Thelansis

 Glomerulonephritis (GN) is a subgroup of renal diseases caused by immune-mediated damage to the basement membrane, mesangium, or capillary endothelium. This leads to symptoms such as hematuria, proteinuria, and azotemia. GN can be classified as acute or progressive, potentially leading to chronic kidney and end-stage renal disease. There are several ways to classify GN based on clinical presentation, including the nephrotic or nephritic syndrome, or based on the underlying immune processes, with five forms: immune-complex, pauci-immune, anti-glomerular basement membrane, monoclonal Ig, and C3 glomerulopathy. Regardless of the classification, the pathogenesis of GN is immune-mediated and involves both humoral and cell-mediated pathways. The following inflammatory response can cause fibrosis and depends on the target of immune-mediated damage, which can vary based on the type of GN. The underlying mechanisms activate the complement system and coagulation cascade, releasing pro-inflammat

 Glomerulonephritis (GN) is a subgroup of renal diseases caused by immune-mediated damage to the basement membrane, mesangium, or capillary endothelium. This leads to symptoms such as hematuria, proteinuria, and azotemia. GN can be classified as acute or progressive, potentially leading to chronic kidney and end-stage renal disease. There are several ways to classify GN based on clinical presentation, including the nephrotic or nephritic syndrome, or based on the underlying immune processes, with five forms: immune-complex, pauci-immune, anti-glomerular basement membrane, monoclonal Ig, and C3 glomerulopathy. Regardless of the classification, the pathogenesis of GN is immune-mediated and involves both humoral and cell-mediated pathways. The following inflammatory response can cause fibrosis and depends on the target of immune-mediated damage, which can vary based on the type of GN. The underlying mechanisms activate the complement system and coagulation cascade, releasing pro-inflammat