Advanced searches left 3/3

Cardiorenal Syndrome - DOAJ

Summarized by Plex Scholar
Last Updated: 10 September 2022

* If you want to update the article please login/register

Cardiotoxicity of Uremic Toxins: A Driver of Cardiorenal Syndrome

In the setting of chronic kidney disease, cardiovascular disease is extremely common. Udocardia is a typical cardiac pathology seen in CKD. Patients with CKD are also vulnerable to heart rhythm disorders, especially atrial fibrillation. Traditional CV risk factors, as well as well as recognized CKD-associated CV risk factors such as anemia, are insufficient to explain CV problems in the CKD population. Accumulation of uremic retention solutes is a characteristic of impaired renal excretory function. In recent years, direct cardiotoxicity of uremic toxins has been on the rise.

Source link: https://doi.org/10.3390/toxins10090352


Beyond the Cardiorenal Syndrome: Pathophysiological Approaches and Biomarkers for Renal and Cardiac Crosstalk

In the last few years, the bi-directional relationship between the heart and kidneys, where dysfunction in one organ exacerbates the functioning of the other, has been the most influential catalyst for scientific research in the last few years. This paper discusses hemodynamic and non-hemodynamic pathways, as well as biomarkers that might be the next target for diagnosis, therapy, and prognosis in cardiorenal syndrome.

Source link: https://doi.org/10.3390/diagnostics12040773


OX-HDL: A Starring Role in Cardiorenal Syndrome and the Effects of Heme Oxygenase-1 Intervention

We'll discuss the potential role of HDL dysfunction in CRS after describing how the HDL and RCT pathways become dysfunctional due to oxidative processes. HDL function and the inducible antioxidant gene heme oxygenase-1 are interconnected, and we'll then discuss how HDL function and the inducible antioxidant gene heme oxygenase-1 are linked, and how injection of HO-1 is safe against HDL dysfunction and vital for the proper functioning of the cardiovascularu2013renal system.

Source link: https://doi.org/10.3390/diagnostics10110976


Cardiorenal Syndrome: Emerging Role of Medical Imaging for Clinical Diagnosis and Management

The interconnection between heart and kidneys is being investigated by cardiorenal syndrome in which one organ's disease causes other abnormalities of the other. The key clinical difficulties associated with cardiorenal syndrome include the lack of diagnostic tools for early diagnosis, prognosis, and evaluation of therapeutic effects. This report details the applicability and the future technological capabilities of each imaging technique in the assessment of CRS.

Source link: https://doi.org/10.3390/jpm11080734


Klotho relieves inflammation and exerts a cardioprotective effect during renal ischemia/reperfusion-induced cardiorenal syndrome

Given this, Klotho therapy may reduce or attenuate the inflammation, as well as preventing electrical cardiac events related to CRS. The purpose of this research was to determine Klotho's therapeutic role in CRS after unilateral renal IRI as a result of its anti-inflammatory intervention. Methods: By excluding the left pedicle for 60 min and reperfusion for 8 days, we investigated renal tissue structure and function, intracellular Ca2+ metabolism, and serum cytokine levels from C57BL/6 mice with unilateral renal IRI. Results: The left renal tissue was damaged after Klotho therapy for eight days, but renal function was restored due to right kidney tissue preservation. In parallel, Klotho also stopped an increase in serum interleukin 6, IL-1u03b2, and tumor necrosis factor alpha values, which were in synchogue.

Source link: https://doi.org/10.1016/j.biopha.2022.113515


Urine N-terminal pro-B-type natriuretic peptide and plasma proenkephalin are promising biomarkers for early diagnosis of cardiorenal syndrome type 1 in acute decompensated heart failure: a prospective, double-center, observational study in real-world

Patients with acute decompensated heart failure with cardiorenal syndrome type 1 are more likely to have a poor outcome. paraphrasedoutput:Methods is a computerized measurement of blood pressure. We established the predictive value of plasma proenkephalin and urine NT-proBNP in ADHF patients before admission to CRS-1 and vulnerable-phase prognosis. b. e. The plasma NT-proBNP, pPENK, and uNT-proBNP were tested in 121 ADHF patients. Conclusions: The pPENK [HR 1. 014], p = 0. 044] and uNT-proBNP/uCr ration [HR 0. 998] were also good predictors of HF readmission and death 90 d after discharge in ADHF patients, as well as independent predictors of CRS-1 incidence and vulnerable-phase outcomes in ADHF patients.

Source link: https://doi.org/10.1080/0886022X.2022.2114367


Grb2 Induces Cardiorenal Syndrome Type 3: Roles of IL-6, Cardiomyocyte Bioenergetics, and Akt/mTOR Pathway

Following acute kidney injury, acute kidney injury, heart damage is the heart of Cardiorenal syndrome type 3. Although many experiments have shown that inflammation, oxidative stress, and cardiomyocyte death play a role in cardiac disease pathophysiological changes during CRS-3, cardiomyocyte pathophysiological changes during CRS-3, they do not have a non-bias approach to determine the primary mediator of cardiac dysfunction. Increasing Grb2 was associated with cardiac diastolic dysfunction and mitochondrial bioenergetics impairment; these pathological changes could be reversed by the introduction of a Grb2-specific inhibitor during AKI. Besides that, Mouse Inflammation Array Q1 identified IL-6 as the upstream trigger of Grb2 upregulation after AKI.

Source link: https://doi.org/10.3389/fcell.2021.630412


Empagliflozin activates Wnt/β-catenin to stimulate FUNDC1-dependent mitochondrial quality surveillance against type-3 cardiorenal syndrome

Objectives: Cardiorenal syndrome type-3 is a sudden increase in cardiac function as a result of acute kidney injury. Mitochondrial dysfunction is a primary pathological cause of CRS-3, and empagliflozin can enhance mitochondrial function by encouraging mitophagy. Conclusions: The CRS-3 model mice had lower heart function, elevated inflammation, and exacerbated myocardial oxidative stress relative to sham-operated controls, but empagliflozin stifled these changes; however, empagliflozin attenuated these changes. Empagliflozin stabilized the mitochondrial membrane potential, stifled mitochondrial reactive oxygen species manufacture, increased mitochondrial respiratory complex formation, and raised the oxygen consumption rate in cardiomyocytes from CRS-3 model mice, thus lowering the oxygen consumption rate in cardiomyocytes. Empagliflozin also normalized the mitochondrial morphology, mitochondrial dynamics, and mitochondrial permeability transition pore opening rate in cardiomyocytes. The protective effects of empagliflozin on mitochondrial homeostasis and myocardial function were destroyed by cardiomyocyte-specific ablation of FUN14 domain-containing protein 1 in mice. Following acute kidney injury, empagliflozin could be used for the clinical care of heart disease.

Source link: https://doi.org/10.1016/j.molmet.2022.101553

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions