Search Results (214)

Heart failure (HF) treatment evolved in the last 5 years with the introduction of new agents capable of reducing HF hospitalization and HF-related mortality. However, some categories such as patients with renal dysfunction tend to be excluded from larger randomized clinical trials. Additionally, most patients with HF experienced unavoidable glomerular filtration rate (GFR) deterioration during the clinical course. This is related to both cardio–renal interaction pathways and common cardiovascular risk factors that affect HF and chronic kidney disease (CKD). However, mineralocorticoid antagonists (MRAs) remain a cornerstone of HF therapy regardless of left ventricular ejection fraction (LVEF) values; some concerns remain about their utilization in CKD. Nevertheless, three studies (FIDELIO, FIGARO, and FINEARTS) have recently showed beneficial effects in both patients with HF and CKD associated with diabetes. Notably, finerenone a new non-steroidal MRA represents a significant step forward in cardiovascular therapy; its application spans a wide spectrum of HF phenotypes and CKD stages, and ongoing investigations will further elucidate its role in combination regimens and in broader patient populations. Further study may investigate the role of the drug in patients with heart failure with reduced ejection fraction (HFrEF) and in the severe CKD stage of non-diabetic etiology. In the current review paper, we provide a chronological overview of major trials evaluating the renal outcomes of MRAs, culminating in the emergence of finerenone as a novel therapeutic option for high-risk CKD populations, particularly those with type 2 diabetes mellitus (T2DM). Full article

Background/Objectives: Impaired kidney function significantly increases mortality in recipients of implantable cardioverter defibrillators (ICDs). However, in the landmark studies evaluating ICDs and cardiac resynchronization therapy with a defibrillator (CRT-D) for the treatment of heart failure (HF) with a reduced ejection fraction (HFrEF), patients with Chagas cardiomyopathy (CC) have been underrepresented. This study aimed to determine whether kidney dysfunction has the same negative impacts on patients with ICDs or CRT-Ds and CC. Methods: We prospectively followed patients with CC and left ventricular ejection fractions (LVEFs) of ≤40% who underwent ICD or CRT-D implantation and had at least one prior creatinine measurement. The primary outcome was the survival rate during follow-up. Variables with a p of <0.10 from the univariate analysis were selected for inclusion in the Cox regression model. Results: A total of 343 patients were enrolled, with a median follow-up duration of 777 days. The mean age was 60.2 (±11.2) years. Fifty percent of patients were observed to have a New York Heart Association (NYHA) functional class of III, and the median left ventricular ejection fraction (LVEF) was 27% (22–32). Overall mortality events occurred in 113 (32.9%) participants during follow-up. Although the estimated glomerular filtration rate (eGFR) was significantly associated with survival in the univariate analysis [HR 0.98 (CI 95% 0.98–0.99), p = 0.007], it did not retain significance in the multivariate model [HR 0.99 (0.98–1.00), p = 0.138], which was adjusted for age, gender, atrial fibrillation (AF), body mass index (BMI), and the use of digoxin, furosemide, anticoagulants, and LVEF. Conclusions: Unlike other cardiomyopathies, impaired eGFR was not an independent predictor of mortality in this cohort of CC patients undergoing ICD or CRT-D implantation, possibly due to the distinctive pathophysiological mechanisms of the disease. These findings suggest that clinicians should not be discouraged from recommending CIEDs in patients with CC and moderately impaired kidney function, although further studies are warranted to assess outcomes in those with advanced CKD. Full article

Background: Ischemia–reperfusion injury (IRI) is a key contributor to graft dysfunction in kidney transplantation. Cell-free mitochondrial DNA (mtDNA) is increasingly recognized as a damage-associated molecular pattern (DAMP) and biomarker in IRI, but its prognostic role in living donor kidney transplantation (LDKT) remains unclear. Methods: This post hoc analysis of the VAPOR-1 study evaluated urinary mtDNA (UmtDNA) in 57 LDKT recipients. MtDNA levels (ND1, ND6, and D-loop) were measured at five early timepoints post-transplantation using qPCR. Associations between early UmtDNA and long-term graft function, defined by estimated glomerular filtration rate (eGFR) at 1, 12, and 24 months, were analyzed. Results: Higher UmtDNA levels in the first urine after reperfusion were significantly associated with improved eGFR at 12 months and a positive change in eGFR between month 1 and 24. These associations were not attributable to urine creatinine levels or mitochondrial copy number. Conclusions: In this LDKT cohort, elevated early UmtDNA may reflect a well-functioning graft capable of clearing systemic mtDNA rather than ongoing tubular injury. These findings suggest that the biological interpretation of mtDNA as a biomarker is context-dependent and call for careful reconsideration of its role in early transplant monitoring. Full article

