A potential mechanism by which obesity could promote hypertension and kidney diseases is through accumulation of adipose tissue in the renal sinus (RS). The aim of the study was to quantify RS and abdominal adipose tissue volumes and to evaluate serum kidney injury molecule (sKIM)-1 and fibroblast growth factor (FGF)-21 association with different adipose tissue compartments. The cross-sectional study included 280 and follow-up study-40 asymptomatic participants; aged 38.30±4.10. For all study participants computed tomography examination was performed, sKIM-1 and FGF-21 levels were measured. The results indicated asymmetrical deposition of adipose tissue into the RS even after corresponding kidney volume adjustment. The cross-sectional and the follow-up studies showed that sKIM-1 level was positively associated with RS adipose tissue volume increase for both genders. FGF-21 was positively associated with RS and retroperitoneal adipose tissue amount. Regardless of gender adipose tissue in RS accumulates asymmetrically-the left RS accumulates a significantly higher amount of adipose tissue. Thus, primarily RS adipose tissue effects should be assessed on the left kidney. Accumulation of adipose tissue in the RS is related with the visceral adipose amount, KIM-1 and FGF-21 concentration increase in the blood serum.

The aim of this study was to test the hypothesis that exercise would induce inflammatory response characterized by increased pro‐inflammatory cytokines – interleukin‐6 (IL‐6) and tumour necrosis factor‐α (TNF‐α), adhesion molecule, matrix metalloprotease‐9 (MMP‐9) and myeloperoxidase (MPO) levels. Additional aim was to elucidate the possible source of maximal exercise‐induced increase in MMP‐9 concentration. To examine our hypothesis, 26 professional male ice hockey players [age 25 ± 1 (mean ± SEM) years; BMI 25.8 ± 0.4 kg/m²] performed an incremental bicycle test until exhaustion, when maximal oxygen consumption was recorded. Venous blood samples were collected 30 min before and 2 min after exercise. There was an increase in the count of leucocytes (8.7 ± 1.8 versus 5.7 ± 1.3 × 10⁹ cells per l) and IL‐6 (1.24 ± 0.17 versus 0.69 ± 0.13 pg/ml), MPO (72 ± 7 versus 50 ± 4 ng/ml) and MPP‐9 (139 ± 9 versus 110 ± 6 ng/ml) concentrations (P < 0.05) comparing post‐ and pre‐exercise levels. Maximal exercise‐induced increase in MPO correlated with the increases in IL‐6 (P < 0.05, R = 0.54) and MMP‐9 (P < 0.01, R = 0.62) concentrations. Furthermore, increase in IL‐6 correlated with the increase in MMP‐9 concentrations (P < 0.05, R = 0.60). Maximal exercise induces an inflammatory response characterized by leucocytosis and increased IL‐6, MPO and MMP‐9 concentrations. Correlations between increased MPO (marker of neutrophils degranulation) and both increased IL‐6 and MMP‐9 concentrations may suggest that neutrophils could be the main source of these inflammatory biomarkers during maximal exercise. Furthermore, correlation between increases in serum IL‐6 and MMP‐9 concentrations may suggest that IL‐6 could exert modulatory effects on MMP‐9 release during maximal exercise.

Background and objectives: Mechanical stress is currently considered as the main factor promoting calcific aortic valve stenosis (AS) onset. It causes endothelial damage and dysfunction. The chronic inflammatory process causes oxidative stress. Oxidative stress-induced high-density lipoprotein cholesterol (HDL-C) dysfunction is an important component of the development of AS. The aim of the study was to evaluate the role of HDL-C in AS patients in three severity grades and in relation to the biomarkers of oxidative stress, thioredoxin reductase 1 (TrxR1) and myeloperoxidase (MPO). Materials and Methods: 18 patients with mild, 19 with moderate. and 15 with severe AS were included in the study, and 50 individuals were enrolled in the control group. Stenosis severity was determined by echocardiography. The TrxR1 and MPO were analyzed by ELISA, and HDL-C by commercially available tests. Data were analyzed using GraphPad Prism 8. Results: HDL-C in AS patients vs. control substantially decreases and this decline was observed in all three AS severity groups: mild (p = 0.018), moderate (p = 0.0002), and severe (p = 0.004). In both the control and the stenosis group, the HDL-C was higher in women than in men. In comparison to control, the HDL-C level was lower in the AS group, and more pronounced in women (p = 0.0001) than in men (p = 0.049). A higher TrxR1 level was observed in patients with mild (p = 0.0001) and severe AS (p = 0.047). However, a clear correlation between TrxR1 and HDL-C was not obtained. Analysis of MPO showed differences in all severity grades vs. control (p = 0.024 mild stenosis; p = 0.002 moderate stenosis; p = 0.0015 severe stenosis). A negative correlation (p = 0.047; rp = −0.28) was found between MPO and HDL-C, which confirms the adverse effects of MPO resulting in HDL-C dysfunction. Conclusions: In this study, we justified HDL-C level association with AS development process. The results unequivocally substantiated the association between HDL-C and AS in all severity grades in women, but only in moderate AS for men, which we explained by the small number of men in the groups. The obtained correlation between the HDL-C and MPO levels, as well as the concurrent decrease in the HDL-C level and increase in the TrxR1 level, indicate in general an HDL-C association with oxidative stress in AS patients.

Sepsis is among the leading causes of critical illness worldwide. It includes physiologic, pathologic, and biochemical abnormalities, induced by infection. Novel methods for recognizing a dysregulated inflammatory response and predicting associated mortality must be developed. Our aim was to investigate biomarkers that characterize a pro-inflammatory and anti-inflammatory response in patients with fever by comparing predictive validity for sepsis. 165 patients with fever were enrolled in this study, 55 of them had sepsis according to pSOFA criteria. All patients had blood samples drawn at the time of inclusion and after 24 h. CRP, PCT and also IL-6, IL-8 and sFAS levels were significantly higher in patients with sepsis. The AUC of CRP to predict sepsis was 0.799, all the other biomarkers had AUC’s lower than that. Cytokines, when used as a single marker, did not show a significant diagnostic performance We analyzed various models of biomarker combinations. CRP combined with sFAS showed increase in sensitivity in predicting sepsis (88% vs. 83%). The highest AUC was achieved, when CRP, IL-6, sFAS and sVCAM-1 markers were combined 0.830 (95% CI 0.762–0.884) with a sensitivity of 70% and specificity of 84%. vs. 0.799 for CRP alone.