Cardiorenal Medicine最新文献

Introduction: Periostin is a matricellular protein. Elevated serum concentrations of periostin have been reported in patients with various cardiovascular diseases, including heart failure. Patients with end-stage renal disease have a substantially increased risk for cardiovascular diseases. However, there is a lack of clinical studies to clarify the prognostic significance of systemic periostin on all-cause mortality in patients with end-stage renal disease on hemodialysis.

Methods: 313 stable end-stage renal disease patients were recruited and followed for 5 years concerning all-cause mortality. At baseline, we collected blood samples and clinical data. Serum periostin concentrations were measured using a certified ELISA.

Results: The optimal cut-off value for serum periostin regarding all-cause mortality, calculated through receiver operating characteristic analysis, was 777.5 pmol/L. Kaplan-Meier survival analysis using this cut-off value demonstrated that higher periostin concentrations are linked to higher all-cause mortality (log-rank test: p = 0.002). Subgroup analysis revealed that serum periostin concentrations only affected all-cause mortality in male but not in female patients (p = 0.002 in male patients and p = 0.474 in female patients). Multivariate Cox regression analyses, adjusted for confounding factors, likewise showed that elevated serum periostin concentrations were positively associated with all-cause mortality in male (p = 0.028) but not in female patients on hemodialysis (p = 0.313).

Conclusion: Baseline serum periostin is an independent risk factor for all-cause mortality in male patients with chronic renal disease on hemodialysis.

Introduction: Sodium-glucose cotransporter-2 inhibitors (SGLT2is) are recommended in kidney disease and heart failure to reduce adverse clinical outcomes, but utilization can vary. To understand potential gaps in clinical practice and identify opportunities for improvement, we aimed to describe the prevalence and factors associated with SGLT2i prescription in patients with reduced kidney function hospitalized for fluid overload and/or heart failure.

Methods: Single-center observational study of patients with reduced kidney function (eGFR 20-59 mL/min/1.73 m2) hospitalized for fluid overload or heart failure between January 2022 and December 2023. Data were retrieved from electronic medical records. The outcome was SGLT2i prescription at discharge. Potential variables affecting SGLT2i prescription were identified during stakeholder engagement and evaluated using multivariable logistic regression.

Results: Among 2,543 patients, the median age was 79 (71, 86) years and admission eGFR was 38.7 (28.4, 49.4) mL/min/1.73 m2. SGLT2i was prescribed to 630 (24.8%) patients at discharge. SGLT2i prescription at discharge was independently associated with cardiovascular disease (OR 1.76, 95% CI: 1.31-2.35), diabetes (OR 1.59, 95% CI: 1.19-2.14), fluid overload or heart failure as the primary discharge diagnosis (OR 1.71, 95% CI: 1.29-2.28), SGLT2i pre-hospitalization (OR 104.91, 95% CI: 63.22-174.08), RAS blocker (OR 2.1, 95% CI: 1.65-2.89), and higher eGFR (OR 1.01, 95% CI: 1.003-1.02) at discharge; but inversely associated with older age (OR 0.97, 95% CI: 0.96-0.98).

Conclusion: SGLT2i prescription at discharge was suboptimal among patients with reduced kidney function hospitalized for fluid overload and/or heart failure, especially in older age and more severe kidney disease. Additionally, cardiovascular disease, diabetes, primary discharge diagnosis of fluid overload or heart failure, prior SGLT2i use, and concurrent RAS blocker at discharge were independently associated with SGLT2i prescription at discharge. Interventions are needed to increase clinicians' knowledge and overcome clinical inertia to increase SGLT2i use in patients with fluid overload and heart failure.

Introduction: Denosumab preceding elective surgery is an alternative option when parathyroidectomy is not immediately possible. Denosumab (an osteoprotegerin mimic) may play a role in the cardiovascular system, which is reflected in the features of epicardial adipose tissue (EAT) and coronary artery calcification (CAC).

Methods: We investigated the effects of denosumab on EAT attenuation (EATat) and CAC in dialysis patients with secondary hyperparathyroidism (SHPT). This cohort study included patients on dialysis with SHPT. The baseline characteristics of dialysis patients and propensity score-matched non-dialysis patients were compared. Computed tomography scans of the dialysis patients (dialysis group with denosumab, n = 24; dialysis group without denosumab, n = 21) were obtained at baseline and at 6 months of follow-up.

Results: At baseline, the dialysis group patients had a higher EATat-median (-71.00 H ± 10.38 vs. -81.60 H ± 6.03; p < 0.001) and CAC (1,223 A [248.50-3,315] vs. 7 A [0-182.5]; p < 0.001) than the non-dialysis group. At follow-up, the dialysis group without denosumab showed an increase in Agatston score (1,319.50 A [238.00-2,587.50] to 1,552.00 A [335.50-2,952.50]; p = 0.001) without changes in EATat-median (-71.33 H ± 11.72 to -70.86 H ± 12.67; p = 0.15). The dialysis group with denosumab showed no change in Agatston score (1,132.2 A [252.25-3,260.5] to 1,199.50 A [324.25-2,995]; p = 0.19) but a significant decrease of EATat-median (-70.71 H ± 9.30 to -74.33 H ± 10.28; p = 0.01).

