Relationship of myocardial fibrosis markers with glomerular filtration rate in patients with arterial hypertension

Abstract

Abstract Funding Acknowledgements Type of funding sources: None. Background. Renal damage in arterial hypertension is considered among the typical damage variants of target organs such as heart, blood vessels and brain. One of the complications of arterial hypertension is nephrosclerosis. Developing quite gradually, arterial hypertension kidney damage goes unnoticed for a long time because clinically it does not cause the patient any discomfort. The most accessible and objective way to assess renal function is to calculate glomerular filtration rate (GFR). Tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) is a protein that is a natural inhibitor of metalloproteinases and forms complexes with matrix metalloproteinase-1 and other metalloproteinases, irreversibly inhibiting their activity. Many studies have demonstrated that TIMP-1 can be considered a serum marker of myocardial and vascular fibrosis Aim of the study. To assess the relationship between GFR and plasma TIMP-1 concentration in patients with arterial hypertension. Materials and Methods. 144 patients (87 men, 67 women) with arterial hypertension with preserved systolic function were examined, mean age was 52.45 ± 4.81 years, duration of AH was 4.82 ± 2.63 years. Calculation of GFR was carried out using the MDRD formula. Tissue matrix metalloproteinase-1 inhibitor concentrations were measured with DSL kit (USA). The reference values were 92-116 ng/ml. The patients were divided into 3 groups depending on GFR: group 1 - GFR over 90 ml/min/1.73m2 (n = 59), group 2 - GFR 60-90 ml/min/1.73m2 (n = 63), group 3 - GFR under 60 ml/min/1.73m2 (n = 22). Results. The highest level of TIMP-1 (481.9 ± 106.4 ng/ml) was found in Group 3 patients (GFR <60 ml/min/1.73m2). The level of TIMP-1 in Group 3 was statistically significantly higher than in patients of Group 1 (p < 0.0001) and Group 2 (p < 0.0001). In group 2 (GFR 60-90 ml/min/1.73m2) the level of TIMP-1 (330.5 ± 108.3 ng/ml) was higher than in group 1 (297.6 ± 104.9 ng/ml), but the difference was not statistically significant (p = 0.091). The correlation analysis revealed a negative association of plasma TIMP-1 level and GFR in patients with arterial hypertension, i.e. the higher TIMP-1, the lower glomerular filtration rate (r=-0.37, p = 0.0001). Conclusions. The increased concentration of TIMP-1 in the blood of patients with arterial hypertension is evidence of increasing fibrosis in the heart and vessels, leading to the emergence and progression of renal dysfunction.