Cardiorenal Medicine最新文献

Background: Systemic inflammation (SI) contributes to increased cardiovascular risk in patients with atherosclerotic cardiovascular disease (ASCVD) and chronic kidney disease (CKD). We assessed clinical perceptions toward SI and usage of high-sensitivity C-reactive protein (hsCRP) among nephrologists.

Methods: FLAME-ASCVD Nephro was an online survey of nephrologists from 10 countries who treat ≥20 patients with ASCVD and CKD a month and were practicing for ≥3 years. Results were analyzed using descriptive statistics.

Results: Of 513 nephrologists who responded, 300 completed and were included in the survey; the mean age was 46 years and the mean time in practice was 16 years. Hypertension (89%), overweight/obesity (81%), and CKD (80%) were the ASCVD risk factors most often discussed with patients (SI was ninth). The most common unmet needs (ranked 1-3) for patients with ASCVD and CKD were "lack of effective SI treatment options" (44%), "limited awareness of the role of SI in ASCVD" (35%), and "higher risk of CV events" (33%). Seventy-four percent of nephrologists wanted to learn more about the role of SI in ASCVD and 71% test for and use SI results when determining management approaches. Seventy percent of nephrologists considered hsCRP testing in patients with ASCVD and CKD (aided), and proven clinical efficacy of hsCRP was the top reason (37%); out-of-pocket cost (30%) was the most common reason for not considering hsCRP testing.

Conclusion: Lack of effective treatment options for SI remains the most common unmet need for patients with ASCVD and CKD. Further medical education is needed to raise awareness among nephrologists about the role of SI and hsCRP testing.

Background: Limited data are available regarding the global burden of heart failure attributable to chronic kidney disease (CKD-HF). The aim of this study was to estimate the disease burden and cross-national disparities in CKD-HF from 1990 to 2021.

Methods: CKD-HF prevalence and years lived with disability (YLDs) were extracted from the Global Burden of Disease (GBD) database. The slope index of inequality (SII) and concentration index were adopted for analyzing absolute and relative health inequalities, and the autoregressive integrated moving average (ARIMA) model was applied to project trends in CKD-HF burden through 2040.

Results: From 1990 to 2021, the CKD-HF age-standardized prevalence rate (ASPR) globally increased from 13.58 per 100,000 (95% uncertainty interval (UI): 11.16-16.22) to 24.21 (95% UI: 19.86-29.23), and the age-standardized years lived with disability (ASYR) increased from 1.73 (95% UI: 1.12-2.56) to 3.07 (95% UI: 1.95-4.44). By 2040, the global ASPR is projected to increase to 30.90 (95% confidence interval (CI): 29.62-32.18), with the ASYR expected to increase to 3.84 (95% CI: 3.59-4.08). In 2021, the highest ASPRs were observed in Western Sub-Saharan Africa, Andean Latin America and Central Latin America, whereas the highest ASYRs were observed in Australasia, Tropical Latin America, and Andean Latin America. Diabetic nephropathy and hypertensive nephropathy have emerged as increasingly significant drivers of the CKD-HF burden. The CKD-HF burden exhibited significant health inequities, with low-sociodemographic index (SDI) regions bearing a disproportionate share of the burden, a trend that is expected to persist through 2040.

Conclusion: Patients with CKD-HF exhibited a sustained increase in disease burden, a shift in the underlying cause distribution, and significant health disparities. There is an urgent need for more region-specific strategies to prevent the underlying causes and improve medical care for patients with CKD-HF to mitigate the future burden of this condition.

Background: We evaluated the effects of sustained low-efficiency dialysis (SLED) as an alternative to palliative care in persistently congested patients with advanced heart failure unsuitable for mechanical circulatory support or heart transplantation.

Methods: In this single-center, non-randomised retrospective cohort study, we included patients hospitalised with advanced heart failure, persistent congestion, and renal dysfunction between September 2002 and December 2024. The index date was defined as the time SLED was considered clinically indicated. Patients who were treated with SLED formed the SLED group, patients who declined SLED and continued with standard medical therapy only were assigned to the standard therapy group. Outcomes included the number and duration of heart failure-related and all-cause hospitalisations 1 year before and after the index date, heart failure medication use, and mortality.

