Overexpression of chemokines, fibrogenic cytokines, and myofibroblasts in human membranous nephropathy

摘要

Overexpression of chemokines, fibrogenic cytokines, and myofibroblasts in human membranous nephropathy.BackgroundProteinuria plays a central role in the progression of glomerular disease, and there is growing evidence suggesting that it may determine tubular cell activation with release of chemokines and fibrogenic factors, leading to interstitial inflammatory reaction. However, most studies on this subject have been performed in experimental models, and the experience in human kidney biopsies has been scarce. We analyzed the tissue sections of patients with idiopathic membranous nephropathy (IMN), a noninflammatory glomerular disease that may follow a progressive disease with heavy persistent proteinuria, interstitial cell infiltration, and decline of renal function.