As the population of adults with congenital heart disease (ACHD) continues to grow, a significant and often underrecognized complication is the development of cardiorenal syndrome (CRS)—a complex, bidirectional interaction between cardiac and renal dysfunction. While CRS has been extensively studied in acquired heart failure, its manifestations and implications in ACHD remain insufficiently understood. Emerging data suggest that renal dysfunction is highly prevalent in ACHD, with significant associations to adverse outcomes regardless of cardiac lesion type or functional status. This review explores CRS within three key physiologic categories in ACHD: patients with a systemic right ventricle, those with a subpulmonary right ventricle, and those with Fontan circulation. Each subgroup presents unique hemodynamic challenges that affect renal perfusion, filtration pressure, and systemic congestion, contributing to both acute and chronic renal impairment. The utility of renal biomarkers such as albuminuria, cystatin C, and estimated glomerular filtration rate (eGFR) is emphasized, alongside the importance of early detection and multidisciplinary management. Heart failure therapy tailored to congenital anatomy, neurohormonal modulation, and careful volume control remain the cornerstones of treatment, while transplantation strategies must consider the potential for irreversible end-organ damage. Given the profound implications of CRS on quality of life and survival, a comprehensive understanding of its pathophysiology and management in ACHD is critical to optimizing long-term outcomes in this increasingly complex patient population. Full article

Background\Objectives: Chronic kidney disease (CKD) is defined as a clinical syndrome secondary to a permanent change in kidney function or structure, making it irreversible. Most patients at the onset of the disease are asymptomatic or present nonspecific symptoms, including signs and symptoms at the oral level. These manifestations, such as hyposalivation, increased calculus index, enamel defects, or changes in saliva composition, contribute to the diagnosis of this pathology and can also significantly affect the patient’s quality of life. The aim is to systematically assess the presence and relevance of oral manifestations in patients with CKD, and to identify correlations between these symptoms and clinical parameters such as glomerular filtration rate or concomitant conditions of the patient. Materials and Methods: A systematic review was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. A search was carried out in the PubMed, Scopus, Scielo, and The Cochrane Library databases on 7 April 2025, using terms related to “chronic kidney disease” and “oral manifestations”. Inclusion criteria referred to observational studies published in the last ten years that reported oral symptoms in patients with CKD. The quality of cohort and case-control studies was assessed using the Newcastle–Ottawa Scale (NOS), while for cross-sectional studies, the Joanna Briggs Institute (JBI) critical appraisal checklist was used. Results: A total of 27 studies met the inclusion criteria, primarily cross-sectional in design. The most frequently reported oral manifestations included hyposalivation, increased calculus and plaque indices, enamel defects, periodontal disease, and oral candidiasis. Significant associations were identified between the duration of dialysis and severity of periodontal disease, as well as between CKD stage and taste dysfunction. Findings varied by age group and CKD stage, with children showing distinct salivary profiles and adults presenting more pronounced periodontal and mucosal conditions. Conclusions: This review highlights a clear relationship between CKD and various oral health disturbances, although more studies are needed to better understand oral–systemic interactions in CKD. What is necessary is the establishment of multidisciplinary care approaches. Full article

Background: Sleep-disordered breathing (SDB), particularly Cheyne–Stokes respiration (CSR), is highly prevalent among patients hospitalized with acute decompensated heart failure (ADHF) and is associated with worse clinical outcomes. Sodium-glucose cotransporter-2 inhibitors (SGLT2i) have demonstrated cardiorenal benefits in heart failure, but their effects on nocturnal respiratory parameters remain underexplored. Objectives: This study aims to evaluate the impact of SGLT2i therapy on key respiratory and cardiac indices including CSR burden, oxygenation, and right heart function in patients with ADHF and reduced left ventricular ejection fraction. Methods: In this single-center prospective cohort study, 60 patients with ADHF, LVEF < 40%, and a baseline apnea–hypopnea index (AHI) > 5 were assessed before and three months after the initiation of SGLT2i therapy. Sleep respiratory parameters were measured using home polygraphy (ApneaLink^TM), while cardiac and renal indices were evaluated by echocardiography, NT-proBNP, and the estimated glomerular filtration rate (eGFR). Structural and functional echocardiographic changes were analyzed both at baseline and following the 3-month treatment period. Patient-reported outcomes were assessed using the Epworth Sleepiness Scale (ESS) and Kansas City Cardiomyopathy Questionnaire (KCCQ). Results: After 3 months of SGLT2i therapy, significant improvements were observed in daytime sleepiness (ESS: −2.68 points; p < 0.001), CSR index (−5.63 events/h; p < 0.001), AHI (−3.07 events/h; p < 0.001), ODI (−6.11 events/h; p < 0.001), and mean nocturnal SpO₂ (+1.95%; p < 0.001). KCCQ scores increased by 9.16 points (p < 0.001), indicating improved quality of life. Cardiac assessments revealed reductions in NT-proBNP (−329.6 pg/mL; p < 0.001) and E/e′ ratio (−1.08; p < 0.001), with no significant change in LVEF or chamber dimensions. Right ventricular function improved, as evidenced by the increased TAPSE/sPAP ratio (+0.018; p < 0.001). Renal function remained stable, with a non-significant upward trend in eGFR. Conclusions: This exploratory study suggests that SGLT2 inhibitors may be associated with the attenuation of Cheyne–Stokes respiration and an improvement in right heart function in patients with ADHF, warranting further investigation in controlled trials. These findings highlight the potential of SGLT2is to address overlapping cardio-respiratory dysfunction in this high-risk population. Full article

Background: According to a study conducted among a relatively healthy population of Mongolia (2017), the prevalence of hepatitis C virus (HCV) infection is 8.5%, which is considered a high prevalence of this infection. In addition to inflammation of the liver, other organ systems are affected by HCV infection, according to research. Our study aimed to evaluate renal dysfunction in patients with HCV infection. Methods: In the study, 111 people with chronic hepatitis C virus infection were included in the study group, and 111 relatively healthy people were included in the control group. Laboratory parameters were analyzed. Liver fibrosis score was assessed and evaluated by renal function. Results: There were 22.9% (51) men and 77.1% (171) women among the 222 participants, and the average age was 40.7 ± 11.1 years. The glomerular filtration rate was 105.3 ± 24.5 in the chronic hepatitis C virus-infected group and 118.7 ± 18.5 in the control group, or the statistically significant difference in the case group compared to the control group was p < 0.01. The liver fibrosis score was higher in the case group than in the control group. According to logistic regression analysis, patients with hepatitis C virus infection are 25 times more likely to have a decrease in glomerular filtration rate than those without viral infection (OR 24.91, 95% CI 3.13–198.38, p = 0.002). Conclusions: Our study showed that HCV infection leads to kidney function loss. In addition, older age, obesity, and severe liver fibrosis contribute to kidney function decline. Full article

Background: Chronic kidney disease (CKD) and its advanced stage, end-stage renal disease (ESRD), affect millions worldwide and are associated with a paradoxical hemostatic imbalance—marked by both increased thrombotic and bleeding risks—which complicates anticoagulant use and demands clearer, evidence-based clinical guidance. Design: This study is a critical review synthesizing the current literature on anticoagulant therapy in CKD and ESRD, with emphasis on altered pharmacokinetics, clinical complications, and therapeutic adjustments. Data Sources: PubMed, Scopus, and Google Scholar were searched for articles discussing anticoagulation in CKD/ESRD, focusing on pharmacokinetics, clinical outcomes, and dosing recommendations. Study Selection: Studies examining the safety, efficacy, and pharmacokinetics of anticoagulants—including heparin, low-molecular-weight heparin (LMWH), warfarin, and direct oral anticoagulants (DOACs)—in CKD and ESRD populations were included. Data Extraction and Synthesis: Key findings were summarized to highlight the dose modifications, therapeutic considerations, and clinical challenges in managing anticoagulation in CKD/patients with ESRD. Emphasis was placed on balancing thrombotic and bleeding risks and identifying gaps in existing guidelines. Results: Patients with CKD and ESRD exhibit a paradoxical hypercoagulable state marked by platelet dysfunction, altered coagulation factors, and vascular endothelial damage. This condition increases the risk of thrombotic events, such as deep vein thrombosis (DVT) and pulmonary embolism (PE), while simultaneously elevating bleeding risks. Hemodialysis and CKD-associated variables further complicate the management of coagulation. Among anticoagulants, unfractionated heparin (UFH) is preferred due to its short half-life and adjustability based on activated partial thromboplastin time (aPTT). Low-molecular-weight heparins (LMWHs) offer predictable pharmacokinetics but require dose adjustments in CKD stages 4 and 5 due to reduced clearance. Warfarin necessitates careful dosing based on the estimated glomerular filtration rate (eGFR) to maintain an international normalized ratio (INR) ≤ 4, minimizing bleeding risks. Direct oral anticoagulants (DOACs), particularly Apixaban, are recommended for patients with eGFR < 15 mL/min or those on dialysis, although data on other DOACs in CKD remain limited. The lack of comprehensive guidelines for anticoagulant use in CKD and ESRD highlights the need for individualized, patient-centered approaches that account for comorbidities, genetics, and clinical context. Conclusions: Managing anticoagulation in CKD/ESRD is challenging due to complex coagulation profiles and altered pharmacokinetics. Judicious dosing, close monitoring, and patient-centered care are critical. High-quality randomized controlled trials are needed to establish clear guidelines and optimize therapy for this vulnerable population. Full article