Results: We compared 107 patients treated with SLED (mean age 75 ± 10 years, 48% male, 58% HFpEF) with 32 patients in the standard therapy group (mean age 79 ± 18 years, 34% male, 53% HFpEF). During the first year after the index date, heart failure hospitalisation occurred in 13% of SLED patients compared to 78% of standard therapy patients. In the SLED group, the annual heart failure hospitalisation rate decreased from 1.5 to 0.3 events (p < 0.001), and duration of hospital stay from 21.4 to 2.5 days (p < 0.001). No significant change was observed in the standard therapy group (1.7 to 1.6 events; 16.3 to 16.3 days). All-cause hospitalisation rates were unchanged in both groups, but duration of all-cause hospital stay (25.1 to 11.5 days, p < 0.001) was significantly reduced in the SLED group. Use and titration of angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, mineralocorticoid receptor antagonists, and β-blockers improved significantly in the SLED group but remained largely unchanged with standard therapy. Median survival was longer in the SLED group (23 months, 95% CI 17-29) compared with standard therapy (3 months, 95% CI 1-7; p < 0.001).

Conclusions: In patients with advanced heart failure and persistent congestion, SLED was associated with fewer heart failure-related hospitalisations, enhanced optimisation of pharmacological heart failure therapy, and prolonged survival relative to standard therapy only.

Background: Cardiovascular-kidney-metabolic (CKM) syndrome is a recently introduced concept that links chronic kidney disease (CKD), cardiovascular disease (CVD), and metabolic risk factors such as obesity or diabetes mellitus (DM). The use of eGFR <60 mL/min/1.73 m² as a CKD indicator often detects more advanced stages of renal disease, even though risk is present at earlier stages, particularly in the presence of albuminuria.

Summary: The non-steroidal mineralocorticoid receptor antagonist finerenone has demonstrated efficacy in reducing cardiovascular and renal outcomes in patients with CKD and type 2 DM. Data from FIDELITY, a pooled analysis of FIDELIO-DKD and FIGARO-DKD, showed significant reductions in kidney failure and cardiovascular outcomes in patients with CKD and type 2 DM. Moreover, data from FINEARTS-HF trial revealed that finerenone prevents onset of albuminuric CKD in patients.

Key messages: These results support a paradigm shift toward earlier intervention in CKM syndrome, with the aim of preserving renal function. Finerenone holds promise for changing the trajectory of CKD within a broader CKM framework. Ongoing trials will further define its role in diverse patient populations and stages of CKM syndrome.

Background: HF and CKD create a mutually reinforcing cycle, escalating disease development, and increasing morbidity and mortality rates. Both are common comorbidities promoting AF and contributing to heightened symptom burden and poorer outcomes in AF. Here our aim was to investigate the relationship of heart failure (HF) and chronic kidney disease (CKD) with cardiorenal outcomes in patients with atrial fibrillation (AF).

Methods: Patients with AF, treated at a tertiary centre between 01/2005 and 07/2019 were included. The primary endpoint was a composite of cardiovascular (CV) death and hospitalization for HF (HHF). Secondary outcomes were the individual components of the primary endpoint, all-cause death, renal death, and dialysis.

Results: We included a total of 7,412 patients (median age 70 years, 39.7% female) with AF and followed them over a median of 4.5 years. There was a significant stepwise increase in 5-year event rates for the composite of CV death/HHF (no CKD and no HF: 23%, HF: 61%, CKD: 63%, CKD and HF: 82%; P log-rank <0.001). Both CKD (adjusted hazard ratio [HR]: 1.87, 95% confidence interval [CI]: 1.55–2.25) and HF (adjusted HR: 2.57, 95% CI: 2.22–2.98) were significantly associated with CV death/HHF after multivariable adjustment. A similar association was observed for the individual components of the primary endpoint and renal death/dialysis.

