Monocyte chemoattractant protein-1 and matrix metalloproteinase-9 in patients with type 2 cardiorenal syndrome with chronic heart failure and diabetes type 2 depending on the rate of glomerular filtration

• Published in: Zaporozhskiĭ medit͡s︡inskiĭ zhurnal no. 5; pp. 24 - 27
• Main Authors: Kravchun, P. G., Narizhnaya, A. V., Rindina, N. G.
• Format: Journal Article
• Language: English
• Published: Zaporozhye State Medical University 20.10.2014
• Subjects: Cardiorenal Syndrome; Chemokine CCL2; Chronic Heart Failure; Diabetes Mellitus; Matrix Metalloproteinase-9
• ISSN: 2306-4145; 2310-1210
• DOI: 10.14739/2310-1210.2014.5.28757

Aim. The purpose of this study was to analyze changes in MCP-1 as a marker of fibrosis and MMP-9 as an indicator of fibrolysis in patients with CRS and with a background of CHF and type 2 diabetes, depending on the level of glomerular filtration rate. Methods and results. 80 patients with CHF FC II-III with coronary heart disease (CHD) and who were treated in the cardiology department of the Kharkiv City Clinical Hospital № 27 were examined (mean age 65,13±8,66 years). The first group included 46 patients with CHF diagnosed with type 2 diabetes, the second - 34 CHF patients without diabetes. The study excluded patients with acute coronary syndrome and acute myocardial infarction. MCP-1 was determined by ELISA using a reagent kit «HUMAN MCP-1» (eBiocience,Austria). MMP-9 was determined by ELISA using a reagent kit «HUMAN MMP-9» (eBiocience,Austria). Conclusion. Progression in patients with type 2 CRS on a background of heart failure and type 2 diabetes associated with a proportional increase fibrosis marker MCP-1, indicating its involvement in tubulointerstitial renal disease. High levels of MMP-9 in patients with type 2 CRS on a background of heart failure and type 2 diabetes in the presence of GFR> 60 mL/min were detected. Reduced GFR <60 mL/min. was not accompanied by a further increase in the activity of an antifibrotic factor. MCP-1 hyperactivity resulted in a cascade of reactions of the progression of interstitial sclerosis.