[The role of monocyte chemotactic peptide (MCP-1) in chronic renal allograft rejection].

Monocyte chemotactic peptide-1 (MCP-1) plays a key role as a mediator of inflammatory infiltration, mainly composed with macrophages. Experimental studies showed that macrophages and their products are pathogenetic factors of chronic renal graft rejection (ch.g.r.). The objective of the present study was to determine the role of MCP-1 in the pathogenesis of human renal ch.g.r. Examined were 34 patients with ch.g.r. (Group I), 50 patients with a stable allograft function (Group II), and 25 healthy subjects (control). Serum and urine levels of MCP-1 were measured by ELISA. The serum level of MCP-1 was found to be higher in transplant patients, than in control group, but this difference was not significant. The serum level of MCP-1 showed a correlation with concentration of triglycerides in both transplant patient groups. This may results from overproduction of MCP-1 through cells of vascular wall affected by hyperlipidemic microenvironment. Considering the lack of relationship between the serum and urine levels of MCP-1, I decided attribute the urine levels of MCP-1 to the secretion through the infiltrating cells and through the kidney cells. In patients with ch.g.r. the urine levels of MCP-1 were significantly higher p < 0.001) than in patients with a stable graft function and control group. MCP-1 levels were particularly high (> 2000 pg/mg creatinine) in patients with enhanced dynamics of ch.g.r. The MCP-1 levels were higher in those patients whose biopsies described cellular infiltration (1385 + 820 pg/mg creatinine vs 680 + 280 pg/mg creatinine). The urine level of MCP-1 showed a correlation with concentration of serum creatinine, cholesterol, level of proteinuria and with arterial pressure in ch.g.r. patients. Increased urine levels of MCP-1 and correlation of MCP-1 with the activity of progressive deterioration of the graft function suggest important role of this chemokine in the pathogenesis of ch.g.r., possibly by activating macrophages and by stimulating their influx into the vascular wall, glomeruli and interstitial tissue. Relationship of urinary MCP-1 excretion with arterial hypertension and lipid disorder suggest that the effect of those risk factors for a progressive deterioration of graft function manifest on the molecular level by affecting the generation of MCP-1.