Conclusions: Both CKD and HF significantly increase the risk of CV death and HHF, as well as renal death/ dialysis in patients with AF. Risk assessment should expand beyond stroke and bleeding to cardiorenal complications including HHF, CV and renal death, as well as kidney failure.

Background: Fluid management is a critical aspect of care in critically ill patients. While fluid overload has been linked to adverse outcomes, the balance between achieving a negative fluid balance and preserving kidney function presents a clinical challenge, and the significance of diuretic responsiveness in patients in the de-resuscitation phase remains unclear.

Objective: This study aimed to evaluate the association between forced diuresis, fluid balance, and clinical outcomes in ICU patients during the de- resuscitation phase. Additionally, we assessed whether changes in kidney function influence prognosis in this patient population.

Methods: A retrospective cohort study was conducted, including 527 critically ill patients treated with furosemide for at least three days during their ICU stay. Fluid balance, kidney function changes (assessed via KDIGO criteria), and clinical outcomes, including ICU mortality and modified SOFA score (excluding renal function), were analyzed.

Results: Patients who achieved both a negative fluid balance and improvement in kidney function had the lowest mortality rates and better outcomes. Conversely, those who remained in positive fluid balance despite forced diuresis and exhibited worsening kidney function had the highest mortality and organ dysfunction progression. The presence of vasopressor use and mechanical ventilation was associated with poorer outcomes.

Conclusion: Among ICU patients undergoing forced diuresis during the de- indicator, non-responsiveness signals a high-risk population. These findings underscore the need for individualized fluid management strategies and highlight the importance of further prospective studies to clarify the role of forced diuresis in critically ill patients.

Aims: Haemodynamic changes in acute heart failure (AHF) are closely linked to renal function alterations. Pulse pressure (PP) may offer insights beyond mean arterial pressure (MAP) in identifying patients with vulnerable renal function during AHF episodes. This study aimed to investigate the association between PP and renal function parameters, including urinary albumin creatinine ratio (UACR) and changes in creatinine, in patients hospitalized for AHF.

Methods and results: We conducted a retrospective observational study involving 695 patients admitted for AHF between June 2020 and April 2023. PP was calculated at admission, and renal function parameters were assessed over the first 48 hours. A multivariable linear regression assessed the association between PP and UACR and creatinine changes, adjusting for possible confounders. Patients in the highest tertile of PP exhibited a significantly higher incidence of worsening renal function (WRF) (p=0.048) and a lower incidence of improved renal function (IRF) (p=0.001). Multivariable analysis identified PP as an independent predictor of changes in creatinine (p=0.010) and UACR (p=0.037). The findings suggest that elevated PP may indicate impaired renal autoregulation and an increased risk of renal deterioration during AHF.

Conclusion: In patients hospitalized for AHF pulse pressure showed a positive and linear association with UACR values and changes in creatinine during the first 48 hours of intravenous furosemide treatment. Pulse pressure may help identifying patients with kidneys more susceptible to haemodynamic changes during hospitalization for AHF.

