THE RELATIONSHIP OF MCP-1 AND TUBULOINTERSTITIAL FIBROSIS IN CHRONIC GLOMERULONEPHRITIS

THE AIM: to study relationship between MCP-1 concentrations with various clinical and morphological manifestations of inflammatory and fibrotic process in renal parenchyma in chronic glomerulonephritis.

PATIENTS AND METHODS: 80 patients with chronic glomerulonephritis were examined. We revealed nephrotic syndrome in 30 patients and nephritic syndrome in 50 patients. Mean age of patients was 35,7±13 years, among them male - 52, female – 28. Average duration of nephritis was 5,0±2,8 years. All patients was performed general examination, estimated creatinine and urea levels of blood serum, calculated glomerular filtration rate (CKD-EPI). Also determined MCP-1 level in blood serum, performed needle nephrobiopsy (optical microscopy, immunofluorescent assay, electron microscopy) with calculation of tubulointerstitial fibrosis activity.

RESULTS. Due to increase of MCP-1 level in blood serum increases fibrosis severity (r = 0,23, p<0,05). Revealed correlation relationship between MCP-1 level and urea of blood initial (before treatment) as well as on treatment and 9 month observation of the patients (r=0,56, p<0,0001, r=0,56, p<0,0001). No statistically significant relationship with creatinine level (r=0,08, p=0,5) or GFR (r=-0,04, p=0,7) was found.

CONCLUSION. Showed relationship between MCP-1 level of blood serum with tubular interstitial fibrosis severity, by that is proved the role of MCP-1-mediated mechanism of tubular interstitial fibrosis progression in chronic glomerulonephritis. Determined no influence of increased MCP-1 levels on tubular interstitial fibrosis and its components occurance which is probably an indication of the prevalence of other MCP-1-mediated mechanisms in formation of tubular interstitial fibrosis, reserving for MCP-1 only the role of tubular interstitial fibrosis progression. Revealing the relationship of MCP-1 with IgA deposits in mesangium and anses capilly loops can probably prove the role of MCP-1 in IgA-nephropathy development, but this study doesn’t show which role is it. 

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