This review has highlighted the cytokine network which is involved in renal damage from an initial, even transient, stage to extensive glomerular and tubulointerstitial sclerosis. Studies of a variety of different proliferative glomerulonephritides have documented the prominent role of macrophages in infiltrating mesangium, subendothelial area and crescentic formation. Thus, they stimulate crescent glomerular cells to produce other cytokines and growth factors. The identification of other mediators, released by the monocytes in the interstitium, exemplifies the important role of these cells in progressive interstitial scarring through the release of fibrogenic cytokines. In addition, renal tubular cells have been found to produce a vast array of cytokines and growth factors which participate in the generation of renal interstitial scarring.
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