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Complement 3 glomerulopathy affects the tiny filtering units in your kidneys. If you have C3G, you may notice changes in your pee, swelling, joint pain, vision problems and fatigue. You may feel a wide range of emotions as you accept your diagnosis and adjust to how C3G affects your life. Give yourself time and space to learn about C3G and your.


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C3 glomerulopathy (glo-mer-u-lop-a-thy) is a disease that affects how well your kidneys work. It causes damage to structures in the kidneys called glomeruli (glo-mer-yuh-lahy). Glomeruli help the kidneys filter toxins out of your blood. Kidney damage from C3 glomerulopathy can be serious and lead to kidney failure.


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A C3 complement blood test measures the levels of a specific type of protein in your blood (C3 proteins). As part of your immune system, C3 proteins destroy microbes (germs) that can make you sick. Sometimes, C3 proteins launch an attack against healthy cells by mistake. The results of this blood test give your healthcare provider information.


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C3G is a disease of the complement system. - The complement system is part of the immune system, and for that reason, immunosuppressants (drugs that "calm down" the immune system) have been used to treat C3G. These drugs include: Glucocorticoids (corticosteroids, steroids) Rituximab. Cyclophosphamide. Mycophenolate mofetil (MMF)


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Along with these signs of C3G, other symptoms of kidney failure include nausea, vomiting, lack of appetite, trouble sleeping, dry and itchy skin, a metallic taste in your mouth, and muscle cramps.


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In recent years, a substantial body of experimental and clinical work has been devoted to C3 glomerulopathy and Ig-mediated membranoproliferative glomerulonephritis. Despite the rapid accumulation of data, several uncertainties about these 2 rare forms of nephropathies persist. They concern their pathophysiology, classification, clinical course, relevance of biomarkers and of pathology.


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C3 glomerulopathy (C3G) is a complex ultra-rare complement-mediated renal disease caused by uncontrolled activation of the complement alternative pathway (AP) in the fluid phase (as opposed to cell surface) that is rarely inherited in a simple mendelian fashion. C3G affects individuals of all ages, with a median age at diagnosis of 23 years. Individuals with C3G typically present with.


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The results suggested that when the serum albumin <30 g/L, C3 had a protective effect on outcomes in patients with anti-GBM disease, and serum albumin could modify the relationship between C3 and kidney failure. In addition, the protective role in outcomes of C3 was observed only in patients without oliguria/anuria.