To explore the associations between the blood urea nitrogen-to-creatinine ratio (BCR), acute kidney injury (AKI), and in-hospital mortality in coronavirus disease 2019 (COVID-19) patients.

COVID-19 patients from Ruijin Hospital LuWan Branch, Shanghai Jiao Tong University School of Medicine were enrolled in this study. Clinical data and laboratory parameters were collected. AKI was defined using two serum creatinine tests according to KDIGO guidelines. Cox regression and receiver operating characteristic (ROC) curve analyses were performed.

Five hundred and sixty-seven COVID-19 patients were enrolled, 44.1% of whom were male. The mean age was 75 years. Among all patients, 17 patients developed AKI, and 30 patients died during hospitalization. Compared to non-AKI patients, the BCR in AKI patients was significantly greater. BCR was significantly associated with AKI (unadjusted HR 1.04, 95% CI: 1.02-1.05, p < 0.001; adjusted HR 1.06, 95% CI 1.02-1.10, p = 0.001). BCR was also a risk factor of in-hospital mortality (unadjusted HR 1.03, 95% CI: 1.02-1.05, p < 0.001; adjusted HR 1.04, 95% CI: 1.01-1.08, p = 0.019). The BCR threshold was 38.9, with 70.6% sensitivity and 87.1% specificity for predicting AKI, while a threshold of 33.0 predicted mortality. Subgroup analysis revealed that BCR could predict AKI and mortality in different subgroups according to sex, age, diabetes mellitus, and estimated glomerular filtration rate.

The BCR, a simple index, is associated with AKI onset and mortality in COVID-19 patients. The BCR possesses certain specificity for AKI screening, which indicates an effective clinical indicator for screening patients at high risk of AKI.

The COVID-19 pandemic, caused by the SARS-CoV-2 virus, has led to a significant burden on global healthcare systems. COVID-19-induced acute kidney injury (AKI) is among one of the complications, that has emerged as a critical and frequent condition in COVID-19 patients. This AKI among COVID-19 patients is associated with poor outcomes, and high mortality rates, especially in those with severe AKI or requiring renal replacement therapy. COVID-19-induced AKI represents a significant complication with complex pathophysiology and multifactorial risk factors. Indeed, several pathophysiological mechanisms, including direct viral invasion of renal cells, systemic inflammation, endothelial and thrombotic abnormalities as well as nephrotoxic drugs and rhabdomyolysis are believed to underlie this condition. Moreover, histopathological and immunohistopathological findings commonly observed in postmortem studies include acute tubular necrosis, glomerular injury, and the presence of viral particles within renal tissue and urine. Identified risk factors for developing AKI vary among studies, depending on regions, underlying conditions, and the severity of the disease. Moreover, histopathological and immunohistopathological findings commonly observed in postmortem studies include show acute tubular necrosis, glomerular injury, and viral particles within renal tissue and urine. While, identified risk factors for developing AKI vary among studies, according to regions, underlying conditions, and the gravity of the disease. This narrative review aims to synthesize current knowledge on the incidence, pathophysiology, risk factors, histopathology, and outcomes of AKI induced by COVID-19.

To date, research on opioid overdose during the COVID-19 pandemic has focused on rates of Emergency Department (ED) visits related to opioids but has not considered how interaction with concurrent COVID-19 infection may have influenced clinical outcomes. We hypothesized that COVID-19 infection increased the need for respiratory support, prolonged hospital stays, and increased mortality among ED patients admitted to the hospital after presenting with opioid overdose.

The 2020 National Emergency Department Sample (NEDS) was used to identify patients admitted to the hospital after presenting to the ED with opioid overdose, and whose COVID-19 infection status could be determined. The primary outcome was the use of respiratory support, and secondary outcomes were hospital length of stay (LOS) and mortality.

Among the 5913 eligible patients, 3 % had a COVID-19 infection diagnosis. Among all included patients, 28 % received respiratory support, in-hospital mortality was 4 %, and the mean hospital length of stay was 3.9 days. After multivariable adjustment, COVID-19 was not associated with the use of respiratory support (odds ratio [OR]: 0.98; 95 % confidence interval [CI]: 0.67, 1.44; p = 0.938). COVID-19 was associated with higher odds of in-hospital mortality (OR: 2.22; 95 % CI: 1.20, 4.11; p = 0.011) and longer hospital stay (incidence rate ratio: 1.57, 95 % CI: 1.22, 2.01; p < 0.001).

This data suggests that COVID-19 infection in patients admitted to the hospital with opioid overdose results in higher morbidity and longer hospital stay, but had no association with the use of respiratory support. The physiologic cause deserves future study.

Rapidly phenotyping patients can inform public health action plans in new pandemics. This study aimed to derive meaningful SARS-CoV-2 reinfected patients' phenotypes based on easily-available patient data and explore key epidemiological factors of reinfections.

We conducted a retrospective study of a cohort of SARS-CoV-2 reinfected adults from the Basque Country between January 1, 2021 and January 9, 2022. Phenotypes were defined in an unsupervised manner with clustering algorithms, incorporating variables like age, Charlson score, vaccination status and pre-existing treatments and comorbidities. Subsequently, clinical characteristics of phenotypes were compared, and their behavioral differences were evaluated through generalized additive models. Finally, their association with clinical outcomes was assessed.

Four phenotypes were identified, which subsequently had a direct relationship with the risk levels for severe COVID-19 outcomes. The highest-risk group, phenotype 4, consisted of older adults -76 years, [62-85] (Median, [Interquartile range])- with multiple comorbidities and extensive baseline medication use. Phenotype 3 was slightly younger -64 years, [58-77]- but presented very low Charlson scores and few comorbidities, representing an intermediate-risk group. Phenotypes 1 and 2 were younger and healthier adults with similar clinical profiles. However, phenotype 1 showed a less protective attitude, with a higher rate of unvaccinated patients and shorter time intervals between infections.

We were able to classify reinfected patients into four distinct groups based on easily available variables, and these phenotypes had a direct relationship with COVID-19 clinical outcomes. Thus, rapidly phenotyping infected individuals can serve as a preventive public health strategy during new pandemics.

While the association between COVID-19 and acute kidney injury (AKI) is well documented, the impact of COVID-19 on the development of advanced chronic kidney disease (CKD) remains unclear, particularly in patients without initial AKI. Using the TriNetX healthcare database, we conducted a matched cohort study comparing 141,587 COVID-19 and 141,587 influenza patients. We excluded patients with AKI within one month of infection and matched groups on demographics, comorbidities, and baseline laboratory values. The primary outcome was the incidence of advanced CKD (stages 3-5) at the 12-month follow-up. COVID-19 patients showed higher 12-month risks of advanced CKD (hazard ratio [HR]:2.02, 95% confidence interval [CI]:1.69-2.42, p < 0.0001), AKI (HR 3.04, 95%CI:2.61-3.55, p < 0.0001), and estimated glomerular filtration rate < 60 mL/min/1.73 m2 (HR:3.01, 95%CI:2.74-3.30, p < 0.0001) compared to influenza patients. Subgroup analyses showed consistently elevated risks across sexes and in patients over 45 years, while younger patients did not demonstrate an increased risk of advanced CKD at the 12-month follow-up. Diabetes mellitus and hypertension have emerged as the strongest predictors of advanced CKD development. In conclusion, COVID-19 is associated with an increased risk of long-term renal dysfunction compared with influenza, suggesting the need for extended monitoring of kidney function in high-risk populations.

