Metabolites and metabolomics in COVID-19

Metabolomics is a comprehensive approach for identifying, quantifying, and characterizing entire metabolites in a biological system using a high-throughput technique. Metabolomics has great potential in discovering biochemical pathways and pathway interactions, disease diagnosis, and biomarker discovery. Viral infections induce changes in the host cell metabolism resulting in cellular reprogramming. In COVID-19, the dysregulation of host metabolites has been implemented in various aspects including diagnosis and management. This chapter summarizes various applications of metabolites and metabolomics approaches in COVID-19. © 2023 Elsevier Inc. All rights reserved.

SARS-CoV-2 cellular tropism and direct multiorgan failure in COVID-19 patients: Bioinformatic predictions, experimental observations, and open questions.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that causes coronavirus disease 2019 (COVID-19), has led to an unprecedented public health emergency worldwide. While common cold symptoms are observed in mild cases, COVID-19 is accompanied by multiorgan failure in severe patients. Organ damage in COVID-19 patients is partially associated with the indirect effects of SARS-CoV-2 infection (e.g., systemic inflammation, hypoxic-ischemic damage, coagulopathy), but early processes in COVID-19 patients that trigger a chain of indirect effects are connected with the direct infection of cells by the virus. To understand the virus transmission routes and the reasons for the wide-spectrum of complications and severe outcomes of COVID-19, it is important to identify the cells targeted by SARS-CoV-2. This review summarizes the major steps of investigation and the most recent findings regarding SARS-CoV-2 cellular tropism and the possible connection between the early stages of infection and multiorgan failure in COVID-19. The SARS-CoV-2 pandemic is the first epidemic in which data extracted from single-cell RNA-seq (scRNA-seq) gene expression data sets have been widely used to predict cellular tropism. The analysis presented here indicates that the SARS-CoV-2 cellular tropism predictions are accurate enough for estimating the potential susceptibility of different cells to SARS-CoV-2 infection; however, it appears that not all susceptible cells may be infected in patients with COVID-19.

Disease Severity and Pathophysiology of COVID-19 in Type 2 Diabetes Mellitus Patients

The world is facing COVID 19 pandemic which has created a chaos among the mankind. It has created a huge burden in the health care facilities. COVID 19 disease is caused by emerging mutants of Severe acute respiratory syndrome corona virus 2(SARS CoV-2). The virus is highly contagious and infects through the respiratory route. It invades the respiratory tract mainly the lungs causing pneumonia. Patient usually presents with fever, nonproductive cough, breathlessness, myalgia and fatigue. Severe cases can rapidly progress to acute respiratory distress syndrome and multi organ failure, death may occur due to complication. Furthermore early identification and diagnosis of high risk cases like hypertension and diabetes and prevention of the serious complication in them help in decreasing the burden on the intensive healthcare facilities. As we know the doctor to patient ratio in a developing country like India is very low, thus it becomes very important for the doctor to know the impending risk in his/her patients. So we have made an effort to understand the pathophysiology involved, the treatment protocols followed in patient of type 2 diabetes mellitus with COVID 19 infection. Regular monitoring of the blood sugar levels during the hospital stay becomes important to detect the red flags of complication. Assessment of the severity of the disease and prognosis in type 2 diabetes mellitus patient and non-diabetics has been contrasted. This might help provide better intensive care management for all the patients at early stage and decrease the morbidity and mortality in the COVID 19 patients. We have tried to unfold the relationship between two hyper inflammatory diseases that is type 2 diabetes mellitus which is chronic inflammatory condition and SARS CoV 2 which causes acute inflammation. It should be noted that both the diseases have tendency to cause multi organ dysfunction and failure.

