Glomerulonephritis
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 kid...
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| Veröffentlicht in: | The Lancet (British edition) 2005-05, Vol.365 (9473), p.1797-1806 |
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| creator | Chadban, SJ Atkins, RC |
| description | 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_str_mv | 10.1016/S0140-6736(05)66583-X |
| format | Article |
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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.</description><identifier>ISSN: 0140-6736</identifier><identifier>EISSN: 1474-547X</identifier><identifier>DOI: 10.1016/S0140-6736(05)66583-X</identifier><identifier>PMID: 15910953</identifier><identifier>CODEN: LANCAO</identifier><language>eng</language><publisher>London: Elsevier Ltd</publisher><subject>Animal models ; Biological and medical sciences ; Bone marrow ; Dialysis ; Disease management ; Epidemiology ; General aspects ; Glomerulonephritis ; Glomerulonephritis - classification ; Glomerulonephritis - immunology ; Glomerulonephritis - physiopathology ; Glomerulonephritis - therapy ; Health risk assessment ; Humans ; Hypertension ; Kidney diseases ; Kidneys ; Medical sciences ; Medical treatment ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. 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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.</description><subject>Animal models</subject><subject>Biological and medical sciences</subject><subject>Bone marrow</subject><subject>Dialysis</subject><subject>Disease management</subject><subject>Epidemiology</subject><subject>General aspects</subject><subject>Glomerulonephritis</subject><subject>Glomerulonephritis - classification</subject><subject>Glomerulonephritis - immunology</subject><subject>Glomerulonephritis - physiopathology</subject><subject>Glomerulonephritis - therapy</subject><subject>Health risk assessment</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Kidney diseases</subject><subject>Kidneys</subject><subject>Medical sciences</subject><subject>Medical treatment</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. 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Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. 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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.</abstract><cop>London</cop><pub>Elsevier Ltd</pub><pmid>15910953</pmid><doi>10.1016/S0140-6736(05)66583-X</doi><tpages>10</tpages></addata></record> |
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| identifier | ISSN: 0140-6736 |
| ispartof | The Lancet (British edition), 2005-05, Vol.365 (9473), p.1797-1806 |
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| language | eng |
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| subjects | Animal models Biological and medical sciences Bone marrow Dialysis Disease management Epidemiology General aspects Glomerulonephritis Glomerulonephritis - classification Glomerulonephritis - immunology Glomerulonephritis - physiopathology Glomerulonephritis - therapy Health risk assessment Humans Hypertension Kidney diseases Kidneys Medical sciences Medical treatment Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure Pathology |
| title | Glomerulonephritis |
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