Please use this identifier to cite or link to this item: https://repository.monashhealth.org/monashhealthjspui/handle/1/27330
Conference/Presentation Title: Glomerulonephritis.
Authors: Chadban S.J.;Atkins R.C.
Institution: (Chadban, Atkins) Department of Nephrology, Monash Medical Centre, Clayton, Vic., Australia (Chadban) Renal Medicine and Transplantation, Royal Prince Alfred Hospital, University of Sydney, Camperdown, NSW, Australia (Chadban) Transplantation, Royal Prince Alfred Hospital, Camperdown, NSW 2050, Australia
Presentation/Conference Date: 17-Oct-2012
Copyright year: 2005
Publisher: Elsevier B.V.
Elsevier Limited (32 Jamestown Road, London NW1 7BY, United Kingdom)
Publication information: Lancet. 365 (9473) (pp 1797-1806), 2005. Date of Publication: 21 May 2005.
Journal: The Lancet
Abstract: The term glomerulonephritis encompasses a range of immune-mediated disorders that cause inflammation within the glomerulus and other compartments of the kidney. Studies with animal models have shown the crucial interaction between bone-marrow-derived inflammatory cells and cells intrinsic to the kidney that is both fundamental and unique to the pathogenesis of glomerulonephritis. The mechanisms of interaction between these cells and the mediators of their coordinated response to inflammation are being elucidated. Despite these pathophysiological advances, treatments for glomerulonephritis remain non-specific, hazardous, and only partly successful. Glomerulonephritis therefore remains a common cause of end-stage kidney failure worldwide. Molecule-specific approaches offer hope for more effective and safer treatments in the future.
DOI: http://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1016/S0140-6736%2805%2966583-X
PubMed URL: 15910953 [http://www.ncbi.nlm.nih.gov/pubmed/?term=15910953]
ISSN: 0140-6736
URI: https://repository.monashhealth.org/monashhealthjspui/handle/1/27330
Type: Conference Paper
Appears in Collections:Conferences

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