High-sodium/low-potassium in the modern diet, potassium excretion, and sodium retention have all been implicated in hypertension. Objectives: This study investigated the differential effects of potassium (K⁺) supplementation on blood pressure, renal function, and oxidative stress in two experimental hypertensive rat models: L-NAME-induced (nitric oxide synthase inhibitor-induced hypertension presenting with reduced NO bioavailability, endothelial dysfunction, vasoconstriction) and DOCA-salt-induced hypertension (deoxycorticosterone acetate + salt mimics volume-dependent hypertension of hypermineralocorticoidism, low renin, high sodium retention and severe cardiac fibrosis and oxidative stress). Methods: Male Sprague Dawley rats were treated with L-NAME or DOCA-salt, with or without 0.75% KCl dietary supplementation for eight weeks. Blood pressure, vascular reactivity, serum electrolytes, renal function markers, and malondialdehyde (MDA) levels were evaluated. Results: Potassium supplementation significantly reduced (20%) mean arterial pressure and (80%) oxidative stress markers in the L-NAME model but not in the DOCA-salt model. In both hypertensive models, K⁺ reduced (15%) vascular contractile response to phenylephrine, though it did not improve acetylcholine-induced vasodilation. Notably, K⁺ supplementation improved glomerular filtration rate (eGFR), sodium–potassium ratio, and renal biomarkers (urea and creatinine) in the L-NAME model, suggesting nephroprotection. However, in the DOCA-salt group, these markers either remained unchanged or worsened. Conclusions: These findings indicate that the antihypertensive and renoprotective effects of potassium are model-specific and depend on the underlying pathophysiological mechanisms, such as nitric oxide bioavailability and mineralocorticoid sensitivity. Dietary potassium may be more effective in patients with endothelial dysfunction-dominant hypertensive subtypes compared with volume-dependent hypertension and may call for K⁺ supplementation studies to be stratified by hypertension subtype. Full article

Background/Objectives: Cognitive impairment is a frequent and underrecognized comorbidity in elderly patients with heart failure with preserved ejection fraction (HFpEF), contributing to poor outcomes and complicating disease management. This study aimed to identify risk factors associated with cognitive impairment in elderly HFpEF patients from Western Romania and to develop a point-based risk score for clinical use. Methods: We conducted a cross-sectional analysis of HFpEF patients aged ≥65 years. Cognitive status was assessed using the Mini-Mental State Examination-2 (MMSE-2), with significant impairment defined as a score <24. Multivariable logistic regression analysis was performed to identify independent predictors of cognitive dysfunction. Results: A total of 326 HFpEF patients were included. Diabetes mellitus, prior stroke or transient ischemic attack (TIA), carotid artery disease, elevated N-terminal pro–B-type natriuretic peptide (NT-proBNP), and reduced estimated glomerular filtration rate (eGFR) were independently associated with cognitive impairment. Higher Kansas City Cardiomyopathy Questionnaire (12-KCCQ) scores and anticoagulant therapy for atrial fibrillation were associated with a lower risk. Based on these variables, a simple point-based cognitive risk score was developed, demonstrating strong discriminatory ability (area under the curve = 0.84). A threshold of ≥2 points identified cognitive impairment with 75% sensitivity and 83% specificity. Conclusions: Our findings underscore the importance of integrated cardiovascular and cognitive assessment in elderly HFpEF patients. The developed risk score offers a pragmatic tool for the early identification of cognitive dysfunction, potentially informing timely interventions and preventive strategies. Full article