Clinical features and risk predictor markers in COVID-19 patients in correlation with disease severity and comorbidities- A data-based retrospective study

Background: COVID-19 infection displays a highly heterogeneous spectrum of severities. Laboratory findings are pivotal cues to assess disease severity and aid in retarding/ reversing disease progression. This study aims to identify the haematological, biochemical, and immunological specifics of COVID-19 patients with varying severity and associated comorbidities. Methods: This retrospective study recruited a total of 192 RT PCR confirmed COVID-19 patients. Data on laboratory findings, clinical characteristics, treatment, and hospital stay were obtained and analysed. Results: The patients were grouped into mild, moderate, and severe categories based on disease severity. 96 patients had mild disease, 31 were classified as having moderate COVID-19, and 67 patients had severe COVID-19. 39.58% of the patients were females. The overall death rate among admitted COVID-19 patients is observed to be 19.02%, sepsis and multi-organ failure as the most common cause. The variation in laboratory variables and comorbidities as CAD, CKD, HTN, DM strongly correlate with the severity and increases with the age factor. Pre-existing chronic liver disease emerged to be a comorbidity of significance for acquiring severe COVID-19. Conclusion: Presence of comorbidities, advanced age and male sex emerged as important risk factors while derangements in thrombo-inflammatory markers and haematological indices might be crucial predictors of disease progression. Thromboembolism or superinfection induced sepsis, and multi-organ failure emerged as leading contributors to mortality. High-risk patterns in thrombo inflammatory and immunohematological markers allow for early detection of the disease progression and aid in the institution of personalized intensive therapeutic interventions and monitoring to avoid further deaths. © 2022 University of Stockholm. All rights reserved.

COVID-19-induced multisystem inflammatory syndrome in a child with Wilson disease: a case report.

Background: Infection with coronavirus disease 2019 (COVID-19) can progress to the multisystem inflammatory syndrome in children (MIS-C). Patients with liver cirrhosis are at increased risk of complications. Case presentation: We report on a 13-year-old Wilson's disease patient who was referred for liver transplantation because of rapid deterioration in his hepatic condition. After admission, he developed fever, respiratory distress, coronary arteries dilatation on echocardiography, laboratory evidence of inflammation, and positive severe acute respiratory syndrome coronavirus (SARS-CoV-2) PCR. SARS-CoV-2-induced MIS-C was diagnosed. Inspite of aggressive management of MIS-C, progressive deterioration of the respiratory, liver, kidney, and cardiac functions occurred and he passed away. Conclusion: MIS-C is a serious possible complication leading to multiorgan failure and higher death rate especially in cirrhotic children. So, early diagnosis and management with higher level of care by a multidisciplinary team are warranted.

Long-short-term memory machine learning of longitudinal clinical data accurately predicts acute kidney injury onset in COVID-19: a two-center study.

OBJECTIVES: This study used the long-short-term memory (LSTM) artificial intelligence method to model multiple time points of clinical laboratory data, along with demographics and comorbidities, to predict hospital-acquired acute kidney injury (AKI) onset in patients with COVID-19. METHODS: Montefiore Health System data consisted of 1982 AKI and 2857 non-AKI (NAKI) hospitalized patients with COVID-19, and Stony Brook Hospital validation data consisted of 308 AKI and 721 NAKI hospitalized patients with COVID-19. Demographic, comorbidities, and longitudinal (3 days before AKI onset) laboratory tests were analyzed. LSTM was used to predict AKI with fivefold cross-validation (80%/20% for training/validation). RESULTS: The top predictors of AKI onset were glomerular filtration rate, lactate dehydrogenase, alanine aminotransferase, aspartate aminotransferase, and C-reactive protein. Longitudinal data yielded marked improvement in prediction accuracy over individual time points. The inclusion of comorbidities and demographics further improves prediction accuracy. The best model yielded an area under the curve, accuracy, sensitivity, and specificity to be 0.965 ± 0.003, 89.57 ± 1.64%, 0.95 ± 0.03, and 0.84 ± 0.05, respectively, for the Montefiore validation dataset, and 0.86 ± 0.01, 83.66 ± 2.53%, 0.66 ± 0.10, 0.89 ± 0.03, respectively, for the Stony Brook Hospital validation dataset. CONCLUSION: LSTM model of longitudinal clinical data accurately predicted AKI onset in patients with COVID-19. This approach could help heighten awareness of AKI complications and identify patients for early interventions to prevent long-term renal complications.

Rare Case of Refractory Hypoxia and Severe Multiorgan Failure from Secondary Lymphohistiocytosis Successfully Bridged to Treatment with Extracorporeal Membrane Oxygenation Support.

