Objective: to study the effect of the total expression of vascular endothelial growth factor A (VEGF A), tissue growth factor β1 (TGF-β1) and monocytic chemoattractant factor 1 (MCP-1) on the course of glomerulonephritis.Material and methods: the study was a prospective (12-month) open comparative clinical and morphological study with the inclusion of 75 patients aged 18 to 75 years (males - 52, females - 23) with glomerulonephritis in the acute stage. All patients were initially examined, including assessment of clinical, laboratory and instrumental parameters, including puncture nephrobiopsy. In addition to the standard, sections of biopsies were stained with labeled antibodies to VEGF A, TGF-β1 and MCP-1 to assess their expression in kidney tissue. After 12 months, the development of remission of glomerulonephritis, parameters of the general analysis of urine, creatinine, urea, uric acid of blood, calculation of GFR were evaluated.Results: it was found that the severity of the total expression of MCP-1+VEGF-A+TGFß1 is observed to a greater extent in hematuric forms of glomerulonephritis, occurring without changes in the level of blood albumin. The same follows from the results demonstrating the relationship of the total expression of MCP-1+VEGF-A+TGFß1 with morphological manifestations more characteristic of nephritic forms of glomerulonephritis (IgA deposits, mesangial hypercellularity). The increased expression of the studied factors has shown its influence on the development of fibrosis and thickening of the walls of renal vessels, glomerular fibrosis and interstitium, reflecting the whole complex of reparative remodeling of renal tissue in the inflammatory process. The effect of the total expression of MCP-1+VEGF-A+TGFß1 on the further course of glomerulonephritis, accompanied by the progression of the disease in the form of a decrease in GFR after 12 months of observation of patients, was revealed.Conclusions: an increase in the total expression of MCP-1+VEGF-A+TGFß1 in hematuric forms of glomerulonephritis indicates the role of these factors in the development of the inflammatory process to a greater extent in these forms of the disease. It was found that an increase in the severity of the total expression of MCP-1+VEGF-A+TGFß1 is associated with manifestations of renal remodeling in glomerulonephritis. It has been shown that an increase in the severity of the total expression of MCP-1+VEGF-A+TGFß1 is accompanied by an increase in the likelihood of a rapid decrease in renal function in glomerulonephritis at 12-month follow-up.

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BACKGROUND. To date, the study of the factors involved in the glomerular-tubular pathological connections leading to damage to the tubulointerstitial tissue is one of the topical areas of nephrology. THE AIM: to study the effect of MCP-1 in the development of tubulointerstitial fibrosis as a factor in the irreversible progression of chronic renal failure. PATIENTS ANDMETHODS. Prospective observation and retrospective analysis of case histories were carried out, which included a total of 75 patients with primary chronic glomerulonephritis. RESULTS. The average age of the patients was 36.7 ± 12.3 years, of which 52 were males, 23 were women. The average length of service in a nephrological disease was 3.0 [1.0; 5.0] years. The calculated GFR values are 87.3 ± 31.2 ml / min / 1.73 m2. In the general population, the moderate degree of MCP-1 expression, estimated at 2 points, was 35 %, pronounced expression was found in 25 % of the respondents. In the mesangium of the glomeruli and in macrophages, the expressed degree of MCP-1 expression was 20 % and 16 %, respectively, which characterizes MCP-1 as a marker produced by resident cells. When studying the relationship of MCP-1 in blood with clinical parameters, a correlation was found with the values of total protein (Rs= –0.43; p <0.05), with erythrocyturia (Rs= –0.28; p <0.05), as well as with an albumin level (Rs= –0.5; p <0.05), which indicates the role of MCP-1 in the development of nephritic forms of glomerulonephritis. Depending on the severity of MCP-1 expression in biopsy specimens, the incidence of focal tubulointerstitial fibrosis with MCP-1 expression estimated at 1 point was 13.3 %, 2 points – 14.3 %, 3 points – 44.0 %. The revealed significant correlation between the serum level of MCP-1 and the severity of tubulointerstitial fibrosis confirms the MCP-1-mediated mechanism of progression of CKD. CONCLUSION. The relationship of serum and tissue forms of MCP-1 with the progression of tubulointerstitial fibrosis in chronic glomerulonephritis has been demonstrated. MCP-1-induced mesangial cell plays a critical role in the development of renal tubular damage, and its increased expression is associated with progressive tubulointerstitial fibrosis and decreased renal function.