Several studies suggest that the heterogeneous spread of SARS-CoV-2 pandemics started on December 2019 could be partially upheld by the prevalence of permissive class I HLA alleles in specific populations. Such HLA alleles are in fact unable to shape an efficient anti-viral immune-response in the hosts or sustain an exaggerated inflammatory T cell mediated response responsible for the COVID-19 disease. We previously reported an ecologic correlation between the risk of COVID-19 spreading across Italy and the germinal expression of permissive HLA-C*01 and -B*44 alleles in specific inter and intraregional populations along the first spreading wave.

Considering that SARS-CoV-2 has undergone multiple adaptative mutations since the beginning of pandemics related to a natural immunization and to the worldwide campaign of anti-SARS-CoV-2 vaccination, we have carried out further analyses to evaluate whether the predictive value of class I HLA-allele gene prevalence and COVID-19 incidence has changed with time along the first four pandemics spreading waves in Italy. To this purpose we carried out an ecologic study followed by a case-control study.

| Our data revealed that the direct correlation of HLA-C*01, and HLA-B*44 gene expression and COVID-19 risk was completely lost just after the first pandemics wave in Italy. On the contrary, the expression of HLA-B*49 allele in specific populations emerged as inversely correlated to the risk of COVID-19 and could be considered as a protective factor. The statistical significance of this correlation was progressively enforced in each subsequent spreading wave until February 2022. The following case-control study in the two Regions of Campania and Calabria in Italy confirmed the protective value of HLA-B*49 allele gene expression (OR = 0.289; p = 0.041), although statistical significance is lost after adjustment by logistic regression model. The analysis also detected multiple class I HLA-alleles whose expression was strongly correlated with COVID-19 risk: HLA-B*08 (ORadj = 3.193; p = 0.015); -B*14:01 (ORadj = 3.596; p = 0.018); -B*15:01 (ORadj = 5.124; p = 0.001); -B*35 (ORadj = 2.972; p = 0.002).

Our study not only identifies specific HLA alleles related to COVID-19 risk but also exemplifies a rapid and inexpensive approach that can be used to identify individuals needing prioritization during vaccination campaigns.

This study aimed to identify possible early biomarkers of mortality among clinical and biochemical parameters, iron metabolism parameters, and cytokines detected within 24 h from admission in hospitalized COVID-19 patients. We enrolled 80 hospitalized patients (40 survivors and 40 non-survivors) with COVID-19 pneumonia and acute respiratory failure. The median time from the onset of COVID-19 symptoms to hospital admission was lower in non-survivors than survivors (p < 0.05). Respiratory failure, expressed as the ratio of arterial oxygen partial pressure to the fraction of inspired oxygen (P/F), was more severe in non-survivors than survivors (p < 0.0001). Comorbidities were similar in both groups. Among biochemical parameters and cytokines, eGFR and interleukin (IL)-1β were found to be significantly lower (p < 0.05), while LDH, IL-10, and IL-8 were significantly higher in non-survivors than in survivors (p < 0.0005, p < 0.05 and p < 0.005, respectively). Among other parameters, LDH values distribution showed the most significant difference between study groups (p < 0.0001). LASSO feature selection combined with Cox proportional hazards and logistic regression models was applied to identify features distinguishing between survivors and non-survivors. Both approaches highlighted LDH as the strongest predictor, with IL-22 and creatinine emerging in the Cox model, while IL-10, eGFR, and creatinine were influential in the logistic model (AUC = 0.744 for Cox, 0.723 for logistic regression). In a similar manner, we applied linear regression for predicting LDH levels, identifying the P/F ratio as the top predictor, followed by IL-10 and eGFR (NRMSE = 0.128). Collectively, these findings underscore LDH's critical role in mortality prediction, with P/F and IL-10 as key determinants of LDH increases in this Italian COVID-19 cohort.

Background: Heart failure with preserved ejection fraction (HFpEF) is a condition with limited large-scale data on the short- and long-term effects of SARS-CoV-2 infection. This study aimed to evaluate the prevalence of major adverse cardiac and cerebrovascular events (MACCEs) in HFpEF patients hospitalized with SARS-CoV-2 and identify sex-specific risk factors and predictors of MACCEs in this population. Methods: This retrospective study analyzed HFpEF patients hospitalized with SARS-CoV-2 from the 2020 National Inpatient Sample (NIS) using ICD-10 codes. Patients hospitalized with HFpEF and SARS-CoV-2 were categorized by age (18-44, 45-64, ≥65 years). Multivariate logistic regression was used to adjust for potential confounders, with the statistical significance set at a two-tailed p-value < 0.05. Results: Among 109,750 HFpEF patients hospitalized with SARS-CoV-2, 31,960 (29.1%) experienced MACCEs. Males experienced a higher rate of MACCEs than females (31.1% vs. 27.5%, OR: 1.20, 95% CI: 1.12-1.28, p < 0.001). Adjusted analysis revealed that elderly patients (≥65 years, OR: 1.47, 95% CI: 1.33-1.62) compared with the 45-64 age group and males (OR: 1.20, 95% CI: 1.12-1.28, p < 0.001) had a higher risk of MACCEs. Key predictors included prior coronary artery bypass grafting (CABG; OR: 1.15, 95% CI: 1.02-1.30), cancer (OR: 1.24, 95% CI: 1.08-1.42), and chronic kidney disease (OR: 1.15, 95% CI: 1.08-1.23). Subgroup analysis identified additional sex-specific risk factors. In males, hyperlipidemia, obesity, tobacco use disorder, prior stroke/transient ischemic attack (TIA), prior venous thromboembolism (VTE), alcohol abuse, depression, and valvular disease were significant predictors of MACCEs. In females, hyperlipidemia, tobacco use disorder, prior stroke/TIA, prior VTE, and depression were significant predictors. Conclusions: HFpEF patients hospitalized with SARS-CoV-2 have a high risk of MACCEs, with male sex, older age, prior CABG, cancer, and chronic kidney disease as key risk factors. This study provides the first large-scale analysis of sex-specific predictors of MACCEs in HFpEF patients hospitalized with SARS-CoV-2. These findings underscore the need for focused research and clinical gender-based strategies to mitigate cardiovascular risks in this unique and high-risk population.

COVID-19 became a pandemic disease in 2020, with multisystem involvement and high renal morbidity during the acute phase. Some affected patients began to present new or persistent symptoms in a condition known as Long COVID. The study aimed to evaluate renal function using clinical and laboratory findings, and to establish the frequency and staging of renal function decline in Long COVID patients, as well as the associated factors.

