The description in the abstract lacks clear logic and a comprehensive summary of this study, so please revise and improve it according to the design theme and main content of this study, and describe it in the order o...The description in the abstract lacks clear logic and a comprehensive summary of this study, so please revise and improve it according to the design theme and main content of this study, and describe it in the order of (research background), purpose/aim, method, results and conclusions. The introduction of the abstract and preface is rather lengthy, but the summary of the whole study and the presentation of the research background are not perfect (mainly because the logic of the context is not clear and orderly), so it will appear a bit messy. Hope to be able to modify (this has been mentioned in the preliminary opinion). Cardiovascular events (CVE) pose a significant threat to individuals with end-stage renal disease (ESRD), yet these patients are often excluded from cardiovascular clinical trials, leaving prognostic factors associated with CVE in ESRD patients largely unexplored. Recent human studies have demonstrated elevated circulating aldosterone levels in ESRD patients, correlating with left ventricular hypertrophy. Additionally, animal models have shown improvements in uremic cardiomyopathy with spironolactone therapy, prompting interest in assessing the efficacy of spironolactone or eplerenone in reducing mortality and improving cardiovascular function in dialysis patients. Clinicians have historically been cautious about prescribing mineralocorticoid receptor antagonists (MRAs) to congestive heart failure patients with chronic kidney disease (CKD) due to hyperkalemia risk. However, the emergence of finerenone, a novel MR antagonist with a favorable safety profile and lower hyperkalemia risk, has renewed interest in MRA therapy in this population. Heart disease, including coronary artery disease, hypertension, and left ventricular failure, is alarmingly prevalent in dialysis patients, contributing significantly to elevated mortality rates compared to the general population. Arterial stiffness, as indicated by pulse wave velocity (PWV), progressively worsens with advancing CKD stages, peaking in severity 展开更多
At the cellular level, reduced kidney perfusion in atherosclerotic renal arthery disease (ARVD), induces hypoxia, activation of the renin-angiotensin-aldosterone system (RAAS) and cytokine activation. Impaired blood f...At the cellular level, reduced kidney perfusion in atherosclerotic renal arthery disease (ARVD), induces hypoxia, activation of the renin-angiotensin-aldosterone system (RAAS) and cytokine activation. Impaired blood flow in the kidneys creates a microenvironment triggering significant cytokine production, contributing to vascular damage and endothelial disfunction. Interactions between cytokines and endothelial, glomerular, and tubular cells often result in increased vessel permeability, and fibrosis, and contribute to the development of chronic kidney disease (CKD). Molecules such as endothelins, prostaglandins, and nitric oxide play a crucial role at the molecular level. The imbalance between vasoconstrictor and vasodilator factors contributes to vascular dysfunction. Oxidative stress and inflammatory processes at the cellular level contribute to endothelial damage and structural changes in blood vessels. Mineralocorticoid receptor antagonists (MRAs) therapy in the context of ARVD holds promise in reducing fibrosis, promoting angiogenesis and enhancing overall outcomes in patients with this pathology. Recent data also indicates the antioxidative, anti-inflammatory, and antifibrotic effects of SGLT2 inhibitors. They reduce oxidative stress caused by hypoxic conditions and enhance renal perfusion, contributing to the preservation of cellular function. Studies employing Blood Oxygen Level-Dependent (BOLD) imaging have identified adaptations to reduced blood flow, volume, and glomerular filtration rate in post-stenotic kidneys that preserve oxygenation in the medulla and cortex during medical therapy. Data from the literature indicate that despite the partial recovery of renal hypoxia and restoration of blood flow after revascularization, inflammatory cytokines and injury biomarkers remain elevated, and the glomerular filtration rate (GFR) does not recover in ARVD. Restoration of vascular patency alone has failed to reverse tubulointerstitial damage and partially explains the limited clinical benefit of renal stent展开更多
文摘The description in the abstract lacks clear logic and a comprehensive summary of this study, so please revise and improve it according to the design theme and main content of this study, and describe it in the order of (research background), purpose/aim, method, results and conclusions. The introduction of the abstract and preface is rather lengthy, but the summary of the whole study and the presentation of the research background are not perfect (mainly because the logic of the context is not clear and orderly), so it will appear a bit messy. Hope to be able to modify (this has been mentioned in the preliminary opinion). Cardiovascular events (CVE) pose a significant threat to individuals with end-stage renal disease (ESRD), yet these patients are often excluded from cardiovascular clinical trials, leaving prognostic factors associated with CVE in ESRD patients largely unexplored. Recent human studies have demonstrated elevated circulating aldosterone levels in ESRD patients, correlating with left ventricular hypertrophy. Additionally, animal models have shown improvements in uremic cardiomyopathy with spironolactone therapy, prompting interest in assessing the efficacy of spironolactone or eplerenone in reducing mortality and improving cardiovascular function in dialysis patients. Clinicians have historically been cautious about prescribing mineralocorticoid receptor antagonists (MRAs) to congestive heart failure patients with chronic kidney disease (CKD) due to hyperkalemia risk. However, the emergence of finerenone, a novel MR antagonist with a favorable safety profile and lower hyperkalemia risk, has renewed interest in MRA therapy in this population. Heart disease, including coronary artery disease, hypertension, and left ventricular failure, is alarmingly prevalent in dialysis patients, contributing significantly to elevated mortality rates compared to the general population. Arterial stiffness, as indicated by pulse wave velocity (PWV), progressively worsens with advancing CKD stages, peaking in severity
文摘At the cellular level, reduced kidney perfusion in atherosclerotic renal arthery disease (ARVD), induces hypoxia, activation of the renin-angiotensin-aldosterone system (RAAS) and cytokine activation. Impaired blood flow in the kidneys creates a microenvironment triggering significant cytokine production, contributing to vascular damage and endothelial disfunction. Interactions between cytokines and endothelial, glomerular, and tubular cells often result in increased vessel permeability, and fibrosis, and contribute to the development of chronic kidney disease (CKD). Molecules such as endothelins, prostaglandins, and nitric oxide play a crucial role at the molecular level. The imbalance between vasoconstrictor and vasodilator factors contributes to vascular dysfunction. Oxidative stress and inflammatory processes at the cellular level contribute to endothelial damage and structural changes in blood vessels. Mineralocorticoid receptor antagonists (MRAs) therapy in the context of ARVD holds promise in reducing fibrosis, promoting angiogenesis and enhancing overall outcomes in patients with this pathology. Recent data also indicates the antioxidative, anti-inflammatory, and antifibrotic effects of SGLT2 inhibitors. They reduce oxidative stress caused by hypoxic conditions and enhance renal perfusion, contributing to the preservation of cellular function. Studies employing Blood Oxygen Level-Dependent (BOLD) imaging have identified adaptations to reduced blood flow, volume, and glomerular filtration rate in post-stenotic kidneys that preserve oxygenation in the medulla and cortex during medical therapy. Data from the literature indicate that despite the partial recovery of renal hypoxia and restoration of blood flow after revascularization, inflammatory cytokines and injury biomarkers remain elevated, and the glomerular filtration rate (GFR) does not recover in ARVD. Restoration of vascular patency alone has failed to reverse tubulointerstitial damage and partially explains the limited clinical benefit of renal stent
