Cardiorenal Medicine最新文献

Introduction: Approximately 70% of patients with heart failure (HF) also have kidney disease. Mortality is increased both by cardiorenal syndrome (CRS) and by the exacerbation of other comorbidities. The purpose of this study is to evaluate the clinical performance of patients with CRS who are followed up by the Cardiorenal Unit (CRU).

Methods: We conducted a retrospective observational study of patients referred to the CRU from April 1, 2022, to April 30, 2023. Demographics, laboratory and ultrasonographic tests, and outcomes were evaluated.

Results: Fifty-four patients were seen in the CRU. A total of 45 (83%) and 16 (30%) patients completed follow-up in the CRU at 6 and 12 months, respectively. The mean age was 70 years±1.6, and 65% were men. Almost 50% of patients had ischemic heart disease-related HF. The mean cardiac ejection fraction (EF) was 40%±1.6, and 61% of patients had HF with reduced EF (HFrEF). NYHA functional classes II and III were the most frequent (60% and 35%, respectively). At six months after follow-up, treatment was optimized with sacubitril-valsartan in 33% vs. 49% (p=0.02) and SGLT2 inhibitors in 48% vs. 72% (p=0.008), without significant deterioration in renal function (creatinine: p=0.61; eGFR: p=0.19). There was also a reduction of more than 50% in the number of hospital admissions (p=0.002). A total of 22% required peritoneal dialysis, and 20% required hemodialysis. Ten (19%) patients died, five of them due to cardiovascular (CV) events.

Conclusions: The CRU is vital for the management of complex patients, as it ensures the implementation of medications that reduce CV mortality and decrease the number of hospital admissions in HF.

Introduction: The objective of this research is to explore the possible link between markers of liver fibrosis and survival rates in a group of adults who have been diagnosed with both chronic kidney disease (CKD) and coronary artery disease (CAD).

Methods: The National Health and Nutrition Examination Survey (NHANES) data (1999-2018) for participants with both CAD and CKD were analyzed. The Fibrosis-4 Index (FIB-4), Nonalcoholic Fatty Liver Score (NFS), Forns index and Aspartate Aminotransferase/Alanine Aminotransferase (AST/ALT) ratio were identified as crucial biomarkers. All-cause and cardiovascular disease (CVD) mortality were primary outcomes, assessed using Cox models, Kaplan-Meier curves, and ROC analysis.

Results: A total of 1,192 CKD and CAD patients were included. The Cox regression analysis revealed substantial correlations between elevated FIB-4, NFS, Forns index and AST/ALT levels and a heightened risk of all-cause (HR 1.188, 95%CI 1.108-1.274; HR 1.145, 95%CI 1.069-1.227; HR 1.142, 95%CI 1.081-1.201; HR 1.316, 95%CI 1.056-1.639, respectively) and CVD mortality (HR 1.133, 95%CI 1.007-1.275; HR 1.155, 95%CI 1.024-1.303; HR 1.208, 95%CI 1.109-1.316 and HR 1.636, 95%CI 1.203-2.224, respectively). The ROC analysis indicated comparable predictive accuracy for all three biomarkers, with AST/ALT showing slightly superior performance.

Conclusion: Liver fibrosis markers, including AST/ALT, NFS, Forns index and FIB-4, are significant mortality predictors in CAD-CKD patients. The AST/ALT ratio, being easily measurable, may serve as an effective predictive tool for risk stratification in this population.

Background: Hyperkalemia, generally defined as serum potassium levels greater than 5.0 mEq/L, poses significant clinical risks, including cardiac toxicity and muscle weakness. Its prevalence and severity increase in patients with chronic kidney disease (CKD), diabetes mellitus, and heart failure (HF), particularly when compounded by medications like Angiotensin converting inhibitors, Angiotensin receptor blockers, and potassium sparing diuretics. Hyperkalemia arises from disruptions in potassium regulation involving intake, excretion, and intracellular-extracellular distribution. In CKD and acute kidney injury, these regulatory mechanisms are impaired, leading to heightened risk. The management of chronic hyperkalemia presents a challenge due to the necessity of balancing effective cardiovascular and renal therapies against the risk of elevated potassium levels.

