Coronavirus-related disease-2019 (COVID-19)-associated coagulopathy presents predominantly with thrombosis and leads to complications in close association with inflammatory process. Soluble endothelial protein C receptor (sEPCR), which is the soluble form of EPCR, reduces the anticoagulant and anti-inflammatory activity of activated protein C. The purpose of this study is to investigate the relationship between sEPCR and the laboratory parameters and thorax computed tomography (CT) findings in the course of COVID-19. Twenty-five laboratory-confirmed [reverse transcription-quantitative polimerase chain reaction (RT-qPCR) positive] and 24 clinically diagnosed (RT-qPCR negative) COVID-19 patients were enrolled in the study. Blood specimens were collected for sEPCR and haematological and biochemical parameter measurement. Thorax CT was performed to detect COVID-19 findings. These parameters from RT-qPCR positive and negative patients were then compared. Although there was no difference between the groups in terms of symptoms, the time between the onset of symptoms and the admission time was shorter in RT-qPCR positive group ( P = 0.000). sEPCR levels were significantly higher in the RT-qPCR positive group ( P = 0.011). Patients with ground-glass opacity and bilateral involvement on thorax CT have higher serum sEPCR levels ( P = 0.012 and 0.043, respectively). This study has shown for the first time that serum sEPCR levels, which is a member of coagulation cascade and has also been reported to be associated with inflammation, is higher in patients with positive RT-qPCR test and patients with GGO or bilateral involvement on thorax CT regardless of the PCR result.

Introduction:The kidneys are some of the most frequently affected organs during coronavirus disease 2019 . This multicenter study evaluated the incidence of and risk factors for acute kidney injury (AKI) in COVID-19 patients followed up in intensive care unit (ICU) and its association with mortality.Methods: Three hundred twenty-eight patients diagnosed with COVID-19 and hospitalized in ICU were included. Risk factors associated with AKI and mortality were evaluated. Results: Eighty-eight patients (27.9%) were diagnosed with AKI. AKI was significantly associated with older age, higher baseline creatinine level, lower albumin level, and coexistence of cardiovascular disease and chronic obstructive pulmonary disease. Mortality in the entire study group was significantly associated with AKI, older age, requirement of invasive mechanical ventilation, higher neutrophil level, lower lymphocyte, and albumin levels.

No abstract

No abstract

Aim: In this study, we aimed to evaluate the presence of oxidative stress in chronic kidney disease (CKD) by measuring dynamic thiol/disulphide homeostasis. Material and Method:A hundred fifty patients (57 men, 93 women) followed with a diagnosis of CKD (stages 1-5, not on dialysis) and 76 healthy, disease-free individuals (30 men, 46 women) were included in the study. Blood thiol/ disulphide homeostasis was measured by newly developed automatic and colorimetric method by Erel and Neselioglu. Results:The mean serum native thiol (p=0.001), total thiol (p=0.001) and disulphide (p=0.041) levels were lower in CKD than in the control group. No significant difference was found between the CKD and control groups in terms of disulphide/thiol, disulphide/total thiol and thiol/total thiol ratios (p>0.05). Serum native thiol and total thiol levels were correlated negatively with both BMI and serum phosphorous level while both the parameters were correlated positively with glomerular filtration rate, total protein level and albumin level. A negative correlation was found between total thiol and age. Disulphide levels were correlated positively with albumin and total protein and negatively with uric acid levels. Conclusion:Our study shows that low serum thiol levels in CKD is due to a decrease in total thiol reserve of the body and not due to conversion of thiol groups into disulphides.

The SPPB is a promising, easily applicable, inexpensive, and sensitive tool that can indicate functional decline independent of age in predialysis CKD patients and can be used in clinical practice to monitor these patients.

Background. Hypertension is one of the leading causes of cardiovascular mortality. Although the pathogenetic process involved is not yet fully understood, the disease involves endothelial damage and inflammation. Calprotectin is an inflammatory marker that rises in parallel with disease activity in conditions such as systemic inflammatory diseases, infection, and atherosclerosis. The purpose of this study was to evaluate inflammation through serum calprotectin levels in newly diagnosed primary hypertension patients. Methods. Forty-nine newly diagnosed hypertensive patients and 38 healthy adults were included in the study. Patients’ office blood pressure values, biochemical findings, and demographic characteristics were recorded. Serum calprotectin levels were measured using ELISA. Parameters affecting serum calprotectin levels and determinants of hypertension were evaluated. Results. Serum calprotectin levels were 242.8 (72.4–524) ng/mL in the control group and 112.6 (67.4–389.8) ng/mL in the hypertensive patient group, the difference being statistically significant ( p = 0.001 ). There was no correlation between serum calprotectin levels and other parameters (blood pressure values, age, gender, serum creatinine, uric acid, and calcium levels) in the hypertensive group. A lower serum calprotectin level was found to be independently related to hypertension (β = −0.009, p = 0.005 ). Serum calprotectin at a cutoff level of 128.6 ng/mL differentiated hypertensives from healthy controls with a sensitivity of 69.4% and specificity of 68.4% (AUC = 0.767). Conclusions. The results of this study were the opposite of our hypothesis that a higher calprotectin level may reflect subclinical endothelial damage in newly diagnosed hypertensive patients. Further comparative studies involving patients at different stages of hypertension may contribute to clarifying the relationship between calprotectin and hypertension. We conclude that molecular studies seem essential for understanding the place of calprotectin in hypertension-associated inflammation, a complex process.

No abstract