Conclusions: Denosumab may reverse EATat and retard CAC progression in dialysis patients with SHPT.

Introduction: Phase angle value, derived from bioelectrical impedance analysis, represents the body cell mass and nutritional status of patients undergoing hemodialysis. Although the phase angle value has clinical significance in these patients, its relationship with electrocardiogram (ECG), another clinically relevant bioelectrical examination, has not yet been well clarified.

Methods: Two hundred and twenty-four patients undergoing dialysis (80 females and 144 males; mean ± SD, 72.2 ± 12.0 years old; 117 diabetic and 107 nondiabetic patients) were studied retrospectively. Multifrequency bioelectrical impedance analysis was performed immediately after the end of dialysis therapy. The phase shift was geometrically converted into a phase angle value. The ECG was recorded simultaneously, and the upper limits of the PR interval, QRS width, and corrected QT interval (QTc) were set at 0.20, 0.12, and 0.44 s, respectively. The geriatric nutritional risk index (GNRI), a representative nutritional index, was also determined. In addition, we examined the incidence of cardiac events, including heart failure, myocardial infarction, cardiac revascularization procedure, cardiac arrhythmia, and cardiac death, or all-cause death.

Results: Of 224 patients undergoing dialysis, the prolongation of the PR interval, QRS width, and QTc was found in 30.7, 17.4, and 62.1%, respectively. The prevalence of QTc prolongation was higher in females and diabetic patients than in males and nondiabetic patients. An inverse relationship between phase angle value and QTc was observed only in males and nondiabetic patients. The relationships of GNRI both with phase angle value and QTc were stronger in males and nondiabetic patients. In addition, PR interval was inversely correlated with a phase angle value only in nondiabetic patients. No significant correlation was found between phase angle value and QRS width. Five-year survival probability for the composite endpoints was significantly worse in patients with lower phase angle values. QTc prolongation was associated with survival in males and nondiabetic patients. Prolonged PR was associated with survival in nondiabetic patients.

Discussion: Relationships between phase angle value and ECG findings were demonstrated in patients undergoing dialysis, especially in males and nondiabetic patients. Although the phase angle value has been considered as an index for evaluating nutritional status, another clinical application of phase angle value in predicting cardiac complications seems to be useful.

Background: Heart failure remains a significant public health burden given its prevalence, morbidity, mortality as well its untoward financial consequences.

Summary: The assessment of congestion and its treatment are integral in heart failure pathophysiology and outcomes. Renal venous congestion and its suboptimal response to diuretic-based and novel pharmacological therapeutic regimens have thus positioned ultrafiltration as a promising therapeutic option for patients with acute decompensated heart failure. As a corollary, peritoneal dialysis has had success establishing itself as a relevant therapeutic option for chronic cardiorenal syndrome in patients with heart failure.

Key messages: Herein, we will discuss the pathophysiologic basis of ultrafiltration and peritoneal dialysis in heart failure with a review of the relevant clinical trials on safety and efficacy profiles in these patient populations.

Background: There is a marked increase in the global prevalence of obesity over the last decades with an estimated 1.9 billion adults living with overweight or obesity. This is associated with a sharp rise in prevalence of cardiorenal metabolic diseases such as type 2 diabetes mellitus, chronic kidney disease, and heart failure. With recent evidence of the efficacy of sodium glucose cotransporter-2 inhibitors and glucagon-like peptide-1 receptor agonists on cardiorenal protection and weight reduction, it is reasonable to investigate common causative pathways for cardiorenal metabolic diseases.

Summary: Central obesity is a common condition with 41.5% prevalence worldwide. It is associated with adverse outcomes even in people with a normal body mass index. Central obesity develops when the personal fat threshold for expansion in the subcutaneous adipose tissue exceeds a certain level. Multiple factors such as age, gender, genetics, and hormones may play a role in determining personal susceptibility to central obesity. Cardiorenal metabolic diseases usually cluster in certain populations - commonly in people with central obesity - and cause a substantial burden on health services and increase the risk of all-cause mortality. In this review, we investigate the pathophysiological pathways between central obesity and cardiorenal metabolic diseases. These pathways include activation of the renin-angiotensin-aldosterone system and the sympathetic nervous system, inflammation and oxidative stress, haemodynamic impairment, insulin resistance, and endothelial dysfunction.

Key message: Central obesity has a pivotal role in the development of cardiorenal metabolic diseases and should be targeted with population-based approaches, such as dietary and lifestyle interventions, as well as the development of pharmacotherapy to reduce the burden of cardiorenal metabolic diseases.