Introduction: Acute respiratory distress syndrome (ARDS) is an uncommon complication of hemophagocytic lymphohistiocytosis (HLH). Non-specific findings that mimic other diseases make timely diagnosis and treatment challenging. We present a rare case of severe ARDS and multiorgan failure from secondary HLH due to peripheral T-cell lymphoma. Case presentation: A middle-aged female presented with dry cough and fever for three days. On presentation, the patient was febrile to 105°F and hypoxic to 88% on room air. Chest X-ray showed bilateral interstitial infiltrates. Laboratory investigations showed lymphopenia and elevated inflammatory markers. The viral panel, including coronavirus disease-2019 (COVID-19), influenza, and respiratory syncytial virus (RSV), was negative. Her respiratory status progressively worsened, requiring invasive mechanical ventilation for ARDS. Despite lung-protective ventilation, prone positioning, and the use of paralytic agents, the patient continued to remain hypoxic, necessitating extracorporeal membrane oxygenation (ECMO) support. The patient was started on antibiotics and high-dose steroid. Thereafter, she developed a leukemoid reaction, and the ferritin level started rising; raising suspicion for lymphophagocytosis. During this time, she also developed acute liver and kidney failure and required multiple vasopressors and renal replacement therapy. Eventually, a diagnosis of mature peripheral T-cell lymphoma was established. Subsequently, her respiratory status and multiorgan failure significantly improved, and ECMO was explanted after 2 weeks. She was started on etoposide and steroid, and eventually discharged after 6 weeks. Discussion: This is the first case describing a successful implementation of ECMO in an adult diagnosed with ARDS secondary to mature peripheral T-cell lymphoma; allowing for recovery of respiratory status, which was compromised during the initial cytokine storm and provided time to establish the diagnosis and initiate appropriate treatment of secondary HLH mature due to peripheral T-cell lymphoma, and in the end, prevented a fatality. We believe that ECMO may be appropriately instituted in rapidly deteriorating patients with an unknown illness refractory to conventional therapy, to allow for end-organ recovery, to reach a diagnosis, and to administer appropriate therapy. How to cite this article: Hundal J, Bowers D, Gadela NV, Jaiswal A. Rare Case of Refractory Hypoxia and Severe Multiorgan Failure from Secondary Lymphohistiocytosis Successfully Bridged to Treatment with Extracorporeal Membrane Oxygenation Support. Indian J Crit Care Med 2022;26(8):970-973. Statement of Ethics: This is a case report and does not contain any images or patient identifying information.

Systematic Review on Pathophysiological Complications in Severe COVID-19 among the Non-Vaccinated and Vaccinated Population.

COVID-19, caused by SARS-CoV-2, is one of the longest viral pandemics in the history of mankind, which have caused millions of deaths globally and induced severe deformities in the survivals. For instance, fibrosis and cavities in the infected lungs of COVID-19 are some of the complications observed in infected patients post COVID-19 recovery. These health abnormalities, including is multiple organ failure-the most striking pathological features of COVID-19-have been linked with diverse distribution of ACE2 receptor. Additionally, several health complications reports were reported after administration of COVID-19 vaccines in healthy individuals, but clinical or molecular pathways causing such complications are not yet studied in detail. Thus, the present systematic review established the comparison of health complication noted in vaccinated and non-vaccinated individuals (COVID-19 infected patients) to identify the association between vaccination and the multiorgan failure based on the data obtained from case studies, research articles, clinical trials/Cohort based studies and review articles published between 2020-2022. This review also includes the biological rationale behind the COVID-19 infection and its subsequent symptoms and effects including multiorgan failure. In addition, multisystem inflammatory syndrome (MIS) has been informed in individuals post vaccination that resulted in multiorgan failure but, no direct correlation of vaccination with MIS has been established. Similarly, hemophagocytic lymphohistiocytosis (HLH) also noted to cause multiorgan failure in some individuals following full vaccination. Furthermore, severe complications were recorded in elderly patients (+40 years of age), indicates that older age individuals are higher risk by COVID-19 and post vaccination, but available literature is not sufficient to comply with any conclusive statements on relationship between vaccination and multiorgan failure.

A Cross-Sectional Study of the Association of ABO Blood Group and Rh Type With Severity of COVID-19 Infection in a Tertiary Care Center of South India.

