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.

Under the term cardiorenal syndrome (CRS) falls an increasing number of patients who present with combined heart and kidney dysfunction. Despite the increasing knowledge concerning CRS pathophysiology, diagnosis, and treatment, many of the aforementioned aspects remain obscure in everyday clinical practice. Some of the challenges that clinicians face when they treat CRS nowadays is the need for a patient-centered management with early diagnosis, early intervention, the distinction of true kidney injury from permissive renal function deterioration during decongestion therapy, and the development of therapeutic algorithms to guide therapy.

Cardiorenal syndrome (CRS) reflects the intricate and bidirectional interplay between cardiac and renal dysfunction, commonly resulting in diagnostic uncertainty, therapeutic dilemmas and poor outcomes. While traditional biomarkers like serum creatinine (Cr) and natriuretic peptides remain widely used, their limitations in specificity, timing and contextual interpretation often hinder optimal management. This narrative review synthesizes the current evidence on established and emerging biomarkers in CRS, with emphasis on their clinical relevance, integration into real-world practice, and potential to inform precision therapy. Markers of glomerular filtration rate beyond creatinine—such as cystatin C—offer more accurate assessment in frail or sarcopenic patients, while tubular injury markers such as NGAL, KIM-1, and urinary L-FABP (uL-FABP) provide early signals of structural renal damage. The FDA-approved NephroCheck^® test—based on TIMP-2 and IGFBP7— enables risk stratification for imminent AKI up to 24 h before functional decline. Congestion-related markers such as CA125 and bio-adrenomedullin outperform natriuretic peptides in certain CRS phenotypes, particularly in right-sided heart failure or renally impaired patients. Fibrosis and inflammation markers (galectin-3, sST2, GDF-15) add prognostic insights, especially when combined with NT-proBNP or troponin. Rather than presenting biomarkers in isolation, this review proposes a framework that links them to specific clinical contexts—such as suspected decongestion-related renal worsening or persistent congestion despite therapy—to support actionable interpretation. A tailored, scenario-based, multi-marker strategy may enhance diagnostic precision and treatment safety in CRS. Future research should prioritize prospective biomarker-guided trials and standardized pathways for clinical integration.

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.

Congestion drives most hospitalizations for acute and chronic heart failure (HF), reflecting the pivotal role of sodium and water retention in disease progression. Loop diuretics remain the first-line decongestive therapy, yet up to one-third of patients exhibit an inadequate natriuretic response—defined as diuretic resistance (DR)—which is strongly associated with prolonged hospitalization, readmissions and adverse outcomes. DR is a multifactorial phenomenon arising from pharmacokinetic limitations, tubular adaptations, neurohormonal activation, and hemodynamic disturbances. Impaired renal perfusion, elevated venous pressures, and chloride depletion are key contributors that mutually reinforce one another and blunt diuretic efficacy. Early recognition through urinary sodium measurement and urine output monitoring is essential to guide therapy before resistance becomes entrenched. Beyond optimizing loop diuretic delivery, management strategies should include sequential nephron blockade, correction of electrolyte and acid–base imbalances and avoidance of excessive sodium restriction. Certain patient phenotypes—right heart failure (RHF), advanced chronic kidney disease (CKD), obesity-related HF with preserved ejection fraction (HFpEF), and frail or elderly patients—pose additional challenges due to overlapping mechanisms of resistance and increased treatment vulnerability. Each requires a tailored approach that balances decongestion with preservation of renal function and systemic perfusion. In refractory cases, extracorporeal fluid removal or peritoneal dialysis may be necessary, while newer pharmacologic agents—such as sodium–glucose cotransporter 2 inhibitors (SGLT2i), mineralocorticoid receptor antagonists (MRAs), and glucagon-like peptide-1 receptor agonists GLP-1 RAs)—offer complementary benefits. This review synthesizes mechanistic insights, bedside monitoring tools and phenotype-specific strategies for the management of DR in cardiorenal syndrome (CRS).

Introduction: Acute cardiorenal syndrome (ACRS) is a common complication of acute heart failure (AHF), leading to worse outcomes and therapeutic challenges. This study aimed to identify clinical parameters associated with ACRS and evaluate its impact on prognosis in hospitalized AHF patients. Methods: This prospective observational study included patients hospitalized for AHF at the Venizelio Cardiology Department from February to November 2023. Demographic characteristics, comorbidities, medications, laboratory and echocardiographic parameters, hospital stay, and in-hospital mortality were recorded. Patients with incomplete data or end-stage chronic kidney disease (CKD) were excluded. Survivors were followed for six months to assess renal function changes, readmissions, initiation of renal replacement therapy (RRT), and mortality. ACRS was defined as a serum creatinine increase of ≥0.3 mg/dL or ≥1.5 times baseline. Results: Among 218 hospitalized AHF patients, 112 (51.3%) developed ACRS. These patients were older, had higher CKD prevalence, worse New York Heart Association (NYHA) functional class, lower hemoglobin, and higher N-terminal Pro-B-type Natriuretic peptide (NT-proBNP) levels. Multivariate analysis identified CKD stage (OR 2.30, 95% CI 1.64–3.23, p < 0.001) and creatinine change on admission (OR 3.53, 95% CI 2.02–6.18, p < 0.001) as independent predictors of ACRS. ACRS was associated with higher in-hospital mortality, longer hospital stays, increased vasoactive medication use, worsening renal function, and higher six-month all-cause readmission and mortality rates. Conclusions: ACRS is a frequent and severe complication in AHF. CKD stage and creatinine on admission are key predictors. Early recognition for risk stratification and individualized management are crucial to improving outcomes in this high-risk population.