la biopsia hepática (muestra de 2 cilindros de 2 y 1,5<span class="elsevierStyleHsp" style=""></span>cm con 10 espacios porta). A) Apreciamos el depósito de material extracelular (azul claro, flechas) en forma de cordones alterando la arquitectura sinusiodal. B) Observamos, a mayor aumento, cómo el depósito de material fibrilar (círculo) desplaza y arrincona a los hepatocitos (rectángulo), que sería la causa de la hipertensión portal. C) Se muestra el material de depósito (marrón) mediante positividad para cadenas lambda en la inmunohistoquimia. D) Visualizamos, mediante microscopía electrónica, las fibrillas de 20<span class="elsevierStyleHsp" style=""></span>nm y distribución desordenada que componen el material de depósito. El color de la figura solo puede apreciarse en la versión electrónica del artículo.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Carlos Alventosa Mateu, Ana Vilar Gimeno, Irene Pérez Álvarez, Javier Carbonell Zamorano, Inmaculada Castelló Miralles, Mercedes Latorre Sánchez, Juan José Urquijo Ponce, Encarnación Martínez Leandro, Liria Terrádez Mas, Moisés Diago" "autores" => array:10 [ 0 => array:2 [ "nombre" => "Carlos" "apellidos" => "Alventosa Mateu" ] 1 => array:2 [ "nombre" => "Ana" "apellidos" => "Vilar Gimeno" ] 2 => array:2 [ "nombre" => "Irene" "apellidos" => "Pérez Álvarez" ] 3 => array:2 [ "nombre" => "Javier" "apellidos" => "Carbonell Zamorano" ] 4 => array:2 [ "nombre" => "Inmaculada" "apellidos" => "Castelló Miralles" ] 5 => array:2 [ "nombre" => "Mercedes" "apellidos" => "Latorre Sánchez" ] 6 => array:2 [ "nombre" => "Juan" "apellidos" => "José Urquijo Ponce" ] 7 => array:2 [ "nombre" => "Encarnación" "apellidos" => "Martínez Leandro" ] 8 => array:2 [ "nombre" => "Liria" "apellidos" => "Terrádez Mas" ] 9 => array:2 [ "nombre" => "Moisés" "apellidos" => "Diago" ] ] ] ] ] "idiomaDefecto" => "es" "Traduccion" => array:1 [ "en" => array:9 [ "pii" => "S2444382424000580" "doi" => "10.1016/j.gastre.2023.08.004" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2444382424000580?idApp=UINPBA00004N" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0210570523003771?idApp=UINPBA00004N" "url" => "/02105705/0000004700000004/v2_202406091228/S0210570523003771/v2_202406091228/es/main.assets" ] ] "itemSiguiente" => array:18 [ "pii" => "S2444382424001871" "issn" => "24443824" "doi" => "10.1016/j.gastre.2023.03.011" "estado" => "S300" "fechaPublicacion" => "2024-04-01" "aid" => "2065" "copyright" => "Elsevier España, S.L.U." 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"documento" => "simple-article" "crossmark" => 1 "subdocumento" => "crp" "cita" => "Gastroenterol Hepatol. 2024;47:380-1" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "en" => array:11 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Scientific letter</span>" "titulo" => "Beyond Crohn's disease: Deferasirox as possible agent for drug-induced ileocolitis" "tienePdf" => "en" "tieneTextoCompleto" => "en" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "380" "paginaFinal" => "381" ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Más allá de la enfermedad de Crohn. Deferasirox como posible agente etiológico de ileocolitis farmacológica" ] ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1505 "Ancho" => 1874 "Tamanyo" => 478991 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">A: notice the right colonic wall thickening. B: Diffuse ileitis with large superficial and ulcers in the terminal ileum. C: Pathological study revealed non-specific features with neutrophilic, eosinophilic and lymphocytic infiltration. D: A second colonoscopy 4 months later showing mucosal healing in the terminal ileum.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Esteban Fuentes-Valenzuela, Ana Yaiza Carbajo, Samuel Juan Fernández-Prada, Beatriz Madrigal Rubiales, Natalia Carpizo Jimenez" "autores" => array:5 [ 0 => array:2 [ "nombre" => "Esteban" "apellidos" => "Fuentes-Valenzuela" ] 1 => array:2 [ "nombre" => "Ana Yaiza" "apellidos" => "Carbajo" ] 2 => array:2 [ "nombre" => "Samuel Juan" "apellidos" => "Fernández-Prada" ] 3 => array:2 [ "nombre" => "Beatriz Madrigal" "apellidos" => "Rubiales" ] 4 => array:2 [ "nombre" => "Natalia Carpizo" "apellidos" => "Jimenez" ] ] ] ] ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2444382424002001?idApp=UINPBA00004N" "url" => "/24443824/0000004700000004/v1_202405220556/S2444382424002001/v1_202405220556/en/main.assets" ] "en" => array:14 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Scientific letter</span>" "titulo" => "Extrarenal fibrillary glomerulonephritis as an unknown etiology of advanced liver disease" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "381" "paginaFinal" => "383" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "Carlos Alventosa Mateu, Ana Vilar Gimeno, Irene Pérez Álvarez, Javier Carbonell Zamorano, Inmaculada Castelló Miralles, Mercedes Latorre Sánchez, Juan José Urquijo Ponce, Encarnación Martínez Leandro, Liria Terrádez Mas, Moisés Diago" "autores" => array:10 [ 0 => array:4 [ "nombre" => "Carlos" "apellidos" => "Alventosa Mateu" "email" => array:1 [ 0 => "almacar84@hotmail.com" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "*" "identificador" => "cor0005" ] ] ] 1 => array:3 [ "nombre" => "Ana" "apellidos" => "Vilar Gimeno" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] 2 => array:3 [ "nombre" => "Irene" "apellidos" => "Pérez Álvarez" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 3 => array:3 [ "nombre" => "Javier" "apellidos" => "Carbonell Zamorano" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">c</span>" "identificador" => "aff0015" ] ] ] 4 => array:3 [ "nombre" => "Inmaculada" "apellidos" => "Castelló Miralles" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 5 => array:3 [ "nombre" => "Mercedes" "apellidos" => "Latorre Sánchez" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 6 => array:3 [ "nombre" => "Juan José" "apellidos" => "Urquijo Ponce" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 7 => array:3 [ "nombre" => "Encarnación" "apellidos" => "Martínez Leandro" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">c</span>" "identificador" => "aff0015" ] ] ] 8 => array:3 [ "nombre" => "Liria" "apellidos" => "Terrádez Mas" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">d</span>" "identificador" => "aff0020" ] ] ] 9 => array:3 [ "nombre" => "Moisés" "apellidos" => "Diago" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] ] "afiliaciones" => array:4 [ 0 => array:3 [ "entidad" => "Unidad de Hepatología, Servicio de Patología Digestiva, Valencia, Spain" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Servicio de Nefrología, Valencia, Spain" "etiqueta" => "b" "identificador" => "aff0010" ] 2 => array:3 [ "entidad" => "Servicio de Anatomía Patológica, Consorcio Hospital General Universitario de Valencia, Valencia, Spain" "etiqueta" => "c" "identificador" => "aff0015" ] 3 => array:3 [ "entidad" => "Servicio de Anatomía Patológica, Hospital Clínico Universitario de Valencia, Valencia, Spain" "etiqueta" => "d" "identificador" => "aff0020" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Glomerulonefritis fibrilar extrarrenal como nueva etiología de enfermedad hepática avanzada" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:8 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1220 "Ancho" => 1867 "Tamanyo" => 585821 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0005" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Histopathology images of the liver biopsy (sample of 2 cylinders of 2 and 1.5 cm with 10 portal spaces). A) The image shows the deposit of extracellular material (light blue, arrows) in the form of cords, altering the sinusoidal architecture. B) At higher magnification, we can see the deposit of fibrillar material (circle) displacing and cornering the hepatocytes (rectangle), which would be the cause of the portal hypertension. C) Deposit material (brown) is shown by being positive for lambda chains in immunohistochemistry. D) Electron microscopy shows the 20 nm fibrils and disordered distribution which make up the deposit material. The colours in the figure can only be appreciated in the electronic version of the article.</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Fibrillary glomerulonephritis (FGN) is a rare non-amyloid deposit disease considered to exclusively involve the kidneys.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> However, there was one case where fibrillar material was found in the liver at autopsy, with no clinical repercussions.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> This raises the possibility that FGN may lead to advanced liver disease.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Case report</span><p id="par0010" class="elsevierStylePara elsevierViewall">This was a 78-year-old male, with BMI 22.7, hypertension and dyslipidaemia, normal blood glucose and glycosylated haemoglobin, and no history of liver or kidney disease. Tests to investigate albuminuria showed normal kidney function and 24-h urine compatible with nephrotic syndrome, with no associated oedema or effusion. Complement C3 and C4 values were normal. The patient reported non-specific abdominal discomfort, with no weight loss or elevated transaminases.</p><p id="par0015" class="elsevierStylePara elsevierViewall">Suspecting membranous nephropathy, a renal biopsy was performed, showing glomerular expansion (without an increase in cellularity) due to the deposit of eosinophilic material in the glomerular basement membrane, which was fragmented. This deposit stained positive for PAS and negative for Congo red. Immunohistochemistry was positive for Kappa and Lambda light chains, negative for amyloid P protein and IgG4, and positive for DNA-J heat-shock protein family member B9 (DNAJB9). Electron microscopy showed the deposit to be made up of disordered fibrils of 20 nm in diameter, consistent with FGN.</p><p id="par0020" class="elsevierStylePara elsevierViewall">In order to rule out the FGN being secondary to a cancerous process, we performed a chest, abdomen and pelvis CT scan, followed by an abdominal ultrasound, which showed splenomegaly and portal dilation as indirect signs of portal hypertension (PHT), as well as homogeneous hepatomegaly with no signs of steatosis, tumours or pre- or post-hepatic vascular thrombosis. Gastroscopy confirmed the presence of small oesophageal varices. At that time (two months after the diagnosis of FGN) total bilirubin, platelets, albumin, coagulation and renal function values were normal, but we observed alterations in liver biochemistry (AST 38, alkaline phosphatase 233 and GGT 368 U/l).</p><p id="par0025" class="elsevierStylePara elsevierViewall">The aetiological study of liver disease was negative, including normal serum IgG4 levels. Lastly, we performed a percutaneous liver biopsy to rule out invasive cancer and to assess for deposition disease. We observed distorted lobular and sinusoidal architecture due to extensive accumulation of eosinophilic extracellular material, leading to sinusoidal rupture and hepatocyte atrophy, without fibrosis. The results of staining and immunohistochemistry and the fibrils seen on electron microscopy were identical to those obtained in the renal biopsy, and positive for DNAJB9 (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>).</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0030" class="elsevierStylePara elsevierViewall">Four months after the diagnosis of FGN, ultrasound showed a thin layer of perihepatic free fluid, while the patient had normal liver function, unchanged transaminases and altered renal function (creatinine 1.35 mg/dl; glomerular filtration rate 72 ml/min/1.73 m<span class="elsevierStyleSup">2</span>). Once underlying cancer had been ruled out, with the main objective of improving his renal impairment, we started him on rituximab 1 g IV, with two doses 15 days apart. Despite this treatment, the patient's kidney function slowly and progressively deteriorated. Six months after the diagnosis of FGN, his ascites became moderate-to-severe, with characteristics of transudate (serum albumin gradient >1.1 and protein <2.5 mg/dl). This ascites was refractory to diuretics, requiring periodic paracentesis.</p><p id="par0035" class="elsevierStylePara elsevierViewall">Nine months after being diagnosed with FGN, the patient’s renal failure continued to progress (creatinine 3.92 mg/dl; glomerular filtration rate 19 ml/min/1.73 m<span class="elsevierStyleSup">2</span>) together with hypoalbuminemia (2.2 g/dl), coagulation disorder (prothrombin time 70%) and worsening of cytolysis/cholestasis enzymes, with bilirubin 1.5 mg/dl. Given the patient's advanced clinical deterioration and the lack of response to treatment, we opted for exclusively symptomatic treatment. The patient died three weeks later of multi-organ dysfunction syndrome.</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">Discussion</span><p id="par0040" class="elsevierStylePara elsevierViewall">FGN is a rare form of glomerulonephritis, the diagnosis of which requires pathology examination. It is distinguished from amyloidosis by being negative for Congo red staining and from immunotactoid glomerulonephritis by the absence of larger diameter microtubular structures (30−50 nm). As it is usually associated with the presence of a systemic disease such as lupus, idiopathic thrombocytopenic purpura, diabetes mellitus, hepatitis C virus infection or cancer, it is recommended that these be ruled out.