Background The novel coronavirus disease 2019 (COVID-19) was declared a pandemic that had affected 224 countries, causing >2.1 million deaths worldwide. The association of the different ABO blood groups with the risk and severity of COVID-19 infections has been speculated in many studies. This study aims to determine the incidence of COVID-19 infections among various blood groups and the association of ABO blood groups and Rh type with the severity of COVID-19 infection as well as with other outcome predictors of COVID-19 infection including neutrophil-to-lymphocyte ratio, D-dimer, ferritin, lactate dehydrogenase, and C-reactive protein. Methodology This was a retrospective study conducted among 150 serologically positive patients >18 years of age who underwent treatment in a district government hospital over two months. Patients were categorized into severity groups, and laboratory data were divided into those corresponding to severe disease and otherwise, in accordance with national guidelines. Appropriate statistical analysis was performed. Results The frequency of blood groups A, B, AB, and O was 30.7%, 29.4%, 13.7%, and 39%, respectively. There was a statistically significant number of patients belonging to non-O blood groups who developed a severe COVID-19 infection (group C) (p = 0.005). There was an increased risk of multiorgan failure (p = 0.035), non-invasive ventilation (p = 0.005), intubation, and mortality among non-O blood groups, and was the maximum for A blood group even after adjusting for age and pre-existing comorbidities. Increased D-dimer levels were noted in non-O blood groups (p = 0.037). No statistically significant association was found between Rh typing and the severity of COVID-19 infection. Conclusions Our findings provide evidence that individuals with non-O blood groups are susceptible to developing more severe COVID-19 infections and should take active preventive measures. Moreover, they should be cautiously monitored and treated once infected.

Mechanism of Multi-Organ Injury in Experimental COVID-19 and Its Inhibition by a Small Molecule Peptide.

Severe disease from SARS-CoV-2 infection often progresses to multi-organ failure and results in an increased mortality rate amongst these patients. However, underlying mechanisms of SARS- CoV-2-induced multi-organ failure and subsequent death are still largely unknown. Cytokine storm, increased levels of inflammatory mediators, endothelial dysfunction, coagulation abnormalities, and infiltration of inflammatory cells into the organs contribute to the pathogenesis of COVID-19. One potential consequence of immune/inflammatory events is the acute progression of generalized edema, which may lead to death. We, therefore, examined the involvement of water channels in the development of edema in multiple organs and their contribution to organ dysfunction in a Murine Hepatitis Virus-1 (MHV-1) mouse model of COVID-19. Using this model, we recently reported multi-organ pathological abnormalities and animal death similar to that reported in humans with SARS-CoV-2 infection. We now identified an alteration in protein levels of AQPs 1, 4, 5, and 8 and associated oxidative stress, along with various degrees of tissue edema in multiple organs, which correlate well with animal survival post-MHV-1 infection. Furthermore, our newly created drug (a 15 amino acid synthetic peptide, known as SPIKENET) that was designed to prevent the binding of spike glycoproteins with their receptor(s), angiotensin- converting enzyme 2 (ACE2), and carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) (SARS-CoV-2 and MHV-1, respectively), ameliorated animal death and reversed altered levels of AQPs and oxidative stress post-MHV-1 infection. Collectively, our findings suggest the possible involvement of altered aquaporins and the subsequent edema, likely mediated by the virus-induced inflammatory and oxidative stress response, in the pathogenesis of COVID- 19 and the potential of SPIKENET as a therapeutic option.

Association between thrombocytopenia and the severity of Covid-19 infection among hospitalized Egyptian patients.

Background: COVID-19, which is caused by the corona virus 2 that causes severe acute respiratory syndrome, causes a respiratory and systemic illness that in 10-15% of patients escalates to a severe form of pneumonia. Thrombocytopenia is frequent in patients with COVID-19. We aimed to evaluate the association between thrombocytopenia and the severity of COVID-19 infection in hospitalized patients. Methods: A cross-sectional study was done on 800 Egyptian patients with confirmed covid-19 infection. They were divided into Group I (Mild): 200 symptomatic patients meeting the case definition for COVID-19 without radiological evidence of pneumonia or hypoxia. Group II (Moderate): 200 patients with clinical signs of non-severe pneumonia and radiological evidence of pneumonia. Group III (Severe): 200 patients with clinical signs of pneumonia plus: respiratory or lung dysfunction. Group IV: 200 critically ill patient in ICU: Acute respiratory distress syndrome (ARDS).Results: there was a highly statistically significant difference between the studied groups regarding thrombocytopenia (p < 0.001). Thrombocytopenia was statistically higher in severe and critically ill patients. In addition, a statistically significant difference found in outcome among the studied groups (p < 0.05) {critically ill (40%), severe (17.5%)}. The most common cause of death was respiratory failure, which occurred in 28 severe patients (80%) and 65 critically ill patients (81.25%), followed by hemorrhage due to thrombocytopenia, which occurred in 7 severe patients (20%) and 15 critically ill patients, respectively (18.75%). Conclusion: The Platelet count is a straightforward, inexpensive, as well as easily available laboratory parameter that is frequently linked to severe covid-19 infection and a significant death risk.