This is a cross-sectional observational study that selected participants from a Long COVID clinical care program between 2020 and 2022.

A total of 246 patients were selected for this study, and renal function decline was found in 83 (33.7%). Patients over 60 years (29.6%) and those who developed glycaemic alterations (41.8%) exhibited a higher prevalence of renal outcomes in long COVID. Some laboratory test as LDH levels and glycated hemoglobin seems to have a statistic relation with a decrease in renal function (p < 0.05).

A decline in renal function was common in patients with Long COVID in this study, and older age and glycaemic alterations were relevant to this condition. Some laboratory markers can be used to predict this outcome.

Maintaining iron homeostasis is necessary for kidney functioning. There is more and more research indicating that kidney disease is often caused by iron imbalance. Over the past decade, ferroptosis' role in mediating the development and progression of renal disorders, such as acute kidney injury (renal ischemia-reperfusion injury, drug-induced acute kidney injury, severe acute pancreatitis induced acute kidney injury and sepsis-associated acute kidney injury), chronic kidney disease (diabetic nephropathy, renal fibrosis, autosomal dominant polycystic kidney disease) and renal cell carcinoma, has come into focus. Thus, knowing kidney iron metabolism and ferroptosis regulation may enhance disease therapy. In this review, we discuss the metabolic and molecular mechanisms of iron signaling and ferroptosis in kidney disease. We also explore the possible targets of ferroptosis in the therapy of renal illness, as well as their existing limitations and future strategies.

Diverse psychological consequences of the COVID-19 pandemic have been reported for 6 months after infection. We conducted a prospective study to evaluate the psychological impact of COVID-19 infection in newly diagnosed cases that were followed up at 1, 6, and 9 months after infection. 137 people were recruited and divided into four groups based on the COVID-19 Treatment Guidelines. They were evaluated using the Pittsburgh Sleep Quality Index (PSQI), Post-traumatic stress disorder Checklist for DSM-5 (PCL-5), and Symptom Checklist 90 (SCL-90). We found that 9 months after infection, patients continued to report poor sleep (74.5%), PTSD (78.3%), somatization (17%), anxiety (17%), aggression (5.7%), phobic anxiety (4.7%), psychoticism (1.9%), paranoid (3.8%), and obsessive-compulsive (9.4%) symptoms, as well as depression and interpersonal sensitivity. The most significant risk factors for psychiatric complications were older age, level of education, smoking, hospitalization duration, hypertension, and critical severity. The negative mental health effects of COVID-19 persist after hospital discharge, and many patients continue to experience moderate-to-severe issues that may endure for 9 months. Notably, there was a progressive improvement in these symptoms over that time.

Pregnant women need special attention during emergencies and infectious disease outbreaks. Pregnancy is a standalone risk factor for the severity of COVID-19, heightening the vulnerability of both the mother and foetus. Neonatal admission, foetal distress, and low birth weight were correlated to the severity of COVID-19. The aim of this study was to provide a clinical overview and characteristics of neonates from mothers who were confirmed with COVID-19.

A cross-sectional study was conducted at Sulianti Saroso Infectious Disease Hospital (SSIDH) from March 2020 to December 2022. Inclusion criteria included pregnant women with confirmed SARS-CoV-2 infection who either gave birth in a hospital according to the regulations of the Ministry of Health of the Republic of Indonesia. All newborns were tested using RT-PCR SARS-COV-2 swab tests within 24 hours after birth. We used electronic medical records as a secondary source.

A total of 181 pregnant women with positive SARS-CoV-2, 103 (56.9%) gave birth, with 101 (98.1%) undergoing caesarean section. Of the 103 who gave birth, a small proportion of mothers with COVID-19 were aged <20 years or >35 years (29.13%) and had preterm deliveries (15.53%). All newborns born to SARS-CoV-2-positive mothers were alive. The severity of illness was associated with the first-minute and fifth-minute APGAR scores of newborns (P < 0.05).

The severity of maternal COVID-19 impacts newborns' 1-minute and 5-minute APGAR scores. Implementing a strict COVID-19 protocol effectively prevents neonatal infections.

Background and Objectives: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) was described in December 2019 for the first time, and it was responsible for a global pandemic. An alarming number of patients with coronavirus disease 2019 (COVID-19) also developed acute kidney injury (AKI), especially those who required extracorporeal membrane oxygenation (ECMO) therapy for acute respiratory distress syndrome (ARDS). The aim of our retrospective observational study was to assess the prognostic significance of AKI in these patients. This study observed, in COVID-19 patients admitted to an intensive care unit (ICU), AKI stages and the need for renal replacement therapy (RRT), assessing the risk factors and outcomes. Moreover, we evaluated the mortality rate of patients treated by ECMO. Materials and Methods: Between November 2020 and December 2022, among 396 patients admitted to our intensive care unit (ICU) diagnosed with SARS-CoV-2 infection, we selected patients with severe ARDS requiring veno-venous (vv) ECMO support and AKI. Results: The 30-day mortality after ECMO positioning was 85.7%. A Cox regression revealed a significant advantage for RRT with a high cut-off (HCO) hemofilter both for ICU mortality (HR 0.17 [95% CI: 0.031-0.935], p = 0.035) and 15 day-mortality after the start of vv-ECMO (HR 0.13 [95%CI: 0.024-0.741], p= 0.021), whereas the early onset of vasoplegic shock after ECMO implantation indicated a higher risk of death (HR 11.55 [95% CI: 1.117-119.567], p = 0.04) during the ICU stay. Conclusions: COVID-19 induces a high risk of AKI and RRT. In our cohort, hypertension, pre-existing renal disease, and mechanical ventilation represented independent risk factors for AKI. Patients requiring ECMO support had a high mortality rate. The early implementation of RRT reduced the risk of death during the ICU stay.

Background: Prone positioning is a standard intervention in managing patients with severe acute respiratory distress syndrome (ARDS) and is known to improve oxygenation. However, its effects on other organs, particularly the kidneys, are less well understood. This study aimed to assess the association between prone positioning and the development of acute kidney injury (AKI), specifically in overweight and obese patients. Methods: A retrospective pre-post study was conducted on a cohort of 60 critically ill ARDS patients who were placed in the prone position during hospitalization. The development of AKI was assessed using the Acute Kidney Injury Network (AKIN) criteria, with AKI measured by both creatinine levels (AKINCr) and urine output (AKINUO). Patients were divided into two groups based on body mass index (BMI): overweight/obese (BMI ≥ 25) and non-obese (BMI < 25). Data were collected before and after prone positioning. Results: In overweight/obese patients (n = 39, 57 cases), both the median AKINCr and AKINUO scores increased significantly following prone positioning (from 0 to 1, median p < 0.01, and from 0 to 2, median p < 0.01, respectively). No statistically significant changes in AKIN scores were observed in non-obese patients nor were significant differences found in either group after repositioning to supine. Conclusions: Prone positioning is associated with an increased risk of acute kidney injury in overweight and obese ARDS patients. This may be due to the kidneys' susceptibility to intra-abdominal hypertension in these patients. Further research is needed to explore optimal proning strategies for overweight and obese populations.