Summary: The emergency department management of acute hyperkalemia focuses on preventing cardiac complications through strategies that stabilize cellular membranes and shift potassium intracellularly. Chronic management often involves dietary interventions and pharmacological treatments. Pharmacological management of acute hyperkalemia includes diuretics, which enhance kaliuresis, and potassium binders such as patiromer and sodium zirconium cyclosilicate (SZC), which facilitate fecal excretion of potassium. While diuretics are commonly used, they carry risks of volume contraction and renal function deterioration. The newer potassium binders have shown efficacy in lowering chronically elevated potassium levels in CKD and HF patients, offering an alternative to diuretics and other older agents such as sodium polystyrene sulfonate , which has significant adverse effects and limited evidence for chronic use.

Key messages: We convened a consensus panel to describe the optimal management across multiple clinical settings when caring for patients with hyperkalemia. This consensus emphasizes a multidisciplinary approach to managing hyperkalemia, particularly in patients with cardiovascular kidney metabolic (CKM) syndrome, to avoid fragmentation of care and ensure comprehensive treatment strategies. The primary goal of this manuscript is to describe strategies to maintain cardiovascular benefits of essential medications while effectively managing potassium levels.

Background: Heart failure with preserved ejection fraction (HFpEF) and chronic kidney disease (CKD) have a strong pathophysiological interrelationship, and their combination worsens prognosis.

Summary: This article briefly reviews the bidirectional epidemiological burden and the pathophysiological interplay between HFpEF and CKD. It also discusses some of the controversial aspects regarding the diagnosis and screening of HFpEF in CKD patients and focuses on the most effective therapeutic approaches to improve symptoms and prognosis in this high-risk population.

Key messages: Due to its prevalence and prognostic significance, HFpEF screening should be considered in patients with CKD, with careful use of traditional diagnostic tools in this population. Optimal medical therapy has seen major recent advances in patients with both HFpEF and CKD. SGLT2 inhibitors, finerenone, and semaglutide have consistently demonstrated cardio- and renoprotective effects in both conditions.

Introduction: Patients on extracorporeal membrane oxygenation (ECMO) often experience worse renal outcomes and higher mortality rates as the severity of kidney injury increases. Nevertheless, the in-hospital mortality risks of patients with end-stage renal disease (ESRD) are poorly understood. This study evaluated several prognostic factors associated with in-hospital mortality in patients with ESRD receiving ECMO therapy.

Methods: This study reviewed the medical records of 90 adult patients with ESRD on venoarterial ECMO in intensive care units in Linkou Chang Gung Memorial Hospital between March 2009 and February 2022. Fourteen patients who died within 24 hours of receiving ECMO support were excluded; the remaining 76 patients were enrolled. Demographic, clinical and laboratory variables were retrospectively collected as survival predictors. The primary outcome was in-hospital mortality.

Results: The overall in-hospital mortality rate was 69.7%. The most common diagnosis requiring ECMO support was postcardiotomy cardiogenic shock, and the most frequent ECMO-associated complication was infection. Multiple logistic regression analysis revealed that the Acute Physiology and Chronic Health Evaluation II (APACHE II) score on day 1 of ECMO support was an independent risk factor for in-hospital mortality. The APACHE II score demonstrated satisfactory discriminative power (0.788 ± 0.057) in the area under the receiver operating characteristic curve. The cumulative survival rates at the 6-month follow-up differed significantly (P < 0.001) between patients with APACHE II score ≤ 29 versus those with APACHE II score > 29.

Conclusion: For patients with ESRD on ECMO, the APACHE II score is an excellent predictor of in-hospital mortality.