<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1,3</span></a> Testing positive for DNAJB9 is diagnostically useful,<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> and in our patient it was present in both biopsies.</p><p id="par0045" class="elsevierStylePara elsevierViewall">There is one published case of a patient with extra-renal fibrillar deposition at autopsy, specifically in the liver, adrenal glands and lungs, but with no progression to advanced liver disease.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> In contrast, in our patient the hepatic deposition led to PHT, ascites and, ultimately, impaired liver function. Unfortunately, in our case we did not perform an autopsy, so we do not know if there was coexisting fibrillar deposition in other organs. Both our patient and the patient reported by Soma et al.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> had rupture of the glomerular basement membrane, and this was probably a predictor of extrarenal involvement.</p><p id="par0050" class="elsevierStylePara elsevierViewall">The liver involvement in our patient differs in several respects from that seen in the usual aetiologies. On the one hand, the liver disease and PHT were the result of sinusoidal destructuring and compression by fibrillar material (without fibrosis), this being sinusoidal vascular-type involvement. In view of these histological findings, we did not pursue further study with hepatic catheterisation and/or transient elastography, which, theoretically, would have shown an elevated venous pressure gradient of <12 kPa.</p><p id="par0055" class="elsevierStylePara elsevierViewall">On the other hand, the alteration in liver function was unremarkable and only appeared in the advanced stage of renal failure. We did, however, see elevated cholestasis enzymes and indirect signs of PHT in earlier stages of the disease, which would point to a diagnosis of liver involvement due to deposition once the usual aetiologies had been ruled out. Lastly, the development of ascites was in parallel to the deterioration in renal function; therefore, although the study was compatible with ascites of hepatic origin, it is possible that the nephrotic syndrome was a contributory factor and made it refractory to diuretic treatment.</p><p id="par0060" class="elsevierStylePara elsevierViewall">FGN has a poor prognosis, with progression rates to advanced chronic kidney disease of 50% at 4 years.<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> There is no standardised treatment, mainly due to the absence of long series of patients. The most commonly used treatments are steroids, with or without other immunosuppressants such as cyclophosphamide or rituximab, but their effectiveness has not been established.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> The addition of liver disease would make the prognosis even worse.</p><p id="par0065" class="elsevierStylePara elsevierViewall">Our case is the first to describe symptomatic involvement of the liver due to deposition secondary to FGN, which represents a hitherto unknown etiology of advanced liver disease.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:4 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 1 => array:2 [ "identificador" => "sec0010" "titulo" => "Case report" ] 2 => array:2 [ "identificador" => "sec0015" "titulo" => "Discussion" ] 3 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "multimedia" => array:1 [ 0 => array:8 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1220 "Ancho" => 1867 "Tamanyo" => 585821 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0005" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Histopathology images of the liver biopsy (sample of 2 cylinders of 2 and 1.5 cm with 10 portal spaces). A) The image shows the deposit of extracellular material (light blue, arrows) in the form of cords, altering the sinusoidal architecture. B) At higher magnification, we can see the deposit of fibrillar material (circle) displacing and cornering the hepatocytes (rectangle), which would be the cause of the portal hypertension. C) Deposit material (brown) is shown by being positive for lambda chains in immunohistochemistry. D) Electron microscopy shows the 20 nm fibrils and disordered distribution which make up the deposit material. The colours in the figure can only be appreciated in the electronic version of the article.