Understanding the Mechanisms of Proteinuria: Therapeutic Implications
Figure 4
Molecules involved in potential mechanisms in the development of proteinuria-induced renal tubulointerstitial injury. The tubulointerstitial damage induced by persistent proteinuria in glomerular diseases is due to the concomitant injuring effects of multiple cellular and biochemical events. Specific proteins have been shown to stimulate production of cytokines, chemotactants, and matrix proteins by tubular epithelial cells, which may stimulate interstitial inflammation and scarring. Abbreviations: MHC: major histocompatibility complex; ICAM-1: intercellular adhesion molecule 1; MCP1: monocyte chemotactic protein-1; TNF-: tumor necrosis factor-alpha; FGF: fibroblast growth factor; TGF-: transforming growth factor beta; PDGF: platelet-derived growth factor; ET-1: endothelin; RANTES: regulated upon activation, normal T-cell expressed and secreted; ECM: extracellular matrix. (Adapted from [99]).