The onset of the COVID-19 pandemic has had a detrimental impact on the healthcare system. Patients with kidney failure and related kidney disease are notably vulnerable to the COVID-19 pandemic. However, it remains unclear how mortality trends associated with kidney failure have evolved over the past three years. In this study, we investigated temporal trends in excess kidney failure-related mortality during the first three years of the pandemic in the United States.

We aim to estimate time-varying excess kidney failure-related mortality, which is defined as the difference between observed mortality and expected mortality predicted by a Poisson log-linear regression model, in the United States (March 2020-March 2023).

Our findings revealed two distinct peaks in excess kidney failure-related mortality during the first year (March 2020-February 2021) and the second year (February 2021-March 2022), whereas a notable decline in excess mortality was observed in the third year (March 2022-March 2023). Additionally, disparities in mortality were evident among various demographic groups, including age, sex, racial/ethnic subgroups, and geographic regions. Across all age subgroups, an increase in kidney failure-related mortalities was observed, with individuals aged 85 years and above experiencing the most substantial relative increase, reaching 9595.8 per million persons (95% CI: 9438.8, 9752.9). Moreover, excess kidney failure-related mortalities were recorded at 510.3 per million persons (95% CI: 502.6, 517.9) and 721.8 per million persons (95% CI: 713.4, 730.1) for women and men, respectively. Notably, non-Hispanic Blacks exhibited the highest excess mortality within the racial/ethnic group, registering at 772.6 per million persons (95% CI: 756.3, 788.9).

Our study observed high levels of excess kidney failure-related mortality during the first two years of the pandemic, followed by a notable decline in the third year. This highlights the effectiveness of current policies and prevention measures implemented to mitigate the impact of the pandemic.

COVID-19 poses a significant threat to global public health. As the severity of SARS-CoV-2 infection varies among individuals, elucidating risk factors for severe COVID-19 is important for predicting and preventing illness progression, as well as lowering case fatality rates. This work aimed to explore risk factors for developing severe COVID-19 to enhance the quality of care provided to patients and to prevent complications.

A retrospective study was conducted in Saudi Arabia's eastern province, including all COVID-19 patients aged 18 years or older who were hospitalized at Prince Saud Bin Jalawi Hospital in July 2020. Comparative tests as well as both univariate and multivariate logistic regression analyses were performed to identify risk factors for developing severe COVID-19 and poor outcomes.

Based on the comparative statistical tests patients with severe COVID-19 were statistically significantly associated with older age and had higher respiratory rate, longer hospital stay, and higher prevalence of diabetes than non-severe cases. They also exhibited statistically significant association with high levels of potassium, urea, creatinine, lactate dehydrogenase (LDH), D-dimer, and aspartate aminotransferase (AST). The univariate analysis shows that having diabetes, having high severe acute respiratory infection chest X-ray scores, old age, prolong hospitalization, high potassium and lactate dehydrogenase, as well as using insulin, heparin, corticosteroids, favipiravir or azithromycin were all statistically significant associated with severe COVID-19. However, after adjustments in the multivariate analysis, the sole predictor was serum LDH (p = 0.002; OR 1.005; 95% CI 1.002-1.009). In addition, severe COVID-19 patients had higher odds of being prescribed azithromycin than non-severe patients (p = 0.001; OR 13.725; 95% CI 3.620-52.043). Regarding the outcomes, the median hospital stay duration was statistically significantly associated with death, intensive care unit admission (ICU), and mechanical ventilation. On the other hand, using insulin, azithromycin, beta-agonists, corticosteroids, or favipiravir were statistically significantly associated with reduced mortality, ICU admission, and need of mechanical ventilation.

This study sheds light on numerous parameters that may be utilized to construct a prediction model for evaluating the risk of severe COVID-19. However, no protective factors were included in this prediction model.

Early reports have indicated that the Omicron variant of coronavirus disease 2019 (COVID-19) may be associated with low mortality. However, the mortality rate of critical patients in Taiwan with COVID-19 caused by different variants has not been well described.

This retrospective cohort study was conducted at the Linkou Branch of Chang Gung Memorial Hospital, Taiwan, from April 2020 to September 2022. Critically ill patients who had confirmed SARS-CoV-2 infection and were on mechanical ventilation (MV) were enrolled. Demographic data, laboratory results, and treatment information were collected and analyzed. In addition, clinical outcomes for different SARS-CoV-2 variants were analyzed.

This study included 110 critical patients with COVID-19 who required intubation and intensive care unit (ICU) admission. Among these patients, 46 (41.8%) required intensive care during Alpha predominance period and 64 (58.2%) during the Omicron predominance period. The Alpha group had a higher body mass index, had a longer ICU stay, and included more patients with acute respiratory distress syndrome, and the Omicron group included more active smokers, had more comorbidities, had worse initial laboratory data (including higher white blood cell counts, prothrombin time [PT], activated partial prothrombin time, blood urine nitrogen levels, and creatine levels), and had higher in-hospital mortality rates (40.6% vs 15.2%, p = 0.004). The independent risk factors for in-hospital mortality, were Charlson Comorbidity Index (CCI) ≥ 3 and higher PT and creatine levels.

Our study discovered that CCI ≥ 3, elevated serum creatine levels, and prolonged PT were independently associated with a high mortality rate in patients with critical COVID-19. Patients with those risk factors may require intensive monitoring during their treatment course.

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) mainly affects the respiratory tract, but different organs may be involved including the kidney. Data on acute kidney injury (AKI) in critical forms of coronavirus disease 2019 (COVID-19) are scarce. We aimed to assess the incidence, risk factors and prognostic impact of AKI complicating critical forms of COVID-19.

A retrospective descriptive case/control monocentric study conducted in a medical intensive care unit of a tertiary teaching hospital over a period of 18 months.

We enrolled 144 patients, with a mean age of 58±13 years old and a male predominance (sex-ratio: 1.25). Forty-one (28%) developed AKI within a median of 4 days (Q1: 3, Q3: 8.5) after hospitalization. It was staged KDIGO class 3, in about half of the cases. Thirteen patients underwent renal replacement therapy and renal function improved in seven cases. Diabetes (OR: 6.07; 95% CI: (1,30-28,4); p: 0.022), nephrotoxic antibiotics (OR: 21; 95% CI: (3,2-146); p: 0.002), and shock (OR: 12.21; 95% CI: (2.87-51.85); p: 0.031,) were the three independent risk factors of AKI onset. Mortality was significantly higher in AKI group (HR:12; 95% CI: (5.81-18.18); p:0.041) but AKI didn't appear to be an independent risk factor of poor outcome. In fact, age > 53 years (p: 0.018), septic shock complicating hospital acquired infection (p: 0.003) and mechanical ventilation (p<0.001) were the three prognostic factors in multivariate analysis.

