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Kallistatin Concentration and Hypertension in Heart Transplant Recipients.
Transplantation Proceedings 2018 September
Development of arterial hypertension is to some extent related to decreased activity of the kallikrein-kinin system. This poorly understood hormonal system consists of blood proteins playing a role in the process of inflammation, coagulation, blood pressure control, and pain conduction. The system consists of kallikreins (plasma and tissue), kallistatin, kininogens, kinins (bradykinin, kallidin-lizynobradykinin), kininases (I and II), and membrane receptors of bradykinin. The aim of the study was the assessment of kallistatin in correlation to blood pressure value in heart transplant recipients.
PATIENTS AND METHODS: Kallistatin level was estimated in 131 heart transplant recipients on standard 3 drugs immunosuppressive regimens (calcineurin inhibitor, mycophenolate mofetil/mycophenolic acid, and steroids) in correlation to inflammation markers and blood pressure values. Additionally, 22 healthy volunteers served as controls. In cross-sectional study, kallistatin and catecholamine concentrations were assessed using commercially available assays.
RESULTS: Kallistatin concentration did not differ significantly among heart transplant recipients in comparison with controls; serum noradrenaline concentration was lower in the study group. In the orthotopic heart transplant group, kallistatin correlated with renal function; estimated glomerular filtration rate was calculated by Modification of Diet in Renal Disease formula (r = -0.28, P < .01; hemoglobin r = -0.19, P < .05; cholesterol level r = -0.23, P < .01; low-density lipoprotein r = 0.25, P < .01; ferritin r = 0.21, P < .05; noradrenaline r = -0.28, P < .01). No correlation with blood pressure values were revealed. In multivariate analysis, cholesterol serum level and age predicted 32% of variability of kallistatin concentration.
CONCLUSION: Kallistatin among heart transplant recipients does not seem to be the pathogenetic factor of arterial hypertension but may be involved in the development of hyperlipidemia often present in this group of patients.
PATIENTS AND METHODS: Kallistatin level was estimated in 131 heart transplant recipients on standard 3 drugs immunosuppressive regimens (calcineurin inhibitor, mycophenolate mofetil/mycophenolic acid, and steroids) in correlation to inflammation markers and blood pressure values. Additionally, 22 healthy volunteers served as controls. In cross-sectional study, kallistatin and catecholamine concentrations were assessed using commercially available assays.
RESULTS: Kallistatin concentration did not differ significantly among heart transplant recipients in comparison with controls; serum noradrenaline concentration was lower in the study group. In the orthotopic heart transplant group, kallistatin correlated with renal function; estimated glomerular filtration rate was calculated by Modification of Diet in Renal Disease formula (r = -0.28, P < .01; hemoglobin r = -0.19, P < .05; cholesterol level r = -0.23, P < .01; low-density lipoprotein r = 0.25, P < .01; ferritin r = 0.21, P < .05; noradrenaline r = -0.28, P < .01). No correlation with blood pressure values were revealed. In multivariate analysis, cholesterol serum level and age predicted 32% of variability of kallistatin concentration.
CONCLUSION: Kallistatin among heart transplant recipients does not seem to be the pathogenetic factor of arterial hypertension but may be involved in the development of hyperlipidemia often present in this group of patients.
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