Outcomes of Acute Kidney Injury among Hospitalized Patients with Infective Endocarditis: A National Inpatient Sample Analysis.

Background/Objectives: Patients with infective endocarditis (IE) are more susceptible to acute kidney injury (AKI). The presence of AKI increases in-hospital complications in these patients. Methods: The 2016-2020 National Inpatient Sample (NIS) database consisting of adult admissions with IE and AKI was utilized. The primary outcome was all-cause inpatient mortality. Secondary outcomes included fluid and electrolyte disorders, stroke, septic arterial embolism, septic shock, cardiogenic shock, valve surgery, vasopressor support, mechanical ventilation, length of stay (LOS), and total hospital charges. Results: Out of a total of 63,725 adult admissions with IE, 16,295 (25.5%) admissions had AKI. Patients with AKI were more likely to be males (63% vs. 57.6%, p < 0.001) and older (55.8 vs. 50.4, p < 0.001). A higher proportion of these patients were admitted to large hospitals (60.6 vs. 55.3%, p < 0.001) and urban teaching hospitals (81.9 vs. 75%, p < 0.001). Patients with AKI had higher LOS (17 ± 16.1 vs. 11.32 ± 11.7, p < 0.001) and hospital charges (USD 239,046.8 ± 303,977.3 vs. USD 124,857.6 ± 192,883.5, p < 0.001). Multivariable analysis showed higher odds of all-cause inpatient mortality (aOR: 2.22, 95% CI: 1.81-2.73, p < 0.001). They also had higher risk for fluid and electrolyte disorder (aOR: 2.31, 95% CI: 2.10-2.53, p < 0.001), septic arterial embolism (aOR: 1.61, 95% CI: 1.42-1.84, p < 0.001), septic shock (aOR: 3.78, 95% CI: 2.97-4.82, p < 0.001), cardiogenic shock (OR: 3.37, 95% CI: 2.65-4.28, p < 0.001), valve surgery (aOR: 1.52, 95% CI: 1.35-1.71, p < 0.001), vasopressor requirement (aOR: 1.99, 95% CI: 1.52-2.60, p < 0.001), and mechanical ventilation (aOR: 2.75, 95% CI: 2.33-3.24, p < 0.001). The association with stroke was elevated but not statistically significant. Conclusions: This large retrospective analysis demonstrated that patients with AKI and infective endocarditis had increased mortality, adverse hospital outcomes, increased LOS, and hospital costs.

Depression and incident cardiovascular disease among patients with chronic kidney disease.

Background: Depression is associated with an increased risk of cardiovascular disease (CVD) and is prevalent among patients with chronic kidney disease (CKD). We aimed to identify the association of depression with incident CVD. Methods: We studied patients with CKD stages 2-4 enrolled in the Chronic Renal Insufficiency Cohort (CRIC) and excluded participants with preexisting CVD. The Cox proportional hazard model was used to examine the association between baseline depression [Beck's Depression Inventory (BDI) score ≥11] and incidence of CVD (cerebrovascular accident, myocardial infarction, heart failure, or peripheral artery disease). Models were adjusted for age, sex, race, estimated glomerular filtration rate (eGFR), urine albumin-creatinine ratio (UACR), systolic and diastolic blood pressure, and 10-year estimated CVD risk. Results: Among 2585 CRIC study participants, 640 (25%) patients had depression at study baseline. Compared to patients without depression, patients with depression were more likely to be women (56% vs. 46%), non-White (68% vs. 53%), with household income <$20,000 (53% vs. 26%), without a high school degree (31% vs. 15%), uninsured (13% vs. 7%), with lower eGFR (42 vs. 46 ml/min/1.73 m (Palmer et al., 2013 Jul)22), and with higher UACR (90 vs. 33 mg/g). In multivariate analyses, depression was associated with a 29% increased risk of developing CVD (adjusted hazard ratio 1.29, 95% confidence interval 1.03-1.62, p = 0.03). BDI (as a continuous variable) was associated with CVD (adjusted hazard ratio 1.017, 95% confidence interval 1.004-1.030, p = 0.012). Conclusions: Among patients with CKD stages 2-4 enrolled in CRIC without preexisting CVD, depression was associated with a 29% increased risk of incident CVD.

A Case of Coombs-Negative Hemolytic Anemia Prompting Diagnosis of SARS-CoV-2.

Case reports have discussed coronavirus disease of 2019 (COVID-19) patients presenting with hemolytic anemia, specifically with a positive direct antiglobulin test. However, Coombs-negative hemolytic anemia in COVID-19 patients has been rarely reported. We present an unusual case of Coombs-negative hemolytic anemia caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) which responded with evidence-based COVID-19 treatments. We demonstrate the importance of considering SARS-CoV-2 as a cause of Coombs-negative hemolytic anemia, and we illustrate how treatment of the underlying COVID-19 illness, even if it is just supportive care, will help resolve the associated hemolysis.

Transcription factor NF-κB in a basal metazoan, the sponge, has conserved and unique sequences, activities, and regulation.

Herein, we characterize transcription factor NF-κB from the demosponge Amphimedon queenslandica (Aq). Aq-NF-κB is most similar to NF-κB p100/p105 among vertebrate proteins, with an N-terminal DNA-binding domain, a C-terminal Ankyrin (ANK) repeat domain, and a DNA binding-site profile akin to human NF-κB proteins. Like mammalian NF-κB p100, C-terminal truncation allows nuclear translocation of Aq-NF-κB and increases its transcriptional activation activity. Expression of IκB kinases (IKKs) induces proteasome-dependent C-terminal processing of Aq-NF-κB in human cells, and processing requires C-terminal serines in Aq-NF-κB. Unlike NF-κB p100, C-terminal sequences of Aq-NF-κB do not inhibit its DNA-binding activity. Tissue of a black encrusting demosponge contains NF-κB site DNA-binding activity, as well as nuclear and processed NF-κB. Treatment of sponge tissue with LPS increases both DNA-binding activity and processing of NF-κB. A. queenslandica transcriptomes contain homologs to upstream NF-κB pathway components. This is first functional characterization of NF-κB in sponge, the most basal multicellular animal.