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Josep M. Grau

Researcher at University of Barcelona

Publications -  164
Citations -  5344

Josep M. Grau is an academic researcher from University of Barcelona. The author has contributed to research in topics: Myopathy & Dermatomyositis. The author has an hindex of 36, co-authored 150 publications receiving 4677 citations. Previous affiliations of Josep M. Grau include Elsevier.

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Journal ArticleDOI

Rhabdomyolysis and Acute Kidney Injury

Xavier Bosch, +2 more
- 10 Dec 2009 - 
TL;DR: This review summarizes current views on the pathogenesis of myoglobin-induced kidney injury as well as on its prevention and treatment.
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Large vessel involvement in biopsy-proven giant cell arteritis: prospective study in 40 newly diagnosed patients using CT angiography

Sergio Prieto-González, +9 more
- 01 Jul 2012 - 
TL;DR: CTA-defined LVV occurs in two-thirds of patients with GCA at the time of diagnosis and aortic dilation is already present in 15%.
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Acute axonal Guillain-Barré syndrome with IgG antibodies against motor axons following parenteral gangliosides.

Isabel Illa, +5 more
- 01 Aug 1995 - 
TL;DR: It is concluded that exogenous ganglioside injections can be immunogenic, triggering IgG antigangliosides antibodies with specificity for motor nerve terminals, in some patients with axonal GBS such antibodies may be Marchkersor mediators of axonal involvement.
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Positron emission tomography assessment of large vessel inflammation in patients with newly diagnosed, biopsy-proven giant cell arteritis: a prospective, case–control study

Sergio Prieto-González, +11 more
- 01 Jul 2014 - 
TL;DR: FDG uptake by large vessels has a substantial sensitivity and specificity for GCA diagnosis, which is significantly higher in patients than in controls and correlated with acute-phase reactants and serum IL-6.
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A strong initial systemic inflammatory response is associated with higher corticosteroid requirements and longer duration of therapy in patients with giant-cell arteritis.

José Hernández-Rodríguez, +9 more
- 01 Feb 2002 - 
TL;DR: GCA patients with a strong initial systemic inflammatory reaction have more elevated circulating levels of IL-6 and TNFalpha, have higher and more prolonged corticosteroid requirements, and experience more disease flares during corticosterone therapy than Patients with a weak systemic acute phase response.