scholarly journals Role of macrophages in cardiorenal syndrome development in patients with myocardial infarction

2021 ◽  
Vol 26 (4) ◽  
pp. 4309
Author(s):  
M. A. Kercheva ◽  
V. V. Ryabov
Keyword(s):  
Myocardial Infarction ◽  
Collecting Duct ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Current Data ◽  
Innate Immune ◽  
Macrophages Polarization ◽  
System Activation ◽  
Cellular Components

Cardiorenal syndrome (CRS) in patients with acute myocardial infarction (MI) underlies the development and progression of renal and heart failure. Along with the well-known mechanisms of CRS development based on reninangiotensin system activation, kidney-heart macrophage axis may be one of the key cellular components of CRS. Continuous sympathetic stimulation of collecting duct system cells under ischemia activates the macrophage link of the kidneys, which contributes to cardiac macrophages' polarization and leads to the development of adaptive myocardial hypertrophy and fibrosis. This review article summarizes current data on interaction of macrophages in the kidney-heart axis, which can be considered as the cellular basis for CRS development in patients with MI. The translation of experimental data on the participation of innate immune system on CRS model in humans will make it possible to find new ways to prevent and suppress acute kidney injury in patients with MI.

scholarly journals Renalase and Biomarkers of Contrast-Induced Acute Kidney Injury

2015 ◽  
Vol 6 (1) ◽  
pp. 25-36 ◽  
Author(s):  
Maciej T. Wybraniec ◽  
Katarzyna Mizia-Stec
Keyword(s):  
Acute Kidney Injury ◽  
Renal Injury ◽  
Amine Oxidase ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Creatinine Concentration ◽  
Invasive Cardiology ◽  
Proximal Tubular ◽  
Novel Biomarkers

Background: Contrast-induced acute kidney injury (CI-AKI) remains one of the crucial issues related to the development of invasive cardiology. The massive use of contrast media exposes patients to a great risk of contrast-induced nephropathy and chronic kidney disease development, and increases morbidity and mortality rates. The serum creatinine concentration does not allow for a timely and accurate CI-AKI diagnosis; hence numerous other biomarkers of renal injury have been proposed. Renalase, a novel catecholamine-metabolizing amine oxidase, is synthesized mainly in proximal tubular cells and secreted into urine and blood. It is primarily engaged in the degradation of circulating catecholamines. Notwithstanding its key role in blood pressure regulation, renalase remains a potential CI-AKI biomarker, which was shown to be markedly downregulated in the aftermath of renal injury. In this sense, renalase appears to be the first CI-AKI marker revealing an actual loss of renal function and indicating disease severity. Summary: The purpose of this review is to summarize the contemporary knowledge about the application of novel biomarkers of CI-AKI and to highlight the potential role of renalase as a functional marker of contrast-induced renal injury. Key Messages: Renalase may constitute a missing biochemical link in the mutual interplay between kidney and cardiac pathology known as the cardiorenal syndrome.

Activation of hypoxia-sensing pathways promotes renal ischemic preconditioning following myocardial infarction

2021 ◽  
Author(s):  
Andrew S Terker ◽  
Kensuke Sasaki ◽  
Juan Pablo Arroyo ◽  
Aolei Niu ◽  
Suwan Wang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ischemic Preconditioning ◽  
Renal Injury ◽  
Cardiac Injury ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Experimental Myocardial Infarction ◽  
Common Mechanism ◽  
Cardiac Damage ◽  
Chronic Kidney Injury

Ischemic heart disease is the leading cause of death worldwide and is frequently comorbid with chronic kidney disease. Physiological communication is known to occur between the heart and the kidney and primary dysfunction in either organ can induce dysfunction in the other, a clinical entity known as cardiorenal syndrome, but mechanistic details are lacking. Here, we used a model of experimental myocardial infarction (MI) to test effects of chronic cardiac ischemia on acute and chronic kidney injury. Surprisingly, chronic cardiac damage protected animals from subsequent acute ischemic renal injury, an effect that was accompanied by evidence of chronic kidney hypoxia. The protection observed post-MI was similar to protection observed in a separate group of healthy animals housed in ambient hypoxic conditions prior to kidney injury, suggesting a common mechanism. There was evidence that chronic cardiac injury activates renal hypoxia-sensing pathways. Increased renal abundance of several glycolytic enzymes following MI suggested a shift towards anaerobic glycolysis may confer renal ischemic preconditioning. In contrast, effects on chronic renal injury followed a different pattern with post-MI animals displaying worsened chronic renal injury and fibrosis. These data show that while chronic cardiac injury following MI protected against acute kidney injury via activation of hypoxia-sensing pathways, it worsened chronic kidney injury. The results further our understanding of cardiorenal signaling mechanisms and have implications for the treatment of heart failure patients with associated renal disease.

scholarly journals Autophagy Function and Regulation in Kidney Disease

Biomolecules ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 100 ◽  
Author(s):  
Gur P. Kaushal ◽  
Kiran Chandrashekar ◽  
Luis A. Juncos ◽  
Sudhir V. Shah
Keyword(s):  
Cell Death ◽  
Renal Injury ◽  
Mammalian Target Of Rapamycin ◽  
Kidney Injury ◽  
Therapeutic Approaches ◽  
Regulated Necrosis ◽  
Atg Genes ◽  
Cellular Components ◽  
The Impact

Autophagy is a dynamic process by which intracellular damaged macromolecules and organelles are degraded and recycled for the synthesis of new cellular components. Basal autophagy in the kidney acts as a quality control system and is vital for cellular metabolic and organelle homeostasis. Under pathological conditