Febrile neutropenia (FN) is a common but serious complication encountered in patients with cancer and is associated with significant morbidity and mortality. In this prospective study, 63 patients with solid tumors under chemotherapy or immunotherapy were admitted to the hospital due to febrile neutropenia, confirmed through clinical or microbiological documentation. The aim of this study was to provide a comprehensive overview of the epidemiological and microbiological characteristics of hospitalized neutropenic patients with solid tumors undergoing treatment. Additionally, we aimed to assess the duration of neutropenia and identify factors influencing patient outcomes. The median age of patients was 71 ± 10.2 years, most of which were males (66.7%), and the primitive tumor location was the lung (38.1%), with most patients (82.5%) being at disease stage IV. The median duration of neutropenia was three days (range 1–10), and, notably, mucositis was significantly associated with neutropenia lasting ≥3 days (p = 0.012). Patients with lung cancer (38.1%) and patients with stage IV disease (82.5%) presented a higher risk of FN, although these differences did not reach statistical significance. The site of infection was identifiable in 55.6% of patients, with positive cultures detected in 34.9% and positive blood cultures (BC) drawn in 17.5% of cases. Gram-positive bacteria were the predominant causative agents in BC (63.6%), with Staphylococci being the most prevalent among them (66.7%). The median duration of hospitalization was nine days (range, 3–43 days), and most patients showed improvement or cure of infection (16.9% and 74.6%, respectively). Among recorded risk factors, the Eastern Cooperative Oncology Group (ECOG) performance status (PS) appears to be statistically significant. Patients with an impaired PS score (2–4) experienced worse outcomes and higher likelihood of mortality (p = 0.004). Regarding the outcome, a longer duration of neutropenia was also statistically significant (p = 0.050). Of the patients, 12.7% ultimately succumbed to their conditions, with 37.5% attributed to infections. FN is a common yet serious complication in solid tumor patients. Adequate knowledge of the predictors of mortality and the microbiological causes are of utmost importance to allow accurate diagnosis and prompt treatment as they significantly influence patient outcomes.

Background: Elevated cardiac troponin (cTn) levels in patients with paroxysmal supraventricular tachycardia (PSVT) often prompt coronary artery disease evaluation, though the clinical relevance of this finding remains unclear. This study aimed to identify risk factors for cTn elevation after a PSVT episode and assess its clinical significance, including the role of coronary artery disease (CAD) and long-term outcomes. Methods: We retrospectively collected data on demographics, presenting symptoms, comorbidities, chronic antiarrhythmic medication use, tachycardia duration, admission systolic blood pressure (SBP), heart rate (HR), laboratory findings, and cardioversion method in patients presenting to the Emergency Department (ED) with PSVT over a 4-year period. Patients were stratified into two groups based on the presence or absence of troponin elevation. Individuals with elevated cTn levels and at least one cardiovascular risk factor were further evaluated for CAD. One-year outcomes included SVT recurrence, rehospitalization, ablation, and mortality. Results: Among 120 patients with PSVT, 58 (48.3%) exhibited elevated cardiac troponin (cTn) levels. Independent predictors of cTn elevation included retrosternal chest pain, absence of prior SVT history, higher admission HR, and lower SBP. A heart rate cut-off of 165 bpm was identified as optimal for predicting cTn elevation (sensitivity 62.1%, specificity 72.6%). Of the 58 cTn (+) patients, 25 underwent CAD evaluation, with only 1 case (4%) confirming significant coronary disease. At one-year follow-up (n = 118), troponin elevation was not associated with increased SVT recurrence, rehospitalization, ablation, or mortality. Similarly, CAD evaluation in troponin-positive patients did not predict outcomes. Conclusions: Troponin elevation after PSVT is frequent but not prognostically significant. It is likely due to transient myocardial stress rather than CAD, supporting a conservative, individualized approach to further testing.

