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.

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.

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.

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.

Background: Frailty is highly prevalent in acute heart failure (AHF), yet whether it is more strongly associated with all-cause mortality or with non-fatal heart-failure events, and whether it adds information beyond cardiac severity, is seldom examined. Methods: In a prospective single-center registry of 530 consecutive patients hospitalized for AHF (February 2023–June 2025), frailty was graded at admission by the Clinical Frailty Scale (CFS; strata 1–3, 4–5, 6–9, and CFS ≥ 5) from patient and collateral history. The primary outcome was 12-month all-cause mortality; first AHF rehospitalization was analyzed with death and renal replacement therapy (RRT) as competing events, using Aalen–Johansen cumulative incidence and cause-specific and Fine–Gray models. Incremental value was tested against a cardiorenal model (age, log NT-proBNP, admission estimated glomerular filtration rate and left ventricular ejection fraction [LVEF]). Results: Frailty was highly prevalent (CFS ≥ 5, 66.4%) and was associated with older age, female sex, renal impairment, right heart failure, multivalvular disease and higher, rather than lower, LVEF. Mortality rose steeply across strata (4.5%, 19.3%, 49.7%; hazard ratio 3.29 per stratum, 95% CI 2.43–4.45), whereas the cumulative incidence of first AHF rehospitalization rose less steeply (4.5%, 29.2%, 33.0%; cause-specific hazard ratio 1.86, 95% CI 1.42–2.45; subdistribution hazard ratio 1.51, 95% CI 1.19–1.92). Frail patients with below-median NT-proBNP had mortality comparable to that of patients with CFS < 5 and above-median NT-proBNP (24.3% vs. 22.0%). Adding CFS to the cardiorenal model improved discrimination (C-index 0.701 → 0.734; optimism-corrected 0.694 → 0.726; apparent ΔC-index 0.033, 95% CI 0.007–0.063) and fit (likelihood-ratio χ² = 27.7, p < 0.001). Discharge prescription of disease-modifying therapy declined with increasing frailty. Conclusions: In elderly patients with AHF, frailty was more strongly associated with all-cause mortality than with documented non-fatal AHF rehospitalization, carried prognostic information complementary to natriuretic peptides, and added discrimination beyond cardiorenal variables, supporting structured frailty assessment alongside heart-failure-directed therapy.

Background: Patients with atrial fibrillation (AF) and advanced chronic kidney disease (CKD) face a markedly elevated risk of both thromboembolic and bleeding events. While oral anticoagulation is the cornerstone of stroke prevention in AF, the optimal use of this treatment in patients with stage 4–5 CKD and end-stage renal disease (ESRD) undergoing dialysis remains uncertain, as these populations were largely excluded from the landmark trials that established the efficacy of direct oral anticoagulants (DOACs) in the general AF population. This study aimed to systematically evaluate and compare the efficacy and safety of vitamin K antagonists (VKAs) and DOACs, including factor Xa inhibitors, compared with alternative anticoagulation strategies or no anticoagulation in patients with AF and advanced CKD, including both non-dialysis-dependent stage 4–5 CKD and dialysis-dependent ESRD. Methods: A systematic search of PubMed (MEDLINE), the Cochrane Library, and ClinicalTrials.gov was performed through January 30, 2026. Randomized controlled trials and observational cohort studies evaluating oral anticoagulation in adults with AF and stage 4–5 CKD (estimated glomerular filtration rate (eGFR) <30 mL/min/1.73 m2, not on dialysis) or ESRD on dialysis were included. Outcomes of interest were a composite of stroke, transient ischemic attack or systemic embolism, major bleeding (International Society on Thrombosis and Haemostasis (ISTH) or study-defined), and all-cause mortality. Owing to clinical and methodological heterogeneity, evidence was synthesized narratively for most comparisons; randomized trials comparing factor Xa inhibitors with VKAs in dialysis-dependent patients were pooled in a random-effects meta-analysis. Results: A total of 20 studies met the inclusion criteria, comprising four randomized trials, one subgroup analysis of an RCT (ARISTOTLE), and fifteen observational cohorts. Four studies evaluated patients with advanced CKD not receiving dialysis, while sixteen focused on dialysis populations. In non-dialysis stage 4–5 CKD, DOAC therapy, particularly apixaban, was generally associated with comparable or reduced thromboembolic risk and lower rates of major bleeding compared with warfarin. Observational data also suggested a potential mortality benefit with DOACs compared with no anticoagulation. In contrast, findings in dialysis-dependent ESRD were heterogeneous. Warfarin was not consistently associated with reduced stroke risk compared with no anticoagulation and was frequently linked to elevated bleeding risk. Observational studies suggest that apixaban may confer a lower risk of major bleeding compared with VKAs while maintaining similar thromboembolic protection; however, randomized evidence has been limited and underpowered to demonstrate a definitive net clinical benefit. In a meta-analysis of the four dialysis randomized trials (n = 486), factor Xa inhibitors were associated with less ISTH major bleeding than VKAs (pooled risk ratio (RR) 0.64, 95% confidence interval (CI) 0.42–0.99; not retained in Mantel–Haenszel or Hartung–Knapp sensitivity analyses), with no significant difference in stroke, transient ischemic attack or systemic embolism (pooled RR 0.46, 95% CI 0.20–1.02) or all-cause mortality (RR 0.88, 95% CI 0.58–1.35). Conclusion: The risk–benefit profile of oral anticoagulation differs across the CKD spectrum. In stage 4–5 CKD not requiring dialysis, DOACs appear to offer a more favorable safety profile than VKAs while preserving efficacy. In dialysis-dependent ESRD, the net clinical benefit of anticoagulation remains uncertain, particularly for warfarin. Further adequately powered randomized trials are needed to clarify optimal anticoagulation strategies in this high-risk population. Until then, treatment decisions should remain individualized, balancing thromboembolic and bleeding risk. PROSPERO Registration: https://www.crd.york.ac.uk/PROSPERO/view/CRD420261286449.