Cardiac Arrest as the First Presentation of Gitelman Syndrome

Gitelman syndrome is a salt-wasting tubulopathy characterized by profound hypokalemia, hypomagnesemia, metabolic alkalosis, and hypocalciuria. Cardiac arrest is a relatively rare manifestation of Gitelman syndrome. Here we present a case of Gitelman syndrome in a patient with recurrent cardiac arrest. A 43-year-old female was admitted for out-of-hospital cardiac arrest secondary to ventricular fibrillation. Initial workup revealed severe hypokalemia, hypomagnesemia, metabolic alkalosis, and prolonged QTc. The workup revealed a picture of salt-wasting tubulopathy with hypokalemia, hypomagnesemia, and hypocalciuria. Potassium was repleted aggressively, and the patient received potassium-sparing agents resulting in the stabilization of potassium levels. Before discharge, an implantable cardioverter defibrillator (ICD) was placed for secondary prevention of cardiac arrest. The patient remained symptom-free, and electrolytes remained stable. This case highlights the diagnostic challenges of Gitelman syndrome and the importance of accurate diagnosis in improving patient outcomes

Identification of distinct clinical subphenotypes in critically ill patients with COVID-19

Subphenotypes have been identified in patients with sepsis and acute respiratory distress syndrome (ARDS), and are associated with different outcomes and response to therapies. Can unique subphenotypes be identified among critically ill patients with coronavirus disease 2019 (COVID-19)? & Methods: Using data from a multicenter cohort study that enrolled critically ill patients with COVID-19 from 67 hospitals across the United States, we randomly divided centers into Discovery and Replication cohorts. We utilized latent class analysis independently in each cohort to identify subphenotypes based on clinical and laboratory variables. We then analyzed the associations of subphenotypes with 28-day mortality. Latent class analysis identified four subphenotypes (SP) with consistent characteristics across Discovery (45 centers, n=2,188) and Replication (22 centers, n=1,112) cohorts. SP1 was characterized by shock, acidemia, and multi-organ dysfunction, including acute kidney injury treated with renal replacement therapy. SP2 was characterized by high C-reactive protein, early need for mechanical ventilation, and the highest rate of ARDS. SP3 had the highest burden of chronic diseases, while SP4 had limited chronic disease burden and mild physiologic abnormalities. 28-day mortality in the Discovery cohort ranged from 20.6% (SP4) to 52.9% (SP1). Mortality across subphenotypes remained different after adjustment for demographics, comorbidities, organ dysfunction and illness severity, regional and hospital factors: compared with SP4, SP1 relative risk (RR) 1.67 (95% CI 1.36-2.03); SP2 RR 1.39 (1.17-1.65); SP3 RR 1.39 (1.15-1.67). Findings were similar in the Replication cohort. We identified four subphenotypes of COVID-19 critical illness with distinct patterns of clinical and laboratory characteristics, comorbidity burden, and mortality

Obesity, inflammatory and thrombotic markers, and major clinical outcomes in critically ill patients with COVID‐19 in the US

Objective This study aimed to determine whether obesity is independently associated with major adverse clinical outcomes and inflammatory and thrombotic markers in critically ill patients with COVID‐19. Methods The primary outcome was in‐hospital mortality in adults with COVID‐19 admitted to intensive care units across the US. Secondary outcomes were acute respiratory distress syndrome (ARDS), acute kidney injury requiring renal replacement therapy (AKI‐RRT), thrombotic events, and seven blood markers of inflammation and thrombosis. Unadjusted and multivariable‐adjusted models were used. Results Among the 4,908 study patients, mean (SD) age was 60.9 (14.7) years, 3,095 (62.8%) were male, and 2,552 (52.0%) had obesity. In multivariable models, BMI was not associated with mortality. Higher BMI beginning at 25 kg/m2 was associated with a greater risk of ARDS and AKI‐RRT but not thrombosis. There was no clinically significant association between BMI and inflammatory or thrombotic markers. Conclusions In critically ill patients with COVID‐19, higher BMI was not associated with death or thrombotic events but was associated with a greater risk of ARDS and AKI‐RRT. The lack of an association between BMI and circulating biomarkers calls into question the paradigm that obesity contributes to poor outcomes in critically ill patients with COVID‐19 by upregulating systemic inflammatory and prothrombotic pathways