COVID-19 and Sepsis

The COVID-19 pandemic has created a major alteration in the medical literature including the sepsis discussion. From the outset of the pandemic, various reports have indicated that although there are some unique features pertinent to COVID-19, many of its acute manifestations are similar to sepsis caused by other pathogens. As a consequence, the old definitions now require consideration of this new etiologic agent, namely SARS-CoV-2. Although the pathogenesis of COVID-19 has not been fully explained, the data obtained so far in hospitalized patients has revealed that serum cytokine and chemokine levels are high in severe COVID-19 patients, similar to those found with sepsis. COVID-19 may involve multiple organ systems. In addition to the lungs, the virus has been isolated from blood, urine, faeces, liver, and gallbladder. Results from autopsy series in COVID-19 patients have demonstrated a wide range of findings, including vascular involvement, congestion, consolidation, and hemorrhage as well as diffuse alveolar damage in lung tissue consistent with acute respiratory distress syndrome (ARDS). The presence of viral cytopathic-like changes, infiltration of inflammatory cells (mononuclear cells and macrophages), and viral particles in histopathological samples are considered a consequence of both direct viral infection and immune hyperactivation. Thromboembolism and hyper-coagulopathy are other components in the pathogenesis of severe COVID-19. Although the pathogenesis of hypercoagulability is not fully understood, it has been pointed out that all three components of Virchow's triad (endothelial injury, stasis, and hypercoagulable state) play a major role in contributing to clot formation in severe COVID-19 infection. In severe COVID-19 cases, laboratory parameters such as hematological findings, coagulation tests, liver function tests, D-dimer, ferritin, and acute phase reactants such as CRP show marked alterations, which are suggestive of a cytokine storm. Another key element of COVID-19 pathogenesis in severe cases is its similarity or association with hemophagocytic lymphohistiocytosis (HLH). SARS-CoV-2 induced cytokine storm has significant clinical and laboratory findings overlapping with HLH. Viral sepsis has some similarities but also some differences when compared to bacterial sepsis. In bacterial sepsis, systemic inflammation affecting multiple organs is more dominant than in COVID-19 sepsis. While bacterial sepsis causes an early and sudden onset clinical deterioration, viral diseases may exhibit a relatively late onset and chronic course. Consideration of severe COVID-19 disease as a sepsis syndrome has relevance and may assist in terms of determining treatments that will modulate the immune response, limit intrinsic damage to tissue and organs, and potentially improve outcome.

Clinical aspects and presumed etiology of multisystem inflammatory syndrome in children (MIS-C): A review.

The COVID-19 outbreak sparked by SARS-CoV-2, begat significant rates of malady worldwide, where children with an abnormal post-COVID ailment called the Multisystem Inflammatory Syndrome (MIS-C), were reported by April 2020. Here we have reviewed the clinical characteristics of the pediatric patients and the prognosis currently being utilized. A vivid comparison of MIS-C with other clinical conditions has been done. We have addressed the probable etiology and fundamental machinery of the inflammatory reactions, which drive organ failure. The involvement of androgen receptors portrays the likelihood of asymptomatic illness in children below adolescence, contributing to the concept of antibody-dependent enhancement.

Surviving the Storm: Cytokine Biosignature in SARS-CoV-2 Severity Prediction.

