Objective COVID-19 is a new coronavirus infectious disease. We aimed to study the characteristics of thyroid hormone levels in patients with COVID-19 and to explore whether thyroid hormone predicts all-cause mortality of severely or critically ill patients. Methods The clinical data of 100 patients with COVID-19, who were admitted to Wuhan Tongji Hospital from February 8 to March 8, 2020, were analyzed in this retrospective study. The patients were followed up for 6–41 days. Patients were grouped into non-severe illness and severe or critical illness, which included survivors and non-survivors. Multivariate Cox proportional hazards analysis was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause mortality in association with continuous and the lower two quartiles of thyroid hormone concentrations in severely or critically ill patients. Results The means of free T3 (FT3) were 4.40, 3.73 and 2.76 pmol/L in non-severely ill patients, survivors and non-survivors, respectively. The lower (versus upper) two quartiles of FT3 was associated with all-cause mortality HR (95% CI) of 9.23 (2.01, 42.28). The HR (95% CI) for all-cause mortality in association with continuous FT3 concentration was 0.41 (0.21, 0.81). In the multivariate-adjusted models, free T4 (FT4), TSH and FT3/FT4 were not significantly related to all-cause mortality. Patients with FT3 less than 3.10 pmol/L had increased all-cause mortality. Conclusion FT3 concentration was significantly lower in patients with severe COVID-19 than in non-severely ill patients. Reduced FT3 independently predicted all-cause mortality of patients with severe COVID-19.

Background: Acute kidney injury (AKI) is a common and critical complication of sepsis, and is associated with unacceptable morbidity and mortality. Current diagnostic criteria for AKI was insensitive for early detection. Novel biomarkers including cystatin C, kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), klotho and fibroblast growth factor-23 (FGF-23) can predict AKI earlier and allow immediate interventions. We aimed to determine the diagnostic performance of these biomarkers for detecting AKI in sepsis patients. Methods: This prospective observational study was conducted between May 2018 and November 2020, enrolling 162 sepsis patients eventually. The AKI was defined in accordance with 2012 KDIGO criteria and we divided patients into non-AKI (n = 102) and AKI (n = 60) groups. Serum levels of several AKI biomarkers were detected by ELISA. The relationship between biomarker levels on admission of AKI was analyzed and discrimination performances comparison were performed. Results: AKI incidence was up to 37.0% (60/162) during hospitalization. Compared with non-AKI group, both serum cystatin C, KIM-1, NGAL and FGF-23 were significantly elevated at admission in septic AKI patients. The areas under the receiver operating curves demonstrated that serum cystatin C had modest discriminative powers for predicting AKI after sepsis, and cystatin C combined with serum creatinine in the prediction of septic AKI increased the diagnostic sensitivity prominently. Conclusion: Serum cystatin C, KIM-1, NGAL and FGF-23 levels were both increased in septic AKI patients. Our study provided reliable evidence that cystatin C solely and combined with serum creatinine may accurately and sensitively predict septic AKI of patients on admission.

The new outbreak of Coronavirus Disease 2019 (COVID-19) has emerged as a serious global public health concern. A more in-depth study of blood coagulation abnormality is needed. We retrospectively analyzed 147 consecutive patients with COVID-19 who were admitted to three ICUs in Wuhan from February 9th, 2020 to March 20th, 2020. The baseline coagulation and other characteristics were studied. Our results showed that the prolonged PT, FDP, DD were positively correlated with the levels of neutrophils, ferritin, LDH, total bilirubin, multi-inflammation cytokines, and negatively correlated with the lymphocytes level (p < 0.01). The level of ATIII was significantly negatively correlated with the levels of neutrophils, ferritin, LDH, total bilirubin, IL2R, IL6 and IL8 (p < 0.05). The patients in the ARDS group had a more prominent abnormality in PT, FDP, DD and ATIII, while the patients in the AKI group had more prolonged PT, more severe FDP and DD level, more inferior ATIII and Fib level than those in the non-AKI group (p < 0.01). The value of PT, DD and FDP were positively correlated with the classical APACHE II, SOFA and qSOFA scores, while the ATIII was negatively correlated with them (p < 0.001). The high levels of PT, FDP and DD were correlated with in-hospital mortality (p < 0.001). In conclusion, blood coagulation disorder was prominent in ICU patients with COVID-19 and was correlated with multi-inflammation factors. The abnormality of blood coagulation parameters could be an adverse prognostic indicator for ICU patients with COVID-19.

