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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Bomback, Andrew S. |
| Description | Author Affiliation: Bomback AS ( Division of Nephrology, Department of Medicine, Columbia University Medical Center, New York, NY. Electronic address: asb68@columbia.edu.) |
| Abstract | A major shift in our understanding of glomerular diseases is the focus on which components of the complement pathway are involved in mediating kidney injury. For example, the membranoproliferative glomerulonephritis lesion is no longer classified solely by ultrastructural findings on biopsy and is now divided into immune-complex-mediated lesions vs complement-mediated lesions. In turn, this emphasis on complement leads to interest in therapies that target complement as potential disease-modifying agents. Eculizumab, the first available anti-complement therapy, blocks at the level of C5 and has revolutionized the treatment of atypical hemolytic uremic syndrome. Whether this agent will work equally well for the far more heterogeneous entities of C3 glomerulonephritis and dense deposit disease remains unclear. Instead, newer agents that target C3 may turn out to be the most effective and specific therapy for these C3 glomerulopathies. |
| File Format | HTM / HTML |
| ISSN | 15485595 |
| e-ISSN | 15485609 |
| Journal | Advances in Chronic Kidney Disease |
| Issue Number | 2 |
| Volume Number | 21 |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2014-03-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Discipline Nephrology Complement Inactivating Agents Therapeutic Use Complement System Proteins Immunology Glomerulonephritis, Membranoproliferative Drug Therapy Hemolytic-uremic Syndrome Antibodies, Monoclonal, Humanized Atypical Hemolytic Uremic Syndrome Complement C3 Antagonists & Inhibitors Complement C5 Glomerulonephritis Receptors, Complement 3b |
| Content Type | Text |
| Resource Type | Article |
| Subject | Nephrology |
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