A significant part of the world population has been affected by the devastating SARS-CoV-2 infection. It has deleterious effects on mental and physical health and global economic conditions. Evidence suggests that the pathogenesis of SARS-CoV-2 infection may result in immunopathology such as neutrophilia, lymphopenia, decreased response of type I interferon, monocyte, and macrophage dysregulation. Even though most individuals infected with the SARS-CoV-2 virus suffer mild symptoms similar to flu, severe illness develops in some cases, including dysfunction of multiple organs. Excessive production of different inflammatory cytokines leads to a cytokine storm in COVID-19 infection. The large quantities of inflammatory cytokines trigger several inflammation pathways through tissue cell and immune cell receptors. Such mechanisms eventually lead to complications such as acute respiratory distress syndrome, intravascular coagulation, capillary leak syndrome, failure of multiple organs, and, in severe cases, death. Thus, to devise an effective management plan for SARS-CoV-2 infection, it is necessary to comprehend the start and pathways of signaling for the SARS-CoV-2 infection-induced cytokine storm. This article discusses the current findings of SARS-CoV-2 related to immunopathology, the different paths of signaling and other cytokines that result in a cytokine storm, and biomarkers that can act as early signs of warning for severe illness. A detailed understanding of the cytokine storm may aid in the development of effective means for controlling the disease's immunopathology. In addition, noting the biomarkers and pathophysiology of severe SARS-CoV-2 infection as early warning signs can help prevent severe complications.

Potential therapeutic approaches for targeted inhibition of inflammatory cytokines following COVID-19 infection-induced cytokine storm.

Coronavirus disease 2019 (COVID-19) is a deadly respiratory disease caused by severe acute respiratory syndrome coronavirus 2, which has caused a global pandemic since early 2020 and severely threatened people's livelihoods and health. Patients with pre-diagnosed conditions admitted to hospital often develop complications leading to mortality due to acute respiratory distress syndrome (ARDS) and associated multiorgan failure and blood clots. ARDS is associated with a cytokine storm. Cytokine storms arise due to elevated levels of circulating cytokines and are associated with infections. Targeting various pro-inflammatory cytokines in a specific manner can result in a potent therapeutic approach with minimal host collateral damage. Immunoregulatory therapies are now of interest in order to regulate the cytokine storm, and this review will summarize and discuss advances in targeted therapies against cytokine storms induced by COVID-19.

Longitudinal prediction of hospital-acquired acute kidney injury in COVID-19: a two-center study.

BACKGROUND: To investigate the temporal characteristics of clinical variables of hospital-acquired acute kidney injury (AKI) in COVID-19 patients and to longitudinally predict AKI onset. METHODS: There were 308 hospital-acquired AKI and 721 non-AKI (NAKI) COVID-19 patients from Stony Brook Hospital (New York, USA) data, and 72 hospital-acquired AKI and 303 NAKI COVID-19 patients from Tongji Hospital (Wuhan, China). Demographic, comorbidities, and longitudinal (3 days before and 3 days after AKI onset) clinical variables were used to compute odds ratios for and longitudinally predict hospital-acquired AKI onset. RESULTS: COVID-19 patients with AKI were more likely to die than NAKI patients (31.5% vs 6.9%, adjusted p < 0.001, OR = 4.67 [95% CI 3.1, 7.0], Stony Brook data). AKI developed on average 3.3 days after hospitalization. Procalcitonin was elevated prior to AKI onset (p < 0.05), peaked, and remained elevated (p < 0.05). Alanine aminotransferase, aspartate transaminase, ferritin, and lactate dehydrogenase peaked the same time as creatinine, whereas D-dimer and brain natriuretic peptide peaked a day later. C-reactive protein, white blood cell and lymphocyte showed group differences - 2 days prior (p < 0.05). Top predictors were creatinine, procalcitonin, white blood cells, lactate dehydrogenase, and lymphocytes. They predicted AKI onset with areas under curves (AUCs) of 0.78, 0.66, and 0.56 at 0, - 1, and - 2 days prior, respectively. When tested on the Tongji Hospital data, the AUCs were 0.80, 0.79, and 0.77, respectively. CONCLUSIONS: Time-locked longitudinal data provide insight into AKI progression. Commonly clinical variables reasonably predict AKI onset a few days prior. This work may lead to earlier recognition of AKI and treatment to improve clinical outcomes.

Longitudinal Clinical Profiles of Hospital vs. Community-Acquired Acute Kidney Injury in COVID-19.

