Cardiorenal Medicine最新文献

Introduction: Patients with heart failure (HF) and chronic kidney disease (CKD) are often suboptimally treated due to concerns of hyperkalaemia, declining kidney function, and hypotension. They commonly suffer from fluid overload which can lead to frequent hospitalisations and death. This research aims to determine the characteristics associated with hospital admissions and death in patients with CKD and HF.

Methods: Consecutive patients with CKD stage 3-5 and HF (regardless of ejection fraction) attending a large, specialised CKD-HF clinic between 12/Sept/2019 and 11/Nov/2021 were identified and data were collected on demographic factors, renal and heart function, medications, hospitalisations, and death. Multinomial and Cox regressions determined the characteristics of patients requiring hospitalisation and their risk of death, respectively.

Results: A total of 667 admissions were attributable to 318 patients, 201 admissions were for HF. Men were less likely than women to have been admitted to hospital for HF (risk ratio [RR] 0.43, 95% CI 0.20, 0.94) and non-HF causes (RR 0.21, 95% CI 0.10, 0.47). A serum haemoglobin level greater than 100 g/L was associated with fewer HF and non-HF admissions compared to a serum haemoglobin less than 100 g/L (RR 0.26, 95% CI 0.09, 0.74; RR 0.17, 95% CI 0.06, 0.47). Compared to CKD stage 3, CKD stage 4 was associated with an increased risk of HF and non-HF admissions (RR 4.01, 95% CI 1.04, 15.5; RR 4.33, 95% CI 1.13, 16.5). Having a HF admission (HR 2.41, 95% CI 1.27, 4.60), HFrEF (HR 2.18, 95% CI 1.30, 3.63), CKD stage 4 (HR 1.91, 95% CI 1.16, 3.16), and loop diuretic use (HR 2.24, 95% CI 1.14, 4.40) were associated with a significantly increased risk of death compared to people with no admissions, with HF with reduced preserved ejection fraction, CKD stage 3, and no diuretic use, respectively. The use of RAAS inhibitors halved the risk of death compared to non-prescribed patients (HR 0.44, 95% CI 0.27, 0.72).

Conclusion: Hospital admissions among CKD-HF patients were common, particularly in those with lower serum haemoglobin levels and advanced CKD stage. The risk of death was higher in those with HF admissions, the presence of HFrEF, advanced CKD stage, loop diuretic use, and those not prescribed RAAS inhibitors.

Background: Kidney transplantation is the best treatment for patients with chronic renal failure, capable of improving life expectancy and the risk of death from all causes, which, however, remains higher than in the general population. The leading cause of death in transplant patients is cardiovascular events, burdened by a significant impact brought about by anti-rejection therapy. Experimental and clinical studies to date show that in kidney transplant recipients, traditional cardiovascular risk factors (hypertension, diabetes, dyslipidemia, obesity, tobacco, etc.) may be exacerbated or worsened by the dysmetabolic effects of immunosuppressive drugs, which may also result in additional risk factors such as proteinuria, anemia, and arterial stiffness. The aim of this review was to provide an in-depth evaluation of the effect of immunosuppressive treatments on cardiovascular risk factors.

Summary: We have investigated and described the main cardiovascular risk factors related to immunosuppressive drugs. We searched for relevant scientific articles in medicine, transplant, cardiologic, and nephrological journals in major medical science libraries.

Key messages: Immunosuppressive drugs allow graft survival and successful bunking of the transplant; however, they are not without significant side effects and should always be prescribed weighing the risk/benefit ratio and the individual patient's therapeutic needs.

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, 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 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: Acute decompensated heart failure (ADHF) poses a challenging paradox of renal and cardiac pathophysiology, with volume excess or "congestion" being a key player. Understanding the mechanisms of congestion is crucial for effectively managing fluid overload and improving patient prognosis.

Summary: In this review, we evaluate the physiology of congestion and explore its implications for management in clinical practice. Mechanisms of congestion can largely be broken down under the subtext of fluid accumulation and fluid redistribution. Fluid accumulation develops as a consequence of neurohormonal dysregulation, physiologic maladaptive mechanisms, and detrimental crosstalk between the heart and the kidney. On the other hand, fluid redistribution evolves due to progressive overriding of compensatory vascular mechanisms, renal injury, and hormonal feedback.

Key messages: Understanding the complex pathophysiology of congestion in ADHF is crucial for effective volume management and protection against long-term mortality and morbidity risks. By targeting both fluid accumulation and redistribution mechanisms, clinicians can optimize treatment strategies to alleviate congestion and restore hemodynamic stability in patients with ADHF.

Background: Cardiopulmonary exercise testing (CPET) is an emerging tool in nephrology that has garnered significant interest among clinicians and investigators.

Summary: CPET technology enables the user to accurately assess cardiovascular functional capacity using an integrative approach, to identify multi-organ reserve capacities and interrogate pathophysiological mechanisms underpinning impaired exercise tolerance in patients with chronic kidney disease (CKD). These capabilities provide rationale for accumulating studies exploring the use of this existing technology for new applications in nephrology and to solve current clinical practice barriers. Examples of current clinical interest areas include its potential to help transform diagnostic approaches to cardiovascular complications in patients with CKD, to offer superior cardiovascular risk stratification and to provide a solution to current limitations of traditional resting endpoints in cardiorenal clinical trials.

Key messages: This article reviews the foundational principles, methodologic, and operational implementation of CPET in patients with CKD and those on dialysis.

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 (incidence rate ratio [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.

Background: The growing complexity of patient data and the intricate relationship between heart failure (HF) and acute kidney injury (AKI) underscore the potential benefits of integrating artificial intelligence (AI) and machine learning into healthcare. These advanced analytical tools aim to improve the understanding of the pathophysiological relationship between kidney and heart, provide optimized, individualized, and timely care, and improve outcomes of HF with AKI patients.

Summary: This comprehensive review article examines the transformative potential of AI and machine-learning solutions in addressing the challenges within this domain. The article explores a range of methodologies, including supervised and unsupervised learning, reinforcement learning, and AI-driven tools like chatbots and large language models. We highlight how these technologies can be tailored to tackle the complex issues prevalent among HF patients with AKI. The potential applications identified span predictive modeling, personalized interventions, real-time monitoring, and collaborative treatment planning. Additionally, we emphasize the necessity of thorough validation, the importance of collaborative efforts between cardiologists and nephrologists, and the consideration of ethical aspects. These factors are critical for the effective application of AI in this area.

Key messages: As the healthcare field evolves, the synergy of advanced analytical tools and clinical expertise holds significant promise to enhance the care and outcomes of individuals who deal with the combined challenges of HF and AKI.