Introduction: Antigen carbohydrate 125 (CA125) has emerged as a proxy of fluid overload and inflammation in acute heart failure (AHF). We aimed to evaluate the influence of dapagliflozin on CA125 levels within the first weeks after discharge and whether CA125 changes were related to 6-month adverse clinical outcomes.

Methods: In this retrospective observational study, data from 956 AHF patients discharged from a tertiary hospital were analyzed. CA125 levels were assessed during the index admission (visit 1) and at a median of 26 (15-39) days after discharge (visit 2). The primary endpoint was changes in CA125 and its correlation with the risk of 6-month death and recurrent readmissions (any or AHF-related). Multivariable mixed regression and a two-equation count model regression were used for the analyses.

Results: The mean age of the cohort was 73.1±11.1 years, 54.8% were males, 43.5% showed left ventricular ejection fraction ≥50%, and 18.7% of patients received dapagliflozin at discharge. Dapagliflozin treatment was associated with a greater reduction in CA125 levels at follow-up (-24 U/mL) compared to non-dapagliflozin patients (-14 U/mL, p=0.034). The magnitude of CA125 reduction (per decrease in 10 U/ml) was significantly associated with a lower risk of 6-month death (IRR=0.98, 95% CI=0.96-0.99; p=0.049), all-cause readmissions (IRR=0.99, 95% CI=0.98-0.99; p=0.003), and HF-readmissions (IRR=0.98, 95% CI=0.97-0.99; p<0.001).

Conclusion: Dapagliflozin treatment at discharge following an episode of AHF was associated with a greater reduction in CA125 during the first weeks after discharge. The greater CA125 reduction identified patients with a lower risk of 6-month adverse clinical outcomes.

Introduction: The effects of glucagon-like receptor 1 receptor agonists (GLP-1 RA) in patients with diabetes and established chronic kidney disease (CKD) remain unclear.

Methods: We systematically searched PubMed, Embase, and Cochrane Library from inception to May 2024 for randomized controlled trials (RCTs) and respective post-hoc studies comparing GLP-1 RAs versus placebo in patients with type 2 diabetes mellitus (T2DM) and established CKD (as per study definition or otherwise defined as having an estimated glomerular filtration rate less than 60 mL/min/1.73m2 and/or urine albumin-to-creatinine ratio more than 30 mg/g). We applied a random-effects model to pool risk ratios (RR), hazard ratios (HR) and 95% confidence intervals (CI).

Results: We included 10 RCTs and post-hoc analyses comprising 18,042 patients, of whom 9,164 (50.8%) were treated with GLP-1 RAs. There were significantly lower rates of major adverse kidney events (RR 0.82; 95% CI 0.74-0.90; p<0.001; high certainty) and a slightly lower incidence of all-cause mortality (HR 0.84; 95% CI 0.71-1.00; p=0.046; moderate certainty) with the use of GLP-1 RAs relative to placebo. This kidney protection remained consistent in patients with stage 3b CKD (RR 0.78; 95% CI 0.65-0.94; p=0.009; high certainty). No significant differences were observed in major adverse cardiovascular events (HR 0.89; 95% CI 0.78-1.02; p=0.090; low certainty) or cardiovascular mortality (HR 0.80; 95% CI 0.60-1.09; p=0.155; very low certainty), possibly due to a lack of statistical power.

Conclusion: GLP-1 RAs were tied to a lower incidence of all-cause mortality and major adverse kidney events in patients with T2DM and established CKD.

Background: The complex relationship between heart and kidney dysfunction has been a subject of medical inquiry since the 19th century. The term "cardio-renal syndrome" (CRS) was introduced in the early 2000s and has since become a focal point of research. CRS is typically categorized into five subtypes based on the sequence of cardiovascular and kidney disease events.

