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| ==Classification== | | ==Classification== |
| ==Pathophysiology== | | ==Pathophysiology== |
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| *The generation of the classical pathway of complement occurs by the immune complex.
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| *Immune complex glomerulonephritis, such as lupus, frequently activates the classical pathway by binding C1q to the antibody-containing immune complexes, which can result in glomerular deposition of immunoglobulins, C3, C1q, and C4d.
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| *C4 activation can also ensue by the lectin pathway of complement.
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| *In the lectin pathway, mannose-binding lectins bind to mannose located on the carbohydrates structure or microbial membranes, which activate C4 (and therefore bypass C1q), resulting in the formation of the classical pathway C3 convertase.
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| *Glomerular C4d, is a split creation of C4, is suggestive of C4 activation as a result of activation of either the lectin pathway of the classical complement pathway.
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| *In C4 glomerulopathy, bright streak for C4d indicates mesangial/capillary wall deposits. C4d deposits are present in a few cases of IgA nephropathy and post-streptococcal glomerulonephritis.
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| ==Differential Diagnosis== | | ==Differential Diagnosis== |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Ali Poyan Mehr, M.D. [2]; Associate Editor(s)-in-Chief: Olufunmilola Olubukola M.D.[3]
Overview
Historical Perspective
Classification
Pathophysiology
Differential Diagnosis
Causes
Risk Factors
Screening
Epidemiology and Demographics
Natural History, Complications, and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Imaging Studies
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Prevention
References
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