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.

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.

Heart failure (HF) remains a prevalent, high-risk condition particularly common among the elderly population. The impairment of systolic function, secondary dysregulation of maladaptive neurohormonal systems and HF therapies lead to electrolyte disturbances. Hyponatremia is a well-studied, robust marker of adverse prognosis in HF. Serum chloride has emerged as a promising prognostic marker, accurately predicting adverse outcomes in both acute and chronic settings. Hypochloremia reflects a compound of maladaptive neurohormonal, renal and acid–base mechanisms, frequently worsened by diuretic therapy. In the context of HF, low chloride levels are independently associated with increased cardiovascular mortality, HF hospitalization and diuretic resistance. Urinary chloride (uCl⁻) has recently been shown to serve as a dynamic biomarker of HF severity, Renin–Angiotensin–Aldosterone-system (RAAS) activation, and poor outcomes, offering incremental prognostic value. Our review synthesizes the latest evidence on serum and urinary chloride disturbances in HF, framing key distinctions between acute versus persistent electrolyte disturbances. We also explore the interrelationship between chloride and sodium, the differential impact of hypochloremia in Heart Failure with Preserved Ejection Fraction (HFpEF) versus Heart Failure with Reduced Ejection Fraction (HFrEF), and clinical outcomes stratified by the temporary vs. persistent nature of chloride imbalance. We have also included visual flowcharts for classifying and managing hypochloremia based on the underlying etiology.

Background: Valvular heart disease frequently accompanies acute heart failure (AHF), yet most studies address single valve lesions, and the prognostic weight of concurrent multivalvular involvement is less well defined. We examined the prevalence of single- and multi-valve disease and its relationship with one-year mortality. Methods: We analyzed 530 consecutive patients enrolled in a prospective single-center AHF registry between February 2023 and June 2025 and followed for 12 months. Aortic, mitral and tricuspid disease was graded according to European Society of Cardiology/European Association of Cardiovascular Imaging (ESC/EACVI) criteria, a valve being considered involved when it carried at least moderate stenosis and/or regurgitation; multivalvular disease was defined as involvement of two or more valves. The primary endpoint was one-year all-cause mortality. Cox regression was adjusted for admission log N-terminal pro-B-type natriuretic peptide (NT-proBNP), frailty (Clinical Frailty Scale ≥ 5) and age. In-hospital acute kidney injury was examined descriptively but was not entered into the models, because it is ascertained after admission. Results: Overall, 71.3% of patients had at least one significantly diseased valve—mitral in 44.3%, tricuspid in 43.8% and aortic in 27.5%—and 34.9% had multivalvular involvement. One-year mortality rose stepwise with the number of valves involved: 19.7%, 24.9%, 36.3% and 54.0% for zero, one, two and three valves, respectively (log-rank p < 0.001), corresponding to a crude hazard ratio (HR) of 1.51 (95% confidence interval [CI] 1.28–1.78) per additional valve. Multivalvular versus single or no valve involvement carried a crude HR of 2.07 (1.51–2.84) and remained associated with mortality after adjustment (HR 1.48, 95% CI 1.06–2.07, p = 0.020), as did each additional valve (HR 1.22, 1.03–1.45, p = 0.023). Adjustment for clinically manifest right heart failure (HF) attenuated the association with mortality (HR 1.15, 95% CI 0.96–1.37), whereas the association with the triple composite remained significant (HR 1.19, 95% CI 1.03–1.36). Propensity-score adjustment excluding right HF retained the association with mortality (HR 1.43, 95% CI 1.02–2.00), whereas inclusion of right HF attenuated it (HR 1.33, 0.94–1.87). The association was not detectable in the 304 patients without clinically manifest right HF (HR 1.06, 0.80–1.41, p = 0.69). In a post-discharge sensitivity analysis, the adjusted associations were directionally similar but did not reach statistical significance. Conclusions: In hospitalized AHF, multivalvular involvement was common, followed a predominantly mitral–tricuspid pattern, and identified an older, frailer, more congested phenotype with substantial right-sided and chronic renal involvement. Valve burden showed a graded association with one-year mortality that persisted after adjustment for baseline prognostic characteristics, but was attenuated once right-sided involvement was taken into account, whether by direct adjustment or by propensity methods; the association was retained when right HF was omitted from the propensity model. Because right-sided variables lie downstream of significant tricuspid disease, this attenuation is what adjustment for an intermediate is expected to produce and does not establish absence of prognostic value. Cumulative valve burden is therefore best interpreted as a powerful phenotypic marker of a more advanced HF phenotype with prominent right-heart involvement, rather than as an independent causal determinant of mortality.