Involvement of cytokines and platelet-activating factor in renal pathology.

Platelet-activating factor (PAF) is a phospholipid that exhibits a wide range of biological activities as a secondary mediator of inflammation and anaphylaxis. Primary mediators of inflammation, such as interleukin-1 and tumor necrosis factor, stimulate PAF release by monocytes/macrophages, neutrophils and endothelial cells. PAF has also been implicated in cell-mediated hypersensitivity reactions. This review will focus on recent data suggesting that the local production of these mediators in glomeruli by infiltrating inflammatory cells or resident cells may influence the clinicopathological expression of glomerular disease. Results from in vitro and experimental studies suggest that these mediators alter the growth pattern of glomerular cells and the composition of secreted matrix, leading to scar formation and eventually to glomerulosclerosis.