Background: Whether the patients with coronavirus disease 19 (COVID-19) infected by severe acute respiratory syndrome (SARS)-CoV-2 would commonly develop acute kidney injury (AKI) is an important issue worthy of clinical attention. This study aimed to explore the effects of SARS-CoV-2 infection on renal function through analyzing the clinical data of 116 hospitalized COVID-19-confirmed patients. Methods: One hundred sixteen COVID-19-confirmed patients enrolled in this study were hospitalized in the Department of Infectious Diseases, Renmin Hospital of Wuhan University from January 14 to February 13, 2020. The recorded information includes demographic data, medical history, contact history, potential comorbidities, symptoms, signs, laboratory test results, chest computer tomography scans, and treatment measures. SARS-CoV-2 RNA in 53 urine sediments of enrolled patients was detected by real-time reverse transcription-polymerase chain reaction. Results: Twelve (10.8%) patients showed mild increase of blood urea nitrogen or creatinine (<26 μmol/L within 48 h), and 8 (7.2%) patients showed trace or 1+ albuminuria in 111 COVID-19-confirmed patients without chronic kidney disease (CKD). All these patients did not meet the diagnostic criteria of AKI. In addition, 5 patients with CKD who were undergone regular continuous renal replacement therapy (CRRT) before admission were confirmed infection of SARS-CoV-2 and diagnosed as COVID-19. In addition to therapy for COVID-19, CRRT was also applied 3 times weekly during hospitalization for these 5 patients with CKD. In the course of treatment, the renal function indicators showed stable state in all 5 patients with CKD, without exacerbation of CKD, and pulmonary inflammation was gradually absorbed. All 5 patients with CKD were survived. Moreover, SARS-CoV-2 RNA in urine sediments was positive only in 3 patients from 48 cases without CKD, and 1 patient had a positive for SARS-CoV-2 open reading frame 1ab from 5 cases with CKD. Conclusion: AKI was uncommon in COVID-19. SARS-CoV-2 infection does not result in AKI, or aggravate CKD in the COVID-19 patients.

This study aims to summarize the clinical characteristics of death cases with COVID-19 and to identify critically ill patients of COVID-19 early and reduce their mortality. Methods: The clinical records, laboratory findings and radiological assessments included chest X-ray or computed tomography were extracted from electronic medical records of 25 died patients with COVID-19 in Renmin Hospital of Wuhan University from Jan 14 to Feb 13, 2020. Two experienced clinicians reviewed and abstracted the data. Results: The age and underlying diseases (hypertension, diabetes, etc.) were the most important risk factors for death of COVID-19 pneumonia. Bacterial infections may play an important role in promoting the death of patients. Malnutrition was common to severe patients. Multiple organ dysfunction can be observed, the most common organ damage was lung, followed by heart, kidney and liver. The rising of neutrophils, SAA, PCT, CRP, cTnI, D-dimer, LDH and lactate levels can be used as indicators of disease progression, as well as the decline of lymphocytes counts. Conclusions: The clinical characteristics of 25 death cases with COVID-19 we summarized, which would be helpful to identify critically ill patients of COVID-19 early and reduce their mortality.

confirmed and 1368 patients have died from the disease. However, the clinical characteristics of the dyed patients were still not clearly clarified. This study aims to summarize the clinical characteristics of death cases with COVID-19 and to identify critically ill patients of COVID-19 early and reduce their mortality. MethodsThe clinical records, laboratory findings and radiologic assessments included chest X-ray or computed tomography were extracted from electronic medical records of 25 died patients with COVID-19 in Renmin Hospital of Wuhan University from Jan 14 to Feb 13, 2020. Two experienced clinicians reviewed and abstracted the data. FindingsThe mean age of the dead was 71.48 ± 12.42 years, the average course of the disease was 10.56 ± 4.42 days, all patients eventually died of respiratory failure. All of those who died had underlying diseases, the most common of which was hypertension (16/25, 64%), followed by diabetes (10/25, 40%), heart diseases (8/25, 32%), kidney diseases (5/25, 20%), cerebral infarction (4/25, 16%), chronic obstructive pulmonary disease (COPD, 2/25, 8%), malignant tumors (2/25, 8%) and acute pancreatitis (1/25, 4%). The most common organ damage outside the lungs was the heart, followed by kidney and liver. In the patients' last examination before death, white blood cell and neutrophil counts were elevated in 17 patients (17/25, 68%) and 18 patients (18/25, 72%), lymphocyte counts were decreased in 22 patients (22/25, 88%). Most patients' PCT, CRP and SAA levels were elevated, the percentages were 90.5% (19/21), 85% (19/20) and 100% (21/21) respectively. The levels of the last test of neutrophils (15/16, 93.8%), PCT (11/11, 100%), CRP (11/13, 84.6%), cTnI (8/9, 88.9%), D-Dimer (11/12, 91.6%) and LDH (9/9, 100%) were increased as compared to the first test, while the levels of lymphocytes were decreased (14/16, 87.5%).Interpretation The age and underlying diseases (hypertension, diabetes, etc.) were the most All rights reserved. No reuse allowed without permission. author/funder, who has granted medRxiv a license to display the preprint in perpetuity.

Background Hyperhomocysteinemia is implicated in the pathogenesis of various liver diseases. In this study, the effects of S-adenosylmethionine (SAM) on hyperhomocysteinemia and steatosis with ethanol-induced liver injury in rats were examined and their mechanisms were explored. Methods Forty-eight female Sprague-Dawley rats were randomly divided into four groups as control, model, lowdose, and high-dose SAM groups. Except the control group, all rats were fed high-fat-containing diet plus ethanol and fish oil gavaged for 8 weeks. SAM was administered by intraperitoneal injection after the 4 weeks' exposure of ethanol. Serum homocysteine (Hcy), alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG), tumor necrosis factor a (TNF-a), and transforming growth factor b1 (TGF-b1) levels were determined. The contents of liver malondialdehyde (MDA) and glutathione (GSH) were assayed. Liver histology was also examined. The expressions of TNF-a and TGF-b1 mRNAs in the liver were detected by the reverse transcriptase-polymerase chain reaction assay. Results Compared with the control group, the model group rats developed marked liver damage, accompanied by an increase in Hcy, ALT, AST, TC, TG, TNF-a, TGFb1, and MDA levels. However, the levels of GSH were decreased. These responses were associated with the increased expression of TNF-a and TGF-b1 mRNAs in the livers, as well as the existence of hepatocellular necrosis and neutrophil infiltration in the livers. In treatment groups, SAM provided significant protection from the liver injury induced by alcohol, resulting in a decrease in serum TNFa, TGF-b1 levels, lipid peroxidation, and the expressions of TNF-a and TGF-b1 mRNAs in the livers, as well as an increase in GSH levels. However, no statistical difference was observed in these parameters between the two different dose treatment groups. In the study, SAM did not affect plasma total homocysteine (tHcy) levels significantly. Conclusion SAM prevents alcohol-induced liver injury in rats by reducing liver lipid peroxidation, anti-inflammation, and antihyperplasia. In addition, it does not affect the plasma tHcy levels.

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