The incidence of AKI was high in this study and associated to an increased mortality. Diabetes, use of nephrotoxic antibiotics and shock contributed significantly to its occurrence. This underlines the importance of rationalizing antibiotic prescription and providing adequate management of patients with hemodynamic instability in order to prevent consequent AKI.

SARS-CoV-2 virus infects cells by engaging with ACE2 requiring protease TMPRSS2. ACE2 is highly expressed in kidneys. Predictors for severe disease are high age and male sex. We hypothesized that ACE2 and TMPRSS2 proteins are more abundant (1) in males and with increasing age in kidney and (2) in urine and extracellular vesicles (EVs) from male patients with COVID-19 and (3) SARS-CoV-2 is present in urine and EVs during infection. Kidney cortex samples from patients subjected to cancer nephrectomy (male/female; < 50 years/˃75 years, n = 24; ˃80 years, n = 15) were analyzed for ACE2 and TMPRSS2 protein levels. Urine from patients hospitalized with SARS-CoV-2 infection was analyzed for ACE2 and TMPRSS2. uEVs were used for immunoblotting and SARS-CoV-2 mRNA and antigen detection. Tissue ACE2 and TMPRSS2 protein levels did not change with age. ACE2 was not more abundant in male kidneys in any age group. ACE2 protein was associated with proximal tubule apical membranes in cortex. TMPRSS2 was observed predominantly in the medulla. ACE2 was elevated significantly in uEVs and urine from patients with COVID-19 with no sex difference compared with urine from controls w/wo albuminuria. TMPRSS2 was elevated in uEVs from males compared to female. ACE2 and TMPRSS2 did not co-localize in uEVs/apical membranes. SARS-CoV-2 nucleoprotein and mRNA were not detected in urine. Higher kidney ACE2 protein abundance is unlikely to explain higher susceptibility to SARS-CoV-2 infection in males. Kidney tubular cells appear not highly susceptible to SARS-CoV-2 infection. Loss of ACE2 into urine in COVID could impact susceptibility and angiotensin metabolism.

Acute kidney injury (AKI) in the setting of COVID-19 is associated with worse clinical and renal outcomes, with limited long-term data.

To evaluate critically ill COVID-19 patients with AKI that required nephrologist consultation (NC-AKI) in a tertiary hospital.

Prospective single-center cohort of critically ill COVID-19 adult patients with NC-AKI from May 1st, 2020, to April 30th, 2021. Kidney replacement therapy (KRT), recovery of kidney function, and death at 90-day and 1-year follow-up were evaluated.

360 patients were included, 60.6% were male, median age was 66.0 (57.0-72.0) years, 38.1% had diabetes, and 68.6% had hypertension. AKI stages 1, 2, and 3 were detected in 3.6%, 5.6%, and 90.8% of patients, respectively. KRT was indicated in 90% of patients. At the 90-day follow-up, 88.1% of patients died and 10.0% had recovered kidney function. Female gender (p = 0.047), older age (p = 0.047), AKI stage 3 (p = 0.005), requirement of KRT (p < 0.0001), mechanical ventilation (p < 0.0001), and superimposed bacterial infection (p < 0.0001) were significantly associated death within 90 days. At 1 year, mortality was 89.3%. Amongst surviving patients, 72% recovered kidney function, although with significantly lower eGFR compared to baseline (85.5 ± 23.6 vs. 65.9 ± 24.8 mL/min, p = 0.003).

Critically ill COVID-19 patients with NC-AKI presented a high frequency of AKI stage 3 and KRT requirement, with a high 90-day mortality. Surviving patients had high rates of recovery of kidney function, with a lower eGFR at one-year follow-up compared to baseline.

The aim of the study was to investigate the long-term effects of the novel severe acute respiratory syndrome coronavirus (SARS-CoV-2) infection and novel coronavirus disease (COVID-19) on prognosis of kidney transplant recipients.

A 1-year retrospective study was carried out among 362 domestic kidney transplant recipients who were divided into observational (COVID-19) and control groups. Stratification analysis was then carried out to investigate whether repeated infections and infection severity could influence graft prognosis. Kaplan-Meier curves assessed 1-year graft survival, while one-way analysis of variance (ANOVA) compared graft function and laboratory parameters. Generalized estimating equations and repeated-measures ANOVA confirmed the magnitude of the impact of COVID-19 on kidney grafts. Generalized logistic regression and Cox regression established a model for analyzing COVID-19 risk factors. Meta-analysis and subgroup analysis were performed for validation.

Exposure of COVID-19 had a significant effect on graft function within 1 year (p < 0.001), and this kind of effect was mostly brought by severer infections in the stratification analysis regarding graft survival rate (p < 0.001), estimated glomerular filtration rate (eGFR) level (p < 0.001), and 1-year eGFR slope (p = 0.014). Diagnostic model showed tacrolimus patients are less likely to get severe COVID-19 than cyclosporine (p = 0.004). Hyperglycemia (p = 0.004) and low hemoglobin (p = 0.023) are adverse factors for severe pneumonia. Hemoptysis, hypo-lymphopenia, high procalcitonin and ferritin are linked to poor allograft outcomes with SARS-CoV-2 infection.

COVID-19 severity is linked to poor kidney allograft prognosis. Hyperglycemia, low hemoglobin, and drug protocols including cyclosporine rather than tacrolimus are correlated with COVID-19 pneumonia. Hemoptysis, low lymphocytes, high procalcitonin or ferritin were concerned with kidney allograft prognosis post-COVID-19.

Vitamin D deficiency is prevalent among patients undergoing hemodialysis. This study aimed to investigate the associations between vitamin D levels and clinical parameters with the risk of COVID-19 infection, severity, and mortality in hemodialysis patients with end-stage kidney disease (ESKD).

This retrospective cohort study included 198 hemodialysis patients from a single center. Vitamin D deficiency was defined by the last measurement of 25-hydroxycholecalciferol less than 20 ng/mL. Vitamin D deficiency and vitamin D supplements were combined to categorize patients into three groups: deficiency, uncertain deficiency, and likely sufficient. COVID-19 infection status, severity, and outcomes were recorded. Statistical analyses were performed to assess the associations between vitamin D levels and COVID-19 severity and mortality.

Among the 198 patients, 73 patients (37%) were in the deficiency group, 29 patients (15%) had uncertain deficiency, and 96 patients (48%) were likely sufficient. The overall COVID-19 infection rate was 59%. The deficiency group had a similar infection rate (60.3%) compared to those with likely sufficient levels (54.2%). However, the severity and mortality rates of vitamin D deficiency group had a significantly higher rate than those with likely sufficient levels. Multivariate logistic regression analysis showed that vitamin D deficiency and uncertain deficiency group were significantly associated with an increased risk of COVID-19 severity (OR = 22.57, p = 0.01 and OR = 15.8, p = 0.03, respectively). Uncertain deficiency group was significantly associated with an increased risk of COVID-19 mortality (OR = 12.93, p = 0.04), while the deficiency group should similarly trend but did not reach statistical significance.

