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Childhood-onset systemic lupus erythematosus (i.e., cSLE), also termed juvenile-onset systemic lupus erythematosus, juvenile systemic lupus erythematosus, and pediatric systemic lupus erythematosus, is a form of the chronic inflammatory and autoimmune disease, systemic lupus erythematosus (i.e., SLE), that develops in individuals up to 18 years old. [1]
The proliferative forms of lupus nephritis are associated with a higher risk of progression to end stage kidney disease. [21] Black and Hispanic people with lupus nephritis are more likely to present with severe disease at initial presentation (with more proteinuria and more extensive histopathologic changes) and progress to end stage kidney ...
Mesangial proliferative glomerulonephritis of Lupus nephritis, Class II is also noted by mesangial hypercellularity and matrix expansion. Microscopic haematuria with or without proteinuria may be seen in Class II Lupus nephritis. Hypertension, nephrotic syndrome, and acute kidney injury are very rare at this stage. [6]
Cyclophosphamide (CP), also known as cytophosphane among other names, [3] is a medication used as chemotherapy and to suppress the immune system. [4] As chemotherapy it is used to treat lymphoma , multiple myeloma , leukemia , ovarian cancer , breast cancer , small cell lung cancer , neuroblastoma , and sarcoma . [ 4 ]
The cause of diffuse proliferative glomerulonephritis (DPGN) depends on the severity of the disease. DPGN is a secondary disease, in that a disease that a patient already has causes DPGN to occur. The most common associated disease of DPGN is severe systemic lupus erythematosus(SLE). [4] Specifically, Lupus nephritis class IV. [5]
When treatment with DMARDs fails, cyclophosphamide or steroid pulse therapy is often used to stabilise uncontrolled autoimmune disease. Some severe autoimmune diseases are being treated with bone marrow transplants in clinical trials, usually after cyclophosphamide therapy has failed.
Type II is today more commonly known as dense deposit disease (DDD). [5] Most cases of dense deposit disease do not show a membranoproliferative pattern. [6] It forms a continuum with C3 glomerulonephritis; together they make up the two major subgroups of C3 glomerulopathy.
Acute proliferative glomerulonephritis is a disorder of the small blood vessels of the kidney.It is a common complication of bacterial infections, typically skin infection by Streptococcus bacteria types 12, 4 and 1 but also after streptococcal pharyngitis, for which it is also known as postinfectious glomerulonephritis (PIGN) or poststreptococcal glomerulonephritis (PSGN). [4]
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