Objectives: To establish an early prediction model for acute pancreatitis (AP) complicated with acute kidney injury (AKI) and evaluate its diagnostic value. Method: AP patients were recruited from the Emergency Department at Peking University People's Hospital in 2021 and stratified into AKI and control (no AKI) groups. Their clinical data were analyzed. The risk for AKI development was determined using logistic analyses to establish a risk prediction model, whose diagnostic value was analyzed using a receiver operating characteristic curve. Results: There was no significant difference in the basic renal function between the AKI (n = 79) and control (n = 179) groups. The increased triglyceride glucose index (odds ratio [OR], 2.613; 95% confidence interval [CI], 1.324–5.158; P = 0.006), age (OR, 1.076; 95% CI, 1.016–1.140; P = 0.013), and procalcitonin (OR, 1.377; 95% CI, 1.096–1.730, P = 0.006) were associated with AKI development. A model was established for prediction of AKI (sensitivity 79.75%, specificity 96.65%). The area under the receiver operating characteristic curve was 0.856 which was superior to the Ranson, Bedside Index for Severity in AP, and Acute Physiology and Chronic Health Evaluation II scores (0.856 vs 0.691 vs 0.745 vs 0.705). Conclusions: The prediction model based on age, triglyceride glucose, and procalcitonin is valuable for the prediction of AP-related AKI.

Background. Acute kidney injury (AKI) was a common and serious complication in patients with acute myocardial infarction (AMI). Novel biomarkers and therapies were deficient and imperative for AKI’s early diagnosis and therapy after AMI. α-Klotho was considered as an early biomarker and potential therapy for AKI recently. Previous studies reported that the expression of α-Klotho was decreased in AKI rodents, and supplement of α-Klotho alleviated kidney injury. Nevertheless, its effect has not been studied in patients presenting with AMI. Methods. A total of 155 consecutive diagnosed with AMI at emergency department whose eGFR >60 ml/min 1.73 m² were enrolled in this prospective observational cohort study which conducted between May 2016 and April 2019 in Peking University People’s Hospital. AKI was defined according to the KDIGO criteria in 2012. At admission, the clinical data of patients were collected and serum α-Klotho was tested by ELISA. The relationship between α-Klotho, serum creatinine, eGFR, systolic pressure, BNP, LVEF, and Hgb of AKI were analyzed and their discrimination performances were compared. The association variables were calculated (adjusted odds ratio) with a confidence interval (CI) of 95% by binary logistic regression. And, we followed up the incidence of CKD and rehospitalization after patients’ discharge in one year. Our study was approved by the ethics committee (no. 2016PHB042-01). Results. AKI incidence was 17.4% (27/155) during hospitalization. Compared to patients without AKI, the AKI group had obviously higher mortality and was more female and had higher incidence of chronic kidney disease, worse cardiac function, more cardiac complications, larger doses of diuretics, and less use of angiotensin-converting enzyme inhibitors/angiotensin receptor blocker. By contrary to previous animal experiments, we found serum α-Klotho levels were increased significantly in AKI patients (740.2 ± 306.8 vs. 419.0 ± 272.6 pg/mL, ). And, the areas under the receiver operating curves indicated serum α-Klotho levels had a superior discriminative power for predicting AKI after AMI compared with other risk factors (0.792, 95% CI, 0.706–0.878, ). Meanwhile, logistic regression model indicates extensive anterior myocardial infarction, Killip classification ≥2 grade, α-Klotho ≥516.9 pg/mL, eGFR (decrease per 10 ml/min 1.73 m²), Hgb, and nonuse of ACEI/ARB were the risk factors of AKI after AMI. Moreover, one-year follow-up presented AMI patients developed CKD had higher α-Klotho levels (739.7 ± 315.2 vs. 443.8 ± 292.5 pg/mL, ), but no significant difference in rehospitalization. And, patients with -Klotho ≥516.9 pg/ml was 6.699 times more likely to develop CKD than those with α-Klotho <516.9 pg/ml (relative risk 6.699, 95% CI 1.631–27.519, ). Conclusion. Compared with traditional cardiac and renal biomarkers, serum α-Klotho could be a more appropriate predict biomarker for AKI after AMI in patients’ eGFR >60 ml/min 1.73 m². Higher α-Klotho levels are related to the development of AKI during hospitalization and suggest a higher prevalence of CKD after discharge. By contrary to animal experiments, whether the increased expression of α-Klotho could be a protective factor secreted by AKI after AMI, is remained to be further studied.