Vitamin D deficiency is associated with an increased risk of COVID-19 severity in hemodialysis patients with ESKD. These findings suggest that monitoring and managing vitamin D levels may be important in reducing the risk of COVID-19 severity in this vulnerable population.

Acetaminophen serves as a standard antipyretic and analgesic agent in the intensive care unit (ICU). However, the association between its administration and acute kidney injury (AKI) among critically ill patients remains controversial, particularly lacking research in patients with Clostridioides difficile infection (CDI). Our aim was to explore the potential relationship between early acetaminophen administration and AKI in critically ill patients with concurrent CDI.

Using data from the Medical Information Mart for Intensive Care (MIMIC) IV version 2.2 database, we performed a retrospective cohort study. AKI within 7 days of ICU admission was the main outcome that was measured. We utilized multivariable logistic regression models adjusted for potential confounders based on statistical significance and clinical relevance, to investigate the association between acetaminophen exposure and the risk of AKI in patients with CDI. Additionally, subgroup analyses and sensitivity analysis were conducted to assess the robustness of our primary findings.

The average age of 984 participants was 66.8 ± 16.5 years, and 52.7% (519) were male. The overall proportion of patients who developed AKI was 75.4% (742/984). In patients without and with acetaminophen administration, AKI rates were 79.8% (380/476) and 71.3% (362/508), respectively. Compared to the non-acetaminophen administration group, the risk of AKI was lower in the acetaminophen administration group (absolute risk difference: -8.5%, 95%CI: -13.83%∼-3.17%, P < 0.01).After adjusting for potential confounders, acetaminophen administration was associated with a 32% reduction in the risk of AKI (OR = 0.68, 95%CI:0.48∼0.96, P = 0.027).

Our study suggests that early acetaminophen administration may offer renal protection by reducing the risk of AKI in critically ill patients with CDI. Prospective, multicenter randomized controlled studies are needed to verify this finding.

Background: Understanding the interactions between age and comorbidities is crucial for assessing COVID-19 mortality, particularly in patients with cardiac and pulmonary conditions. This study investigates the relationship between comorbidities and mortality outcomes in a cohort of hospitalized COVID-19 patients, emphasizing the interplay of age, cardiac, and pulmonary conditions. Methods: We analyzed a cohort of 3005 patients hospitalized with COVID-19 between 2020 and 2022. Key variables included age, comorbidities (diabetes, cardiac, pulmonary, and neoplasms), and clinical outcomes. Chi-square tests and logistic regression models were used to assess the association between comorbidities and mortality. Stratified analyses by age, diabetes, and pulmonary conditions were conducted to explore interaction effects. Additionally, interaction terms were included in multivariable logistic regression models to evaluate the combined impact of age, comorbidities, and mortality. Results: Cardiac conditions such as hypertension, ischemic cardiopathy, and myocardial infarction showed significant protective effects against mortality in younger patients and in those without pulmonary conditions (p < 0.001). However, these protective effects were diminished in older patients and those with pulmonary comorbidities. Age was found to be a significant modifier of the relationship between cardiac conditions and mortality, with a stronger protective effect observed in patients under the median age (p < 0.001). Pulmonary comorbidities significantly increased the risk of mortality, particularly when co-occurring with cardiac conditions (p < 0.001). Diabetes did not significantly modify the relationship between cardiac conditions and mortality. Conclusions: The findings highlight the complex interactions between age, cardiac conditions, and pulmonary conditions in predicting COVID-19 mortality. Younger patients with cardiac comorbidities show a protective effect against mortality, while pulmonary conditions increase mortality risk, especially in older patients. These insights suggest that individualized risk assessments incorporating age and comorbidities are essential for managing COVID-19 outcomes.

During the COVID-19 pandemic, it has been observed that acute kidney injury (AKI) especially requiring intervention support of hemodialysis has notably increased mortality rates among COVID-19-positive critically ill patients; however, comprehensive data regarding this from India, especially the eastern territory, remains sparse. This study aims to outline the demographic, clinical, and biochemical characteristics, along with the outcomes, of these patients.

A retrospective study was performed at the All India Institute of Medical Sciences (AIIMS), Patna, from March 1, 2020, to March 31, 2021. Included were patients diagnosed with COVID-19 and AKI necessitating hemodialysis during their intensive care unit (ICU) stay. These patients tested positive for COVID-19 and met the Kidney Disease: Improving Global Outcomes (KDIGO) criteria for AKI stages 1-3, requiring ICU admission and hemodialysis. Medical history, clinical features, laboratory results, comorbidities, and demographic data were collected and analyzed. Patients were tracked from admission to discharge or death. Gaussian-distributed values were compared using the unpaired t-test or Pearson's test, while non-Gaussian continuous variables were analyzed using the Mann-Whitney test or Spearman's test. The study employed the Kolmogorov-Smirnov test to assess Gaussian distribution, while categorical data were compared using the Chi-square test.

Among 773 patients with positive COVID-19 tests who were admitted to the ICU, 236 patients developed AKI, and among them, 139 patients required hemodialysis. The total mortality rate was 167 (70.7%) among people who had AKI and 102 (77%) in patients with AKI who required hemodialysis. AKI was also a risk factor associated with higher mortality rates in older patients (>45 years) (n=150 (73.2%)), those needing invasive ventilation (n=163 (88.1%)), and patients with elevated total leucocyte count (TLC) (n=130 (79.3%)), lactate dehydrogenase (LDH) (n=159 (72.9%)), interleukin-6 (IL-6) (n=153 (72.2%)), and serum ferritin (n=51 (73.7%)) and hypoalbuminemia (n=152 (73.1%)).

AKI requiring hemodialysis significantly increases mortality risk in COVID-19 patients. Other risk factors for mortality with AKI in COVID-19-positive patients include age, elevated leucocyte count, invasive ventilation, and deranged inflammatory markers.

Kidney involvement occurs in almost one third of patients hospitalised with coronavirus disease 2019 (COVID-19) and is associated with increased disease severity. This review aims to outline the spectrum of kidney pathology involved in COVID-19. Literature was reviewed systematically on the databases Medline OVID and Scopus in search of case reports, case series, cohort studies and autopsy studies of patients with COVID-19 who underwent kidney biopsies. Studies were published between August 2020 and November 2021. Fourteen studies consisting of 159 patients were included in this review. Acute tubular necrosis is the most common pathology followed by collapsing glomerulopathy, occurring in 40.1% and 28.9% of patients respectively. Of the 46 patients with collapsing glomerulopathy, 44 were of African descent with high-risk apolipoprotein L1 genotypes. Less common glomerular diseases include membranous nephropathy, secondary focal segmental glomerulosclerosis, minimal change disease and primary focal segmental glomerulosclerosis occurring in 5%, 4.4%, 3.1% and 2.5% of patients respectively. Glomerulonephritis occurred in a minority of patients. Direct viral infection has not been found as a definitive aetiology. Acute kidney injury occurs frequently in hospitalised COVID-19 patients and is associated with increased morbidity and mortality. The mechanisms underpinning acute kidney injury are multifactorial. Acute tubular necrosis is the most common. Collapsing glomerulopathy is the most common glomerular injury and is strongly linked to apolipoprotein L1 genotypes. Improved understanding of COVID-19-related kidney pathologies can guide treatment to improve patient outcomes and reduce progression of chronic kidney disease. The longitudinal impact of COVID-19-related kidney disease requires further research.