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:5 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Fibillary glomerulonephritis: an update" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "J.D. Rosenstock" 1 => "G.S. Markowitz" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:5 [ "tituloSerie" => "Kidney Int Rep" "fecha" => "2019" "volumen" => "4" "paginaInicial" => "917" "paginaFinal" => "922" ] ] ] ] ] ] 1 => array:3 [ "identificador" => "bib0010" "etiqueta" => "2" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Systemic non-amyloidotic fibril deposit disease: a probable variant form of fibrillary glomerulonephritis" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:6 [ 0 => "J. Soma" 1 => "K. Sato" 2 => "I. Nakaya" 3 => "M. Yahata" 4 => "T. Sakuma" 5 => "H. Sato" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:5 [ "tituloSerie" => "Clin Nephrol" "fecha" => "2011" "volumen" => "75" "paginaInicial" => "74" "paginaFinal" => "79" ] ] ] ] ] ] 2 => array:3 [ "identificador" => "bib0015" "etiqueta" => "3" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Fibrillary and immunotactoid glomerulonephritis: distinct entities with different clinical and pathologic features" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:6 [ 0 => "J.L. Rosenstock" 1 => "G.S. Markowitz" 2 => "A.M. Valeri" 3 => "G. Sacchi" 4 => "G.B. Appel" 5 => "V.D. D’Agati" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1046/j.1523-1755.2003.00853.x" "Revista" => array:6 [ "tituloSerie" => "Kidney Int" "fecha" => "2003" "volumen" => "63" "paginaInicial" => "1450" "paginaFinal" => "1461" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/12631361" "web" => "Medline" ] ] ] ] ] ] ] ] 3 => array:3 [ "identificador" => "bib0020" "etiqueta" => "4" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "DNAJB9 is a specific immunohistochemical marker for fibrillary glomerulonephritis" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "S.H. Nasr" 1 => "J.A. Vrana" 2 => "S. Dasari" 3 => "F. Bridoux" 4 => "M.E. Fidler" 5 => "S. Kaaki" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1016/j.ekir.2017.07.017" "Revista" => array:6 [ "tituloSerie" => "Kidney Int Rep" "fecha" => "2018" "volumen" => "3" "paginaInicial" => "56" "paginaFinal" => "64" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/29340314" "web" => "Medline" ] ] ] ] ] ] ] ] 4 => array:3 [ "identificador" => "bib0025" "etiqueta" => "5" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Fibrillary glomerulonephritis: a report of 66 cases from a single institution" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "S.H. Nasr" 1 => "A.M. Valeri" 2 => "L.D. Cornell" 3 => "M.E. Fidler" 4 => "S. Sethi" 5 => "N. Leung" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.2215/CJN.08300910" "Revista" => array:6 [ "tituloSerie" => "Clin J Am Soc Nephrol" "fecha" => "2011" "volumen" => "6" "paginaInicial" => "775" "paginaFinal" => "784" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/21441134" "web" => "Medline" ] ] ] ] ] ] ] ] ] ] ] ] ] "idiomaDefecto" => "en" "url" => "/24443824/0000004700000004/v1_202405220556/S2444382424000580/v1_202405220556/en/main.assets" "Apartado" => array:4 [ "identificador" => "77930" "tipo" => "SECCION" "en" => array:2 [ "titulo" => "Scientific letter" "idiomaDefecto" => true ] "idiomaDefecto" => "en" ] "PDF" => "https://static.elsevier.es/multimedia/24443824/0000004700000004/v1_202405220556/S2444382424000580/v1_202405220556/en/main.pdf?idApp=UINPBA00004N&text.app=https://www.elsevier.es/" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2444382424000580?idApp=UINPBA00004N" ]
Journal Information
Vol. 47. Issue 4.
Pages 381-383 (April 2024)
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Vol. 47. Issue 4.
Pages 381-383 (April 2024)
Scientific letter
Extrarenal fibrillary glomerulonephritis as an unknown etiology of advanced liver disease
Glomerulonefritis fibrilar extrarrenal como nueva etiología de enfermedad hepática avanzada
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Carlos Alventosa Mateua,
, Ana Vilar Gimenob, Irene Pérez Álvareza, Javier Carbonell Zamoranoc, Inmaculada Castelló Mirallesa, Mercedes Latorre Sáncheza, Juan José Urquijo Poncea, Encarnación Martínez Leandroc, Liria Terrádez Masd, Moisés Diagoa
Corresponding author
a Unidad de Hepatología, Servicio de Patología Digestiva, Valencia, Spain
b Servicio de Nefrología, Valencia, Spain
c Servicio de Anatomía Patológica, Consorcio Hospital General Universitario de Valencia, Valencia, Spain
d Servicio de Anatomía Patológica, Hospital Clínico Universitario de Valencia, Valencia, Spain
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