Background/Objectives: In recent decades, shifting demographics and advancements in treating cardiovascular disease have altered the types of patients receiving coronary angiography (CA). However, data investigating the impact of kidney dysfunction stratified by the indication for CA are limited. Methods: Consecutive patients who underwent invasive CA at one institution between 2016 and 2022 were included in this study. Firstly, the prevalence and extent of coronary artery disease (CAD) in patients with different levels of kidney function was assessed. Secondly, the study examined how impaired kidney function affected long-term outcomes—specifically the risk of rehospitalization for heart failure (HF), acute myocardial infarction (AMI), or the need for coronary revascularization—at 36 months of follow-up. Results: A total of 7624 patients undergoing CA were included with a median estimated glomerular filtration rate (eGFR) of 68.9 mL/min/1.73 m² (IQR: 50.8–84.3). In total, 63.7% of patients had an eGFR ≥ 60 mL/min/1.73 m², 29.0% an eGFR of 30–<60 mL/min/1.73 m², and 7.3% an eGFR of <30 mL/min/1.73 m². Compared to patients with an eGFR ≥ 60 mL/min/1.73 m², those with an eGFR 30–<60 mL/min/1.73 m² and eGFR < 30 mL/min/1.73 m² had a higher prevalence of CAD (66.8% vs. 72.9% and 80.1%, respectively; p = 0.001) and three-vessel CAD (25.6% vs. 34.5% and 39.5%, respectively; p = 0.001). At 36 months of follow-up, patients with an eGFR 30–<60 mL/min/1.73 m² and eGFR < 30 mL/min/1.73 m² suffered from significantly higher risk of HF-associated rehospitalization (HR = 1.937, 95% CI: 1.739–2.157, p = 0.001 and HR = 3.223, 95% CI: 2.743–3.787, p = 0.001, respectively) and AMI compared to patients with an eGFR ≥ 60 mL/min/1.73 m² (reference group). The significantly higher risk of HF-related rehospitalization remained after multivariable adjustment. Conclusions: Both groups with impaired kidney function demonstrated a markedly higher risk of rehospitalization for HF at 36 months—even after multivariate adjustments. Increased risk of HF-related rehospitalization in patients with an eGFR < 30 mL/min/1.73 m² was especially evident if they also presented with decompensated HF and LVEF < 35%. In patients with an eGFR 30–<60 mL/min/1.73 m², presenting with angina pectoris and multivessel disease increased the risk of HF-related rehospitalization. Full article

Background: The eye and kidney share embryological, structural, and pathophysiological similarities, suggesting potential interconnections between retinal and renal microvascular changes. Hypertension, a major risk factor for renal impairment, also affects retinal microvasculature. This study investigates the relationship between retinal vascular density, assessed by Optical Coherence Tomography Angiography (OCT-A), and early renal dysfunction in hypertensive patients. Methods: A total of 142 hypertensive patients (mean age 47 ± 13 years; 74% male) were enrolled from the Nephrology and Hypertension Unit at the University of Palermo. Retinal vascular density was measured using OCT-A, and renal function was assessed using estimated glomerular filtration rate (eGFR). Clinical and hemodynamic parameters, including 24-h aortic blood pressure, were also analyzed. Results: Patients with eGFR < 60 mL/min/1.73 m² exhibited significantly lower retinal vascular densities, particularly in the parafoveal region. Superficial parafoveal density was inversely associated with aortic pulse pressure (p = 0.012) and directly correlated with eGFR (p = 0.012). Deep parafoveal density was independently associated with eGFR (p = 0.001). Multiple linear regression confirmed that lower retinal vascular density was significantly linked to reduced renal function, independent of age and blood pressure. Conclusions: Retinal vascular density, particularly in the parafoveal region, is associated with renal function decline in hypertensive patients. These findings suggest that retinal microvascular changes could serve as a non-invasive biomarker for kidney dysfunction, with potential applications in early risk stratification and disease monitoring. Further research is needed to establish causality and clinical utility. Full article

