Diagnostic and prognostic potential of kallistatin in assessment of liver parenchyma changes in patients with non-alcoholic fatty liver disease and hypertension kallistatin in patients with NAFLD and hypertension

Abstract

Abstract Background and aim Non-alcoholic fatty liver disease (NAFLD) is closely linked to hypertension (HT). An important issue remains the search for non-invasive tests to NAFLD detection in the early stages of liver fibrosis. The objective of the study was to evaluate the diagnostic and prognostic value of kallistatin in assessing the liver fibrosis progression in NAFLD and HT patients. Patients and methods One hundred fifteen patients with NAFLD with and without HT were examined, the control group consisted of 20 relatively healthy volunteers. Plasma kallistatin level measurement, ultrasound steatometry and elastography were performed in all patients. Results Kallistatin level was 65.03 ng mL−1 (95% CI 61.38; 68.68), 83.42 ng mL−1 (95% CI 81.89; 84.94) and 111.70 ng mL−1 (95% CI 106.14; 113.22) in patients with NAFLD and HT, isolated NAFLD and control group, respectively. There were significant differences in the liver parenchyma condition between groups. Kallistatin levels strongly inversely correlated with the attenuation coefficient and the mean liver stiffness in NAFLD and HT (rs = −0.70) and in the isolated NAFLD patients (rs = −0.56; rs = −0.68, respectively). Kallistatin level was 71.82 ng mL−1 (95% CI 70.16; 79.51) and 58.62 ng mL−1 (95% CI 55.81; 64.45) in patients with HT stage I and HT stage II, respectively (P < 0.001). Conclusions Concomitant HT in NAFLD patients is associated with greater severity of fatty and fibrotic liver changes. The course of NAFLD is accompanied by decrease in kallistatin level. Increased degree of liver steatosis and fibrosis, inflammation activity, increased BMI and increased stage of HT lead to inhibition of kallistatin activity. Kallistatin may be considered as a biomarker for progression assessment of NAFLD with or without HT.