Background: Salt-sensitive blood pressure (SSBP) represents a prevalent yet underrecognized hypertensive phenotype, in which blood pressure (BP) and volume status are disproportionately influenced by dietary sodium intake. Beyond BP elevation alone, salt sensitivity reflects a convergence of renal sodium handling abnormalities, neurohormonal activation, vascular dysfunction, and inflammatory pathways that link excessive sodium exposure to progressive kidney injury and adverse cardiac remodeling. Given its association with chronic kidney disease (CKD) and the association of heart failure with preserved ejection fraction (HFpEF), improved recognition of SSBP has direct clinical relevance. Objective: This narrative review aims to synthesize current mechanistic and clinical evidence on SSBP, focusing on pathophysiology, cardiorenal interactions, diagnostic challenges, and phenotype-guided therapeutic strategies with practical applicability. Methods: A narrative literature review was conducted using PubMed, Scopus, and Web of Science from inception through January 2026. Experimental, translational, and clinical studies, along with relevant guideline documents, were integrated to provide conceptual and clinical interpretation rather than quantitative analysis. Key Findings: Impaired renal sodium excretion, intrarenal RAAS activation, sympathetic overactivity, endothelial dysfunction, and immune-mediated inflammation contribute to sodium retention, microvascular dysfunction, and fibrotic remodeling across the kidney–heart axis. These pathways are strongly supported by experimental and translational data, but direct interventional clinical validation remains limited for several mechanisms. Clinically, salt-sensitive individuals often exhibit non-dipping BP patterns, albuminuria, salt-induced edema, and a predisposition to HFpEF. Dynamic BP monitoring combined with targeted laboratory assessment improves identification of this phenotype and supports individualized management. Conclusions: Early recognition of SSBP enables targeted interventions beyond uniform sodium restriction. Phenotype-guided strategies integrating lifestyle modification, RAAS blockade, thiazide-like diuretics, mineralocorticoid receptor antagonists, and sodium-glucose co-transporters 2 inhibitors (SGLT2i) may improve cardiorenal outcomes. Emerging precision tools (e.g., wearable blood-pressure sensors, digital sodium tracking technologies, etc.) remain exploratory but may further refine individualized management.

Background: Bloodstream infections (BSIs) represent a severe complication among patients with solid tumors (STs), contributing substantially to morbidity and mortality, especially in the context of increasing antimicrobial resistance (AMR). Evidence in STs remains limited compared to hematologic malignancies. Methods: We conducted a two-center observational study including 282 hospitalized adults with solid malignancies and documented infections; 66 patients (23.4%) had confirmed BSIs. Clinical characteristics, microbiological profiles, resistance patterns, and outcomes were evaluated. Results: Patients had a mean age of 66.4 ± 11.8 years, and 63.6% were male. The majority (84.8%) had stage IV disease and were receiving chemotherapy (95.5%). Gram-negative bacteria predominated (51.5%), mainly Escherichia coli, Klebsiella pneumoniae, and Pseudomonas aeruginosa. Multidrug resistance (MDR) was detected in 45.5% of isolates, while 28.8% of BSIs were polymicrobial; both were associated with worse outcomes and increased infection-related mortality (p = 0.041 and p = 0.032, respectively). Overall infection-related mortality reached 28.8%. In multivariable analysis, poor functional status (ECOG PS ≥ 2), prior hospitalization, and concurrent radiotherapy were independently associated with unfavorable outcomes. Conclusions: BSIs remain a significant cause of morbidity and mortality in patients with STs. The high burden of Gram-negative and MDR pathogens, along with the impact of polymicrobial infections and impaired performance status, highlights the need for early risk stratification and locally adapted empirical antimicrobial strategies. Prospective multicenter studies are warranted to validate these findings and optimize management strategies in this vulnerable population.

Hypertension has traditionally been viewed as a hemodynamic disorder leading to cardiac and renal injury; however, growing evidence suggests that, in many individuals, elevated blood pressure is instead the earliest clinical expression of subtle cardiorenal dysfunction. Early abnormalities—such as low-grade albuminuria, increased renal resistive index, arterial stiffness, and masked or nocturnal hypertension—can appear before estimated glomerular filtration rate decline or elevated office blood pressure, indicating early impairment of pressure–natriuresis, heightened tissue renin–angiotensin–aldosterone system (RAAS) activity, and increased renal microvascular impedance. The aim of this review is to summarize mechanistic, clinical, and phenotypic evidence supporting the concept that hypertension functions as an early biomarker along the cardiorenal continuum. Incorporating vascular and renal biomarkers, ambulatory blood pressure phenotyping, and targeted laboratory indices into routine assessment may identify individuals transitioning from functional disturbances to structural organ damage. These abnormalities reflect a mechanistic triad of arterial stiffening, salt-sensitive RAAS activation, and circadian blood pressure disruption, collectively defining the early cardiorenal–hypertensive phenotype. Viewing hypertension through a cardiorenal lens underscores a critical opportunity for earlier detection and mechanism-oriented intervention, which may modify disease trajectory and prevent progression to overt chronic kidney disease and heart failure.