Summary: The cardiovascular-kidney-metabolic (CKM) syndrome, as defined by the American Heart Association, describes a set of interrelated metabolic risk factors and their effects on the kidneys and cardiovascular system. This syndrome emphasizes the complexity of managing patients with combined conditions and identifies several knowledge gaps, including disease mechanisms, clinical phenotype variability, and the impact of social determinants of health. The chronic cardiovascular-kidney disorder (CCKD) framework proposes a shift from the term "syndrome" to "disorder," focusing on concurrent cardiovascular and kidney problems regardless of their sequence.

Key messages: (i) The CCKD concept calls for simplification and conceptual clarity, arguing that understanding the bidirectional acceleration of disease progression between heart and kidney dysfunction can lead to more effective treatment strategies. (ii) Both CKM and CCKD share common pathophysiological mechanisms and risk factors, including hypertension, diabetes, obesity, and dyslipidemia. Managing these conditions requires a comprehensive approach that addresses the underlying risk factors and pathophysiological mechanisms. (iii) Future directions include embracing precision medicine, public health strategies, interdisciplinary care models, and ongoing research and innovation. Both frameworks underscore the need for comprehensive, interdisciplinary care models and innovative treatment strategies to address the complex interplay between cardiovascular and kidney diseases.

Introduction: Haemodialysis (HD) is a life-sustaining treatment for individuals with end-stage kidney disease. However, the risk of mortality remains significantly higher compared to the general population, even when matched for age and sex. Global longitudinal strain (GLS), derived from speckle tracking echocardiography, has shown promise as a predictor of mortality in HD patients. However, its prognostic utility in patients with multiple cardiovascular risk factors such as diabetes mellitus (DM) and receiving HD remains unclear. This study aimed to evaluate the prognostic value of GLS in HD patients, with and without DM.

Methods: This prospective study was a long-term follow-up extension study of an earlier published study that investigated a cohort of HD patients from a single centre with a comprehensive cardiovascular imaging protocol. All patients had an echocardiography with the use of speckle tracking software to determine GLS. Patients were divided into group A (with DM) and group B (without DM). Patients were followed up until death, major adverse cardiovascular events, transplantation, or the censoring date (29 February 2024). Statistical analyses were performed using univariate and multivariate Cox proportional hazards models.

Results: A total of 184 patients receiving HD were included in the analysis. Patients with DM (group A) had significantly higher all-cause mortality (ACM) (47.1% vs. 20.7%, p < 0.001) and a lower chance of receiving a kidney transplant (13.2% vs. 43.1%, p < 0.001). In group A, GLS did not predict ACM, whereas in group B, a GLS cut-off of -15.76% correlated with higher 5-year ACM (p = 0.036). Left ventricular ejection fraction (LVEF) was a significant predictor of ACM in group A (HR 0.98; p = 0.036).

Conclusion: GLS is a poor predictor of adverse outcomes in HD patients with DM, likely due to their high cardiovascular risk. In contrast, GLS was a significant predictor of mortality in non-diabetic HD patients. LVEF may be a more reliable prognostic indicator in high-risk diabetic patients.

Background: Patients with chronic kidney disease (CKD) have an increased cardiovascular (CV) risk. The lower the glomerular filtration rate, the higher the CV risk.

Summary: Current data suggest that several uremic toxins lead to vascular inflammation and oxidative stress that, in turn, lead to endothelial dysfunction, changes in smooth muscle cells' phenotype, and increased degradation of elastin and collagen fibers. These processes lead to both functional and structural arterial stiffening and explain part of the increased risk of acute myocardial infarction and stroke reported in patients with CKD. Considering that, at least in patients with end-stage kidney disease, the reduction of arterial stiffness is associated with a parallel decrease of the CV risk; vascular function is a potential target for therapy to reduce the CV risk.

Key messages: In this review, we explore mechanisms of vascular dysfunction in CKD, paying particular attention to inflammation, reporting current data in other models of mild and severe inflammation, and discussing the vascular effect of several drugs currently used in nephrology.