Background A newly recognized condition, the cardiovascular-kidney-metabolic (CKM) syndrome,integrated disease spectrum encompassing interlinked renal, cardiovascular, and metabolic dysfunction. Visceral adiposity plays a pivotal role in driving this multisystem deterioration. Although surrogate markers such as the visceral adiposity index (VAI), metabolic score for visceral fat (METS-VF), body roundness index (BRI), and weight-adjusted waist index (WWI) have been proposed to estimate visceral fat burden, their relationship with advanced CKM syndrome remains poorly defined.This study sought to thoroughly examine the links between these indices and advanced CKM risk, and to evaluate their ability to predict such risk. Methods In this study, we performed a cross-sectional analysis using data from the National Health and Nutrition Examination Survey (NHANES) spanning 1999 to 2018, which included 22,019 adults aged 20 years and older. We calculated four indices of visceral fat accumulation (VAI, METS-VF, BRI, WWI) and assessed their associations with advanced CKM syndrome through weighted multivariable logistic regression, restricted cubic spline (RCS) modeling, and receiver operating characteristic (ROC) curve analysis. Subgroup analyses were also conducted to ensure the robustness of the findings, adjusting for demographic and lifestyle factors. Results Advanced CKM syndrome was present in 17.4% of participants. All four indices were significantly associated with advanced CKM (all P < 0.05), with METS-VF showing the strongest association (OR = 1.87, 95% CI: 1.51-2.30). Both METS-VF and VAI demonstrated a non-linear increase in risk for advanced CKM, whereas BRI and WWI showed a positive linear relationship with the risk. Subgroup analyses provided additional evidence, confirming that these associations remained consistent across multiple population subgroups. In ROC analysis, METS-VF demonstrated the highest predictive accuracy (AUC = 0.79), followed by WWI (AUC = 0.73), outperforming traditional markers such as body mass index (BMI) and waist circumference (WC). Conclusions Elevated VAI, METS-VF, BRI, and WWI levels have been significantly linked to advanced CKM syndrome. METS-VF and WWI, as simple and non-invasive markers, show strong predictive capacity and may serve as effective tools for early detection and intervention in clinical settings.

Introduction: The processes of atherosclerosis, inflammation, and carbamylation are closely linked in cardiovascular (CV) disease, but the potential of carbamylation burden as a CV mortality predictor is unclear, especially in patients with no or mild chronic kidney disease (CKD). This study aimed to investigate whether elevated carbamylated albumin (C-Alb), as a surrogate marker for carbamylation burden, is associated with mortality and arterial stiffness/atherosclerotic burden in patients with no or mild CKD, using pulse pressure (PP) as a marker for arterial stiffness.

Methods: We measured C-Alb in 3,193 participants of the Ludwigshafen Risk and Cardiovascular Health study who had been referred for coronary angiography and followed up for 10 years.

Results: The mean age was 62.7 years, and 30.4% were female. Mean blood pressure was 141/81 mm Hg, and mean C-Alb was 5.54 mmol/mol. Increase in C-Alb levels was associated with older age; female sex; increased PP, high-sensitivity C-reactive protein, and interleukin-6 levels; and increased incidence of coronary artery disease (CAD), peripheral artery disease (PAD), and carotid stenosis. In contrast, BMI, diastolic blood pressure (DBP), albumin, and the proportion of active smokers decreased with increasing C-Alb levels. In particular, C-Alb showed a highly significant correlation with CAD severity: Friesinger (Pearson correlation coefficient [r] = 0.082, p < 0.001) and Gensini score (r = 0.066, p < 0.001). The area under the curve (AUC) for all-cause mortality prediction by the European Society of Cardiology Heart Score (ESC-HS) significantly improved from 0.719 to 0.735, and the AUC for CV mortality prediction based on C-Alb increased from 0.726 to 0.750 in patients without previously known CV disease. C-Alb correlated directly and significantly with PP (r = 0.062, p < 0.001), which was consistently the strongest predictor of mortality across all C-Alb tertiles. The hazard ratios (HRs) for all-cause mortality per 10 mm Hg increase (or 1,000 mm Hg/min increase for double product [DP]) in the 1st tertile of C-Alb were 1.18, 1.13, 1.11, and 1.11 for PP, mean arterial pressure (MAP), systolic blood pressure (SBP), and DP, respectively, but the HR for DBP did not reach significance. In the 3rd tertile of C-Alb, the HRs were 1.13, 1.05, and 1.09, for PP, SBP, and DP, respectively, but the HR for MAP did not reach significance.

Conclusion: C-Alb may be a valuable biomarker for assessing CV risk and improving mortality prediction even in patients with no or mild CKD. The findings support the notion of a crosslink between carbamylation, inflammation, atherosclerosis, and mortality. While these results are promising, further research is needed to fully elucidate the role of C-Alb in CV disease progression and risk stratification.