Acute kidney injury (AKI) is associated with high mortality in coronavirus disease 2019 (COVID-19). However, it is unclear whether patients with COVID-19 with hospital-acquired AKI (HA-AKI) and community-acquired AKI (CA-AKI) differ in disease course and outcomes. This study investigated the clinical profiles of HA-AKI, CA-AKI, and no AKI in patients with COVID-19 at a large tertiary care hospital in the New York City area. The incidence of HA-AKI was 23.26%, and CA-AKI was 22.28%. Patients who developed HA-AKI were older and had more comorbidities compared to those with CA-AKI and those with no AKI (p < 0.05). A higher prevalence of coronary artery disease, heart failure, and chronic kidney disease was observed in those with HA-AKI compared to those with CA-AKI (p < 0.05). Patients with CA-AKI received more invasive and non-invasive mechanical ventilation, anticoagulants, and steroids compared to those with HA-AKI (p < 0.05), but patients with HA-AKI had significantly higher mortality compared to those with CA-AKI after adjusting for demographics and clinical comorbidities (adjusted odds ratio = 1.61, 95% confidence interval = 1.1-2.35, p < 0.014). In addition, those with HA-AKI had higher markers of inflammation and more liver injury (p < 0.05) compared to those with CA-AKI. These results suggest that HA-AKI is likely part of systemic multiorgan damage and that kidney injury contributes to worse outcomes. These findings provide insights that could lead to better management of COVID-19 patients in time-sensitive and potentially resource-constrained environments.

Insights into Potential Mechanisms of Injury and Treatment Targets in COVID-19, SARS-Cov-2 Infection.

The severe acute respiratory syndrome coronavirus 2, SARS-CoV-2, is the most serious pandemic in modern times. The disease was first reported in January of 2020 in China's city of Wuhan, Hubei province, and since then it has spread worldwide. Given the rapid spread of the virus and the burden it has taken on the healthcare systems it has swept through, there is the need for a concise description of current understanding of the pathogenesis of organ failure in SARS-CoV-2 infection while acknowledging that more is yet to be uncovered. This review will not only inform decision making at the bedside but will also help illustrate potential therapeutic targets for research. We searched the available literature to-date, and present the pathophysiology underlying increased morbidity and mortality of SARS-CoV-2 infection in the lungs, heart and kidneys in a highly illustrated presentation that is easy-to-understand for the clinician, researcher, and student alike.

COVID-19 and Mesenchymal Stem Cell Treatment; Mystery or Not.

On December 31, 2019, novel SARS-CoV2 spread from Wuhan China to more than 200 territories around world and the World Health Organization declared a COVID-19 pandemic on January 30, 2020. At this time there is no particular therapy, drug or vaccine available to deal with COVID-19. Today actual data indicates that about 17% of closed COVID-19 cases died. Health care professionals, ministry of health in countries and the public are trying to read the runes to see when the COVID-19 pandemic will be over. Although mild cases of COVID-19 can be controlled with antiviral, anti-inflammatory and immunomodulatory treatment, severe cases may need intensive care unit support and ventilation. Cytokine storms cause high inflammatory responses and pneumonia in severe cases. Mesenchymal stem cells are immunomodulatory and they have regenerative capacity. In this sense, mesenchymal stem cells may improve the patient's clinical and immunological response to COVID-19.

Atrial fibrillation: a risk factor for unfavourable outcome in COVID-19? A case report.

BACKGROUND: Fulminant cardiac involvement in COVID-19 patients has been reported; the underlying suspected mechanisms include myocarditis, arrhythmia, and cardiac tamponade. In parallel, atrial fibrillation is common in the elderly population which is at particularly high risk for COVID-19 morbidity and mortality. CASE SUMMARY: A 72-year-old male SARS-CoV2-positive patient was admitted to the intensive care unit due to delirium and acute respiratory failure. Atrial fibrillation known from history was exacerbated, and made complex rate and rhythm control necessary. Progressive heart failure with haemodynamic deterioration and acute kidney injury with the need for continuous renal replacement therapy were further aggravated by pericardial tamponade. DISCUSSION: Treatment of acute heart failure in COVID-19 patients with a cytokine storm complicated by tachycardic atrial fibrillation should include adequate rate or rhythm control, and potentially immunomodulation.