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Background Infective endocarditis (IE) remains a difficult to diagnose condition associated with high mortality. 18 F-fluorodeoxyglucose positron emission tomography/computed tomography ( 18 F-FDG PET/CT) has recently emerged as another IE imaging modality, although diagnostic accuracy varies across observational studies and types of IE. This meta-analysis assessed the diagnostic performance of 18 F-FDG PET/CT for IE and its subtypes. Methods We searched Pubmed, Cochrane, and Embase from January 1980 to September 2019 for studies reporting both sensitivity and specificity of 18 F-FDG PET/CT for IE. Meta-Disc 1.4 was used to pool data for all cases of IE and its subgroups of native valve IE, prosthetic valve IE, and cardiac implantable electronic devices IE. Results We screened 2566 records from the search, assessed 52 full-text articles, and included 26 studies totaling 1358 patients (509 IE cases). Pooled sensitivity and specificity (95% CI, inconsistency I-square statistic) were 0.74 (0.70–0.77, 71.5%) and 0.88 (0.86–0.91, 78.5%) for all cases of endocarditis. Corresponding parameters for native valve IE were sensitivity 0.31 (0.21–0.41, 29.4%) and specificity 0.98 (0.95–0.99, 34.4%); for prosthetic valve IE: sensitivity 0.86 (0.81–0.89, 60.0%) and specificity 0.84 (0.79–0.88, 75.2%); and for cardiac implantable electronic devices IE: sensitivity 0.72 (0.61–0.81, 76.2%) and specificity 0.83 (0.75–0.89, 83.6%). Pooled sensitivities and specificities were higher for the 17 studies since 2015 than the 9 studies published before 2015. Conclusions 18 F-FDG PET/CT had high specificity for all IE subtypes; however, sensitivity was markedly lower for native valve IE than prosthetic valve IE and cardiac implantable electronic devices IE. It is, therefore, a useful adjunct modality for assessing endocarditis, especially in the challenging scenarios of prosthetic valve IE and cardiac implantable electronic devices IE, with improving performance over time, related to advances in 18 F-FDG PET/CT techniques.

Early recognition of acute kidney injury (AKI) is critical to prevent its associated complications as well as its progression to long term adverse outcomes like chronic kidney disease. A growing body of evidence from both laboratory and clinical studies suggests that inflammation is a key factor contributing to the progression of AKI regardless of the initiating event. Biomarkers of inflammation are therefore of interest in the evaluation of AKI pathogenesis and prognosis. There is evidence that the renin angiotensin aldosterone system is activated in AKI, which leads to an increase in angiotensin II (Ang II) formation within the kidney. Ang II activates pro-inflammatory and pro-fibrotic pathways that likely contribute to the progression of AKI. Angiotensinogen is the parent polypeptide from which angiotensin peptides are formed and its stability in urine makes it a more convenient marker of renin angiotensin system activity than direct measurement of Ang II in urine specimens, which would provide more direct information. The potential utility of urinary angiotensinogen as a biomarker of AKI is discussed in light of emerging data showing a strong predictive value of AKI progression, particularly in the setting of decompensated heart failure. The prognostic significance of urinary angiotensinogen as an AKI biomarker strongly suggests a role for renin–angiotensin system activation in modulating the severity of AKI and its outcomes.

We examined if urinary angiotensinogen (uAOG), a marker of intrarenal renin‐angiotensin system activity, antedates stage 3 chronic kidney disease (CKD) using samples from participants in the Diabetes Control and Complications Trial (DCCT) and later in the Epidemiology of Diabetes Intervention and Complications (EDIC) trial. In a nested case–control design, cases were matched at the outcome visit (eGFR less than 60, 21‐59 mL/min per 1.73 m2) on age, gender, and diabetes duration, with controls: eGFR (95, 75‐119, mL/min per 1.73 m2.) Additionally, in an exploratory analysis progressive renal decline (PRD), defined as eGFR loss >3.5 mL/min per 1.73m2/year, was evaluated using only data from EDIC because no progressions were observed during DCCT. At the EDIC visit, which antedated the GFR outcome visit by 2 years (range 1–7years) the median uAOG/creatinine was markedly higher in cases than in controls (13.9 vs. 3.8 ng/mg P = 0.003) whereas at the DCCT visit, which antedated the GFR outcome by 17 to 20 years it was not (2.75 vs. 3.16 ng/mg, respectively). The Odds Ratio for uAOG and CKD stage 3 development was significant after adjusting for eGFR, HbA1c, and systolic blood pressure 1.82 (1.00–3.29) but no longer significant when Albumin Excretion Ratio (AER) was included 1.21 (0.65–2.24).In the PRD analysis, uAOG/creatinine was sixfold higher in participants who experienced PRD than in those who did not (26 vs. 4.0 ng/mg, P = 0.003). The Odds Ratio for uAOG and PRD was significant after adjusting for eGFR, HbA1c, and systolic blood pressure 2.48 (1.46–4.22) but no longer significant when AER was included 1.32 (0.76–2.30). In people with type1 diabetes, a robust increase in uAOG antedates the development of stage 3 CKD but is not superior to AER in predicting this renal outcome. Increased uAOG moreover is associated with PRD, an index of progression to End Stage Kidney Disease (ESKD).

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Erdheim-Chester disease (ECD) is a rare non-Langerhans cell histiocytosis characterized by systemic xanthogranulomatous infiltration. We described the case of a female adult presenting with pericardial effusion. Pericardial infiltration is the most frequent cardiac manifestation of ECD and is the one discussed in this article. We found that the majority of patients with pericardial infiltration needed a cardiovascular procedure.

Background. SARS-CoV-2 is a newly emerged virus that has spread rapidly, exhibiting tremendous morbidity and mortality. Some potential pharmaceutical targets have been identified but are still lacking proper validation. Case Presentation. We describe the case of a young, immunosuppressed and critically ill patient with previous Influenza B infection, requiring extracorporeal membrane oxygenation, which was then followed, in the succeeding months, by SARS-CoV-2 infection complicated by severe adult respiratory distress syndrome. Her clinical course exhibited complications, including pulmonary embolism, acute kidney injury, pneumothorax, pneumomediastinum, multiple cardiac arrests, and eventually death. Conclusion. Coinfection with other respiratory pathogens and opportunistic infections are possible.

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