Background: The coexistence of heart and kidney diseases, also called cardiorenal syndrome, is very common, leads to increased morbidity and mortality, and poses diagnostic and therapeutic difficulties. There is a risk-treatment paradox, such that patients with the highest risk are treated with lesser disease-modifying medical therapies.

Summary: In this document, different scientific societies propose a practical approach to address and optimize cardiorenal therapies and related comorbidities systematically in chronic cardiorenal disease beyond congestion. Cardiorenal programs have emerged as novel models that may assist in delivering coordinated and holistic management for these patients.

Key messages: (1) Cardiorenal disease is a ubiquitous entity in clinical practice and is associated with numerous barriers that limit medical treatment. (2) The present article focuses on the practical approaches to managing chronic cardiorenal disease beyond congestion to overcome some of these barriers and improve the treatment of this high-risk population.

Introduction: The prevalence of heart failure (HF) is more common in people with advanced non-dialysis chronic kidney disease (ND-CKD) compared to the general population. It is well known that HF with reduced ejection fraction (HFrEF) is associated with a higher risk of mortality in people with ND-CKD. However, the impact of HFrEF on progression into end-stage kidney disease (ESKD) is not well studied. Our study aimed to examine the independent association of HFrEF on progression to ESKD after correcting for confounding factors using two methods of propensity scoring.

Methods: This study used data from the Salford Kidney Study, a longitudinal study which has recruited more than 3,000 patients with ND-CKD since 2002. Patients without a history of HF during the recruitment questionnaire were included in the control group. Patients with a reported history of HF and echo showing left ventricular ejection fraction <40% at enrolment were included in the HFrEF group. Two propensity score methods were used to attenuate the effects of confounding factors between the two groups - propensity score matching (PSM) and inverse probability weighting (IPW). Univariate and multivariate Cox-regression analyses were performed.

Results: A total of 2,383 patients were included in the analysis. Patients with HFrEF had significantly higher median age and a higher percentage of male gender compared to patients with no HF (72.5 vs. 66.6 years and 71.8 vs. 61.1%, respectively). Univariate and 5 models of multivariate Cox-regression analysis showed that HFrEF in people with CKD was a strong predictor for a higher incidence of ESKD (model 5: hazard ratio 1.38; 95% confidence interval = 1.01-1.90; p = 0.044). The association between HFrEF and the risk of ESKD remained significant after using the PSM and the IPW methods.

Conclusion: Patients with concomitant advanced ND-CKD and prevalent HFrEF were found to have a higher risk of ESKD when compared to patients with no HF. This risk persists despite the adjustment of confounding factors using PSM and IPW.

Background: The global population is aging. It is estimated that by 2050, the proportion of the elderly population will reach 16%. Various studies have suggested that elderly people have a greater incidence of CKD. These elderly patients are also susceptible to cardiovascular disease (CVD), which is the leading cause of death, resulting in poor prognosis in this population. However, CVD in such patients is often insidious and lacks early markers for effective evaluation. Fortunately, several studies have recently proposed biomarkers associated with this process.

Summary: This study aimed to summarize the early biomarkers of CVD in elderly patients with CKD to provide a basis for its prevention and treatment.

Key messages: This review outlines four categories of potential early biomarkers. All of them have been shown to have some clinical value for these patients, but more research is still needed.

Background: According to the Centers for Disease Control and Prevention (CDC), diabetes affects approximately 37.3 million individuals in the USA, with another estimated 96 million people having a prediabetic state. Furthermore, one or two out of three adult Americans exhibit metabolic syndrome or an insulin-resistant state, depending on their age group.

Summary: Chronic kidney disease (CKD) represents a complication often associated with type II diabetes or the insulin-resistant condition, typically identifiable through proteinuria. Proteinuria serves as both a marker and a contributing factor to kidney damage, and it significantly heightens the risk of cardiovascular (CV) events, including atherosclerosis, heart attacks, and strokes. Renin-angiotensin-aldosterone system inhibitors (RAASis) have demonstrated clinical efficacy in lowering blood pressure, reducing proteinuria, and slowing CKD progression. However, hyperkalemia is a common and serious adverse effect associated with using RAASi.

Key messages: It is imperative to establish personalized management strategies to enable patients to continue RAASi therapy while effectively addressing hyperkalemia risk. Healthcare professionals must be careful not to inadvertently create a low renal perfusion state, which can reduce distal nephron luminal flow or luminal sodium concentration while using RAASi. Nonsteroidal mineralocorticoid receptor antagonists (nsMRAs), such as finerenone, are demonstrated to delay CKD progression and reduce CV complications, all while mitigating the risk of hyperkalemia. Additionally, maintaining a routine monitoring regimen for serum potassium levels among at-risk patients, making dietary adjustments, and considering the adoption of newer potassium-binding agents hold promise for optimizing RAASi therapy and achieving more effective hyperkalemia management.