Diuretics are a class of pharmacological agents that promote the renal excretion of water and electrolytes, increasing urine output and reducing fluid retention. They play a critical role in the management of edematous syndromes, irrespective of their etiology (cardiac, renal, or hepatic), as well as in the treatment of hypertension (HTA). The mechanism of action of diuretics can be classified as either renal, as seen with saluretic diuretics that inhibit sodium and water reabsorption at various segments of the nephron, or extrarenal, involving alterations in the glomerular filtration pressure or osmotic mechanisms. Based on their site of action and mechanism, diuretics are categorized into multiple classes, including loop diuretics, thiazide and thiazide-like diuretics, potassium-sparing diuretics, carbonic anhydrase inhibitors, and osmotic diuretics. These agents are frequently used in combination with other antihypertensive or heart failure medications to optimize therapeutic efficacy. By reducing the blood volume and peripheral vascular resistance, diuretics improve cardiac function, lower blood pressure, and enhance exercise tolerance. Additionally, they are employed in managing chronic kidney disease (CKD), electrolyte imbalances, and specific metabolic disorders. Given the potential for adverse effects such as electrolyte disturbances and renal dysfunction, diuretic therapy should be individualized, with the careful monitoring of the dosage, patient response, and comorbid conditions. Patient education on adherence, lifestyle modifications, and the recognition of side effects is essential for optimizing the therapeutic outcomes and minimizing the risks associated with diuretic therapy. Full article

Background/Objectives: p-Cresyl sulfate (PCS) is implicated in inflammation, oxidative stress and vascular dysfunction. Hypertension is a major risk factor for peripheral arterial disease (PAD), which is linked to increased mortality in patients with hypertension. This study aimed to evaluate the association between serum PCS levels and PAD in hypertension cases. Methods: We analyzed fasting blood samples and clinical data from 105 patients with hypertension in a cardiovascular outpatient clinic. Serum PCS levels were quantified using high-performance liquid chromatography–mass spectrometry. Ankle–brachial index (ABI) was measured using an automated oscillometric device; ABI < 0.9 indicated PAD. Results: A total of 24 patients (22.9%) had PAD. The PAD group had a higher prevalence of diabetes mellitus (p = 0.026), elevated serum C-reactive protein (CRP) levels (p < 0.001) and increased PCS levels (p = 0.002) than the normal ABI group. Multivariate logistic regression showed that PCS (odds ratio [OR]: 1.154, 95% confidence interval [CI]: 1.013–1.315, p = 0.031) and CRP (per 0.1 mg/dL increase, OR: 1.649, 95% CI: 1.138–2.389, p = 0.008) were independently associated with PAD. According to Spearman’s correlation analysis, log-transformed PCS (log-PCS) levels negatively correlated with left or right ABI (p = 0.001 and p = 0.004, respectively) and estimated glomerular filtration rate (p = 0.001) but positively correlated with log-CRP (p = 0.024). Conclusions: Elevated serum PCS and CRP levels are significantly associated with PAD in patients with hypertension, suggesting the potential role of PCS in PAD pathogenesis. Full article

Background/Objectives: This study aimed to investigate the prognostic value of the red cell distribution width-to-estimated glomerular filtration rate (RGR) ratio in patients hospitalized with chronic heart failure (CHF) and its potential interaction with NT-proBNP levels. By integrating anemia and renal dysfunction markers, the RGR may provide enhanced predictive insights regarding extended length of hospital stay (ELOS) > 7 days, in-hospital mortality, and 6-month all-cause mortality across specific CHF phenotypes. Methods: In this retrospective, single-center pilot observational study, 627 CHF admissions (January 2022–August 2024) were analyzed. Patients were classified according to the ESC guidelines into heart failure with reduced (HFrEF), mildly reduced (HFmrEF), or preserved ejection fraction (HFpEF). The RGR was calculated as red cell distribution width standard deviation (RDW-SD) divided by estimated glomerular filtration rate (eGFR). Predictive accuracy was evaluated using logistic regression, receiver operating characteristic (ROC) analyses, and stepwise Cox proportional hazard regression. Results: RGR was significantly higher in HFrEF than in HFpEF (p = 0.042) and predicted ELOS only in HFpEF (AUC = 0.619). In contrast, for in-hospital mortality, RGR achieved excellent discrimination in HFrEF (AUC = 0.945), outperforming RDW and NT-proBNP. In HFmrEF, RDW exhibited the highest predictive power (AUC = 0.826), whereas in HFpEF, NT-proBNP was the strongest predictor (AUC = 0.958), although RGR preserved good discrimination (AUC = 0.746). Across the entire cohort and HF phenotypes, RGR consistently emerged as a significant predictor in univariable analysis. In multivariable models, it improved the significance prognosis especially alongside NT-proBNP in the entire cohort and HFrEF. For 6-month all-cause mortality, RGR surpassed RDW in prediction in all HF phenotypes. Conclusions: The RGR independently predicts prolonged hospitalization, in-hospital, and 6-month mortality in CHF—often outperforming RDW and eGFR and being comparable to NT-proBNP, especially in HFrEF. These findings suggest that RGR may serve as a valuable risk stratification tool in CHF management. Full article