Nephrogenic Systemic Fibrosis: An Overview

Cowper, Shawn E.

doi:10.1016/j.jacr.2007.08.013

Cited by 60 publications

(42 citation statements)

References 18 publications

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“…3. The occurrence of NSF in temporal proximity to inflammatory and thrombotic episodes in affected patients (9,44) suggests that macrophages and inflammatory cells may have been primed by these events and, thus, capable of an enhanced or exaggerated response to noxious agents accords with the observations that monocytes and macrophages can be directly stimulated by GBCA in vitro (38,39). 4.…”

Section: Discussionmentioning

confidence: 77%

Mechanism of NSF: New evidence challenging the prevailing theory

Newton¹,

Jimenez

2009

Magnetic Resonance Imaging

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Nephrogenic systemic fibrosis (NSF) has been associated with the administration of gadolinium‐based contrast agents in patients with severely impaired renal function (SIRF), endstage renal disease (ESRD), or acute renal failure (ARF). Since the vast majority of these patients do not get NSF, it is highly likely that patient factors play a role in its development. Although “free” or dechelated gadolinium is thought by some to be the only trigger of NSF, recent evidence suggests that chelated gadolinium may be important. Chelated gadolinium such as Omniscan (gadodiamide) and Magnevist (gadopentetate) can directly stimulate macrophages and monocytes in vitro to release profibrotic cytokines and growth factors capable of initiating and supporting the tissue fibrosis that is characteristic of NSF. In addition, an effect of chelated gadolinium on fibroblasts has also been demonstrated. Chelated gadolinium in the form of Omniscan, Magnevist, MultiHance, and ProHance increased proliferation of human dermal fibroblasts. Indeed, increased numbers of macrophages, together with activated fibroblasts and fibrocytes, are essential cells in the fibrotic process and are present in NSF skin. Accordingly, it is important that chelated gadolinium, in combination with patient cofactors, is considered in the etiology of NSF associated with enhanced scans. J. Magn. Reson. Imaging 2009;30:1277–1283. © 2009 Wiley‐Liss, Inc.

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Section: Discussionmentioning

confidence: 77%

Mechanism of NSF: New evidence challenging the prevailing theory

Newton¹,

Jimenez

2009

Magnetic Resonance Imaging

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“…55 The present work showed that Gd-DTPA-cholesterol and Gd-DTPA-(cholesterol) 2 could be metabolized into the bile and subsequently secreted via the feces. These Gd-labeled HDL nanoparticles could thus be developed as safer contrast agents, with more detailed studies concerning the exact elimination pathway of these cholesterol-based compounds.…”

Section: Discussionmentioning

confidence: 57%

Recombinant high-density lipoprotein nanoparticles containing gadolinium-labeled cholesterol for morphologic and functional magnetic resonance imaging of the liver

Rui

Guo²,

Ding³

et al. 2012

IJN

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Background: Natural high-density lipoproteins (HDL) possess important physiological functions to the transport of cholesterol from the peripheral tissues to the liver for metabolic degradation and excretion in the bile. Methods and results:In this work, we took advantage of this pathway and prepared two different gadolinium (Gd)-DTPA-labeled cholesterol-containing recombinant HDL nanoparticles (Gd-chol-HDL) and Gd-(chol) 2 -HDL as liver-specific magnetic resonance imaging (MRI) contrast agents. The reconstituted HDL nanoparticles had structural similarity to native HDL, and could be taken up by HepG2 cells via interaction with HDL receptors in vitro. In vivo MRI studies in rats after intravenous injections of 10 µmol gadolinium per kg of recombinant HDL nanoparticles indicated that both nanoparticles could provide signal enhancement in the liver and related organs. However, different T 1 -weighted image details suggested that they participated in different cholesterol metabolism and excretion pathways in the liver. Conclusion: Such information could be highly useful to differentiate functional changes as well as anatomic differences in the liver. These cholesterol-derived contrast agents and their recombinant HDL preparations may warrant further development as a new class of contrast agents for MRI of the liver and related organs.

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“…Estos incluyen condiciones proinflamatorias y alteraciones bioquímicas. Dentro de los primeros se identifican: cirugía vascular reciente, eventos protrombóticos o estados procoagulantes, infecciones severas e hiperparatiroidismo 5,32,33 Fibrosis sistémica nefrogénica -C. Varela et al alteraciones bioquímicas destacan: acidosis metabólica, niveles elevados de hierro, calcio y/o fosfato y terapia con dosis altas de eritropoyetina 8,25,34,35 .…”

Section: Otros Factoresunclassified

Fibrosis sistémica nefrogénica: la pandemia que no fue

U¹,

Prieto-Rayo²

2014

Rev. méd. Chile

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Causal relationship between the use of gadolinium based contrast media and nephrogenic systemic fibrosis L a fibrosis sistémica nefrogénica (FSN) es una grave enfermedad iatrogénica que alarmó a la comunidad médica a partir de la descripción de la relación causal del uso de medios de contraste basados en gadolinio (MC-Gd) para resonancia magnética (RM), en pacientes con enfermedad renal avanzada, el año 2006 1 . Dado el uso masivo y universal de estos fármacos, hasta ese momento con un perfil de seguridad impecable, esta patología se perfilaba como una verdadera pandemia. Ocho años después y como un hecho casi inédito en la historia de la medicina, podemos afirmar que ha sido controlada con simples medidas de prevención 2 .Se trata de una enfermedad poco frecuente, que hasta la fecha se ha desarrollado únicamente en pacientes con disminución severa de la función renal, ya sea aguda o crónica 3 . Clínicamente simula un esclero mixedema que se desarrolla en días o semanas 4,5 . Este artículo tiene como objetivo realizar una revisión actualizada de la FSN, revalorando su relevancia como complicación iatrogénica en pacientes con disfunción renal, con especial énfasis en los factores de riesgo y su prevención y por último conocer su realidad en Chile. Historia de la FSNEsta entidad clínica fue reconocida por primera vez en el año 1997 y descrita en el año 2000 por Cowper y cols. como una enfermedad cutánea escleromixedematosa-símil en pacientes con enfermedad renal crónica (ERC) en diálisis 6 . Inicialmente se pensaba que la enfermedad afectaba sólo la piel de los pacientes, por lo que se le llamó dermatopatía fibrosante nefrogénica. Posteriormente se comprobó la afección de múltiples órganos y sistemas por lo que en el año 2005 se propuso cambiar su nombre a FSN 7 .En el año 2006, múltiples autores notaron una fuerte asociación entre la administración de MC-

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Nephrogenic Systemic Fibrosis: An Overview

Cited by 60 publications

References 18 publications

Mechanism of NSF: New evidence challenging the prevailing theory

Mechanism of NSF: New evidence challenging the prevailing theory

Recombinant high-density lipoprotein nanoparticles containing gadolinium-labeled cholesterol for morphologic and functional magnetic resonance imaging of the liver

Fibrosis sistémica nefrogénica: la pandemia que no fue

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