To explore the risk factors of proteinuria in Omicron variant patients and to construct and verify the risk predictive model.

1091 Omicron patients who were hospitalized from August 2022 to November 2022 at Tianjin First Central Hospital were defined as the derivation cohort. 306 Omicron patients who were hospitalized from January 2022 to March 2022 at the same hospital were defined as the validation cohort. The risk factors of proteinuria in derivation cohort were screened by univariate and multivariate logistic regression analysis, and proteinuria predicting scoring system was constructed and the receiver operating characteristic(ROC)curve was drawn to test the prediction ability. The proteinuria risk model was externally validated in validation cohort.

7 factors including comorbidities, blood urea nitrogen (BUN), serum sodium (Na), uric acid (UA), C reactive protein (CRP) and vaccine dosages were included to construct a risk predictive model. The score ranged from -5 to 16. The area under the ROC curve(AUC) of the model was 0.8326(95% CI 0.7816 to 0.8835, p < 0.0001). Similarly to that observed in derivation cohort, the AUC is 0.833(95% CI 0.7808 to 0.9002, p < 0.0001), which verified good prediction ability and diagnostic accuracy in validation cohort.

The risk model of proteinuria after Omicron infection had better assessing efficiency which could provide reference for clinical prediction of the risk of proteinuria in Omicron patients.

The Coronavirus Disease 2019 (COVID-19) pandemic, driven by the novel coronavirus and its variants, has caused over 518 million infections and 6.25 million deaths globally, leading to a significant health crisis. Beyond its primary respiratory impact, Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) has been implicated in various extra-pulmonary complications. Research studies reveal that the virus affects multiple organs, including the kidneys, liver, pancreas, and central nervous system (CNS), largely due to the widespread expression of Angiotensin Converting Enzyme-2 (ACE-2) receptors. Clinical evidence shows that the virus can induce diabetes by disrupting pancreatic and liver functions as well as cause acute kidney injury. Additionally, neurological complications, including cognitive impairments and neuroinflammation, have been observed in a significant number of COVID-19 patients. This review discusses the mechanisms linking SARS-CoV-2 to acute kidney injury, Type 1 and Type 2 Diabetes Mellitus (T1DM and T2DM), emphasizing its effects on pancreatic beta cells, insulin resistance, and the regulation of gluconeogenesis. We also explore how SARS-CoV-2 induces neurological complications, detailing the intricate pathways of neuro-invasion and the potential to trigger conditions such as Alzheimer's disease (AD). By elucidating the metabolic and neurological manifestations of COVID-19 and the underlying pathogenic mechanisms, this review underscores the imperative for continued research and the development of effective therapeutic interventions to mitigate the long-term and short-term impacts of SARS-CoV-2 infection.

Critically ill COVID-19 patients may exhibit various clinical symptoms of renal dysfunction including severe Acute Kidney Injury (AKI). Currently, there is a lack of bibliometric analyses on COVID-19-related AKI. The aim of this study is to provide an overview of the current research status and hot topics regarding COVID-19 AKI. The literature was retrieved from the Web of Science Core Collection (WoSCC) database. Subsequently, we utilized Microsoft Excel, VOSviewer, Citespace, and Pajek software to revealed the current research status, emerging topics, and developmental trends pertaining to COVID-19 AKI. This study encompassed a total of 1507 studies on COVID-19 AKI. The United States, China, and Italy emerged as the leading three countries in terms of publication numbers, contributing 498 (33.05%), 229 (15.20%), and 140 (9.29%) studies, respectively. The three most active and influential institutions include Huazhong University of Science and Technology, Wuhan University and Harvard Medical School. Ronco C from Italy, holds the record for the highest number of publications, with a total of 15 papers authored. Cheng YC's work from China has garnered the highest number of citations, totaling 470 citations. The co-occurrence analysis of author keywords reveals that 'mortality', 'intensive care units', 'chronic kidney disease', 'nephrology', 'renal transplantation', 'acute respiratory distress syndrome', and 'risk factors' emerge as the primary areas of focus within the realm of COVID-19 AKI. In summary, this study analyzes the research trends in the field of COVID-19 AKI, providing a reference for further exploration and research on COVID-19 AKI mechanisms and treatment.

Literature on the safety of remdesivir in hospitalized COVID-19 patients with severe renal impairment is limited. We aimed to investigate the safety and effectiveness of remdesivir in this population.

We conducted a retrospective cohort study of adult hospitalized COVID-19 patients who received remdesivir between April 2022 and October 2022. Outcomes were compared between estimated glomerular filtration rate (eGFR) <30 mL/min/1.73 m2 and ≥30 mL/min/1.73 m2 groups. The primary safety outcomes were acute kidney injury (AKI) and bradycardia, while the primary effectiveness outcomes included mortality in COVID-19-dedicated wards and hospital mortality. Secondary outcomes included laboratory changes, disease progression, and recovery time.

A total of 1,343 patients were recruited, with 307 (22.9%) in the eGFR <30 group and 1,036 (77.1%) in the eGFR ≥30 group. Patients with an eGFR <30 had higher risks of AKI (adjusted hazard ratio [aHR] 2.92, 95% CI 1.93-4.44) and hospital mortality (aHR 1.47, 95% CI 1.06-2.05) but had comparable risks of bradycardia (aHR 1.15, 95% CI 0.85-1.56) and mortality in dedicated wards (aHR 1.43, 95% CI 0.90-2.28) than patients with an eGFR ≥30. Risk of disease progression was higher in the eGFR <30 group (adjusted odds ratio 1.62, 95% CI 1.16-2.26). No difference between the two groups in laboratory changes and recovery time.

Hospitalized COVID-19 patients receiving remdesivir with severe renal impairment had an increased risk of AKI, hospital mortality, and COVID-19 disease progression compared to patients without severe renal impairment.

