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C3 glomerulopathy encompasses a set of diseases that impair kidney function. Common characteristics include excessive protein excretion in urine (proteinuria), blood in urine (hematuria), decreased urine production, low blood protein levels, and widespread swelling (edema). Individuals with C3 glomerulopathy often exhibit reduced levels of complement component 3 (C3), a protein in the blood.
The kidney dysfunction associated with C3 glomerulopathy typically progresses over time. Approximately 50% of those affected develop end-stage renal disease (ESRD) within a decade of diagnosis. ESRD is a serious, life-threatening condition where the kidneys are unable to adequately filter fluids and waste from the body.
Scientists recognize two primary types of C3 glomerulopathy: dense deposit disease and C3 glomerulonephritis. While both lead to similar kidney issues, dense deposit disease generally manifests earlier, often during adolescence, compared to C3 glomerulonephritis. However, the symptoms of either condition can emerge in adulthood.
Dense deposit disease, one form of C3 glomerulopathy, can also manifest with conditions unrelated to the kidneys. For instance, individuals with dense deposit disease might develop acquired partial lipodystrophy, marked by a loss of subcutaneous fat in the upper body. Furthermore, some individuals with dense deposit disease may accumulate yellowish deposits (drusen) in the retina of the eye. These deposits usually appear during childhood or adolescence and can lead to visual impairments later in life.
Most cases of C3 glomerulopathy occur randomly (sporadically) in individuals without a family history of the condition. Only a small number of families have reported multiple members with C3 glomerulopathy. However, many affected individuals have close relatives with autoimmune diseases, which arise when the immune system mistakenly attacks the body's own tissues and organs. The relationship between C3 glomerulopathy and autoimmune diseases is not completely clear.
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