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Background: COVID-19 can lead to functional disorders and complications, e.g., pulmonary, thromboembolic, and neurological. The neuro-invasive potential of SARS-CoV-2 may result in acute brain malfunction, which manifests as delirium as a symptom. Delirium is a risk factor for death among patients hospitalized due to critical illness. Taking the above into consideration, the authors investigated risk factors for delirium in COVID-19 patients and its influence on outcomes.
Methods: A total of 335 patients hospitalized due to severe forms of COVID-19 were enrolled in the study. Data were collected from medical charts.
Results: Delirium occurred among 21.5% of patients. In the delirium group, mortality was significantly higher compared to non-delirium patients (59.7% vs. 28.5%; < 0.001). Delirium increased the risk of death, with an OR of 3.71 (95% CI 2.16-6.89; < 0.001). Age, chronic atrial fibrillation, elevated INR, urea, and procalcitonin, as well as decreased phosphates, appeared to be the independent risk factors for delirium occurrence.
Conclusions: Delirium occurrence in patients with severe COVID-19 significantly increases the risk of death and is associated with a cardiovascular burden. Hypophosphatemia is a promising reversible factor to reduce mortality in this group of patients. However, larger studies are essential in this area.
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http://dx.doi.org/10.3390/jcm12155049 | DOI Listing |
J Am Soc Nephrol
September 2025
Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN, USA.
Background: Genetic modifiers are believed to play an important role in the onset and severity of polycystic kidney disease (PKD), but identifying these modifiers has been challenging due to the lack of effective methodologies.
Methods: We generated zebrafish mutants of IFT140, a skeletal ciliopathy gene and newly identified autosomal dominant PKD (ADPKD) gene, to examine skeletal development and kidney cyst formation in larval and juvenile mutants. Additionally, we utilized ift140 crispants, generated through efficient microhomology-mediated end joining (MMEJ)-based genome editing, to compare phenotypes with mutants and conduct a pilot genetic modifier screen.
JCI Insight
September 2025
Department of Pharmacology, University of Michigan, Ann Arbor, United States of America.
Cardiac hypertrophy is a common adaptation to cardiovascular stress and often a prelude to heart failure. We examined how S-palmitoylation of the small GTPase, Ras-related C3 botulinum toxin substrate 1 (Rac1), impacts cardiomyocyte stress signaling. Mutation of the cysteine-178 palmitoylation site impaired activation of Rac1 when overexpressed in cardiomyocytes.
View Article and Find Full Text PDFJAMA Netw Open
September 2025
Department of Internal Medicine, University of Arkansas for Medical Sciences, Little Rock.
Importance: Patients with kidney failure (KF) receiving long-term dialysis have increased incidence of atrial fibrillation (AF). Patients with KF and AF have increased risk of stroke, death, and bleeding compared with age-matched cohorts. In KF, the use of oral anticoagulants (OACs) increases hemorrhage risk, offsetting potential benefits and making left atrial appendage occlusion (LAAO) a potentially promising solution for risk reduction in AF.
View Article and Find Full Text PDFHigh Blood Press Cardiovasc Prev
September 2025
Center for Translational and Experimental Cardiology, Department of Cardiology, University Hospital Zurich and University of Zürich, Wagistrasse 12, 8952, Schlieren, Switzerland.
Introduction: Epigenetic changes are important modulators of gene expression. The histone acetyltransferase gene non-derepressible 5 (Gcn5) is emerging as a pivotal epigenetic player in metabolism and cancer, yet its role in obesity and cardiovascular disease remains elusive.
Aims: To investigate Gcn5 role in obesity-related endothelial dysfunction.
Apoptosis
September 2025
Department of Physiology, School of Basic Medical Sciences, Southwest Medical University, Luzhou, 646000, Sichuang, China.
Cardiovascular diseases (CVDs) are a leading cause of death globally, responsible for 32% of all fatalities. They significantly reduce quality of life and life expectancy, while imposing a substantial economic burden on healthcare systems in different countries. High mobility group box 1 (HMGB1), a location-dependent multifunctional protein, plays a significant role in various cell death pathways associated with CVDs.
View Article and Find Full Text PDF