Objectives: Although acute respiratory syndrome is the main manifestation of COVID-19 disease, one of the characteristics of the disease is acute kidney injury (AKI). This study aimed to assess the prevalence of kidney dysfunction and para-clinical outcomes in hospitalized COVID-19 patients and its relationship with mortality.Methods: This cross-sectional analytical study was carried out on 715 patients aged older than 16-years with a diagnosis of COVID-19 admitted to the tertiary teaching Imam Reza Hospital, Mashhad, Iran from February 2020 to February 2021. During hospitalization, these patients were evaluated for AKI based on the Kidney Disease Improving Global Outcomes classification and mortality. Demographic variables and laboratory data were extracted from the hospital information systems electronic database. The significant risk factors for the incidence of AKI were analyzed using SPSS software in the present study.Results: The mortality rate of the included patients was 18.9%, which expired during hospitalization. Mortality was higher among patients with stage 1-2 AKI (34.1%) and stage 3 AKI (44.9%) compared to patients without AKI (8.7%). Individuals in different stages of AKI were significantly older relative to the non-AKI patients; hence, aging could be considered as the predictor of AKI. Leukocytosis, lactate dehydrogenase (LDH), and blood urea nitrogen (BUN) were indicated as significant risk factors for the incidence of AKI.Conclusions: It was found that the prevalence of AKI was 37.2% in hospitalized COVID-19 patients, and there was an association between mortality and the incidence of AKI.

Severe acute respiratory syndrome coronavirus-2 (SARS-COV-2) infection is well established as a systemic disease including kidney damage. The entry point into the renal cell remains the angiotensin-converting enzyme 2 (ACE-2) receptor and the spectrum of renal lesions is broad, with a clear predominance of structural and functional tubular lesions. The most common form of glomerular injury is collapsing glomerulopathy (CG), which is strongly associated with apolipoprotein L1(APOL-1) risk variants. These acute lesions, which are secondary to the direct or indirect effects of SARS-CoV-2, can progress to chronicity and are specific to long COVID-19 in the absence of any other cause. Residual inflammation associated with SARS-CoV-2 infection, in addition to acute kidney injury (AKI) as a transitional state with or without severe histological lesions, may be responsible for greater kidney function decline in mild-to-moderate COVID-19. This review discusses the evidence for renal histological markers of chronicity in COVID-19 patients and triggers of low-grade inflammation that may explain the decline in kidney function in the post-COVID-19 period.

Pediatric patients infected with coronavirus disease 2019 (COVID-19) have unique clinical characteristics. Tumor necrosis factor (TNF) is a proinflammatory cytokine that greatly contributes to tumor pathogenesis.

To describe the presenting characteristics of COVID-19 infection among pediatric patients, and investigate the possible role of the TNF-α signaling pathway.

This prospective case-control study included 50 Egyptian pediatric patients with COVID-19 and 50 healthy controls. Clinical, laboratory, and radiological assessments were performed. Serum TNF-alpha (TNF-α), TNF-α-converting enzyme (TACE), and angiotensin-converting enzyme 2 (ACE2) were measured using enzyme-linked immunosorbent assay. ACE (I/D) (rs4646994), ACE2 rs2285666, and TNF-α-308G/A single nucleotide polymorphisms (SNPs) were performed using conventional polymerase chain reaction techniques with or without restriction fragment length polymorphism.

The median age was 1 year (interquartile range [IQR], 0.31-2.50 years) in the case group and 1.45 years (IQR, 1.00-3.00) in the control group. The main presenting symptoms were fever (92%), dry cough (74%), and dyspnea (72%). The lymphocytic count was normal in 14 patients (28%), decreased in 16 patients (32%), and increased in 20 patients (40%) of the case group. Positive chest computed tomography finding of COVID-19 infection were demonstrated among 40% of patients using COVID-19 Reporting and Data System categories (ground-glass opacity with or without consolidations in the lungs). There were significant increased serum TACE and TNF-α with decreased ACE2 levels among cases versus controls (P< 0.001). The GG genotype and G allele of the TNF-α-308G/A SNP were significantly higher in patients than in controls (P<0.05 for both), with insignificant differences in genotype and allelic frequencies in the ACE (I/D) (rs4646994) and ACE2 rs2285666 SNPs.

The TNF signaling pathway was significantly activated in pediatric COVID-19 infection. Only the TNF-α-308G/A SNP was significantly associated with pediatric COVID-19 infection.

Coronavirus disease 2019 (COVID-19) has been recognised as a risk factor for acute kidney injury (AKI). Our aim was to investigate the risk factors contributing to hospitalised and outpatient paediatric COVID-19-associated AKI.

A retrospective observational study was conducted on patients aged 1 month to 18 years with diagnosed COVID-19-associated AKI applied to a tertiary paediatric referral hospital between March 1, 2020 and March 1, 2022.

A total of 6683 patients were evaluated and 486 patients were included in the study. Acute kidney injury was observed in 3.7% of outpatients and 23.9% of hospitalised patients. Multivariate logistic regression analysis showed that, on admission, a history of contact with a COVID-19 positive person (p < 0.001), age below 12 months (p = 0.004), presence of comorbidities (p < 0.001), abdominal pain (p = 0.008), anorexia (p = 0.003), dyspnoea (p = 0.005), higher lactate dehydrogenase values (p = 0.004), neutrophilia (p < 0.001), higher neutrophil-to-lymphocyte ratio (NLR) (p = 0.003), higher white blood cell counts (p = 0.006), elevated C-reactive protein (CRP) levels (p = 0.002), anaemia (p = 0.015), hypoalbuminaemia (p < 0.001), hyperglycaemia (p = 0.006), and presence of proteinuria (p = 0.003) were independent predictors of AKI. Higher rates of hospitalisation (p < 0.001) and admission to the paediatric intensive care unit (PICU) (p < 0.001), longer length of hospitalisation (p < 0.001), and greater need for mechanical ventilation (p < 0.001) were associated with AKI.

This study reveals that not only hospitalised children, but also paediatric patients are at risk for AKI. The presence of comorbidities, abdominal pain, anorexia, dyspnoea, anaemia, inflammation, hypoalbuminaemia, proteinuria and history of contact with a COVID-19 positive person were the main risk factors for AKI. COVID-19-associated AKI was associated with worse outcomes.

The gut microbiota plays a crucial role in modulating the immune response during COVID-19, with several studies reporting significant alterations in specific bacterial genera, including Akkermansia, Bacteroides, Bifidobacterium, Faecalibacterium, Lactobacillus, Oscillospira, and Ruminococcus. These genera are symbionts of the gut microbiota and contribute to host health. However, comparing results across studies is challenging due to differences in analysis methods and reference databases. We screened 16S rRNA raw datasets available in public databases on COVID-19, focusing on the V3-V4 region of the bacterial genome. In total, seven studies were included. All samples underwent the same bioinformatics pipeline, evaluating the differential abundance of these seven bacterial genera at each level of severity. The reanalysis identified significant changes in differential abundance. Bifidobacterium emerged as a potential biomarker of disease severity and a therapeutic target. Bacteroides presented a complex pattern, possibly related to disease-associated inflammation or opportunistic pathogen growth. Lactobacillus showed significant changes in abundance across the COVID-19 stages. On the other hand, Akkermansia and Faecalibacterium did not show significant differences, while Oscillospira and Ruminococcus produced statistically significant results but with limited relevance to COVID-19 severity. Our findings reveal new insights into the differential abundance of key bacterial genera in COVID-19, particularly Bifidobacterium and Bacteroides.