Infi ltration by mononuclear cells is found within the renal tissue in various types of kidney diseases. The migration of leukocytes through vessels and beyond the vascular compartment is dependent in part on small chemoattractant proteins called chemokines. All types of renal cells can produce chemokines in a cell- and stimulus-specifi c manner. Some chemokines appear to be constitutively expressed, while proinfl ammatory chemokines are expressed only in responses to specifi c stimuli. MCP-1 expression in renal tubuli is enhanced in proteinuric states, irrespective of the types of renal disease, and this increased MCP-1 expression probably contributes to renal tubular damage in proteinuric states. Expression of individual chemokines correlate with intrarenal T cells and monocyte/macrophage infi ltrates as well as with interstitial kidney damage and renal function. Experimental data and studies on human renal tissue in patients with glomerulonephritis and renal allograft rejection indicate that MCP-1, MIP-1α,β, RANTES, and IL-8 play a main role in the resolution and progression of infl ammatory processes in these cases. Renal cells and infl ammatory cells also express chemokine receptors, especially CCR-5, CCR-1, CCR-2, and CXCR3. Analysis of the immunoexpression of chemokines and chemokine receptors in renal tissue of patients with glomerulonephritis and renal allograft rejection may be helpful in evaluating the progression of
kidney disease, whereas monitoring chemokines in the urine may provide a dynamic picture of the infl ammatory state. The pharmacological regulation of chemokine and chemokine receptor expression may be a useful tool in the therapy of kidney diseases.

Keywords: Chemokines - physiology, Glomerulonephritis - immunology, Graft Rejection - immunology, Kidney Transplantation - immunology, Receptors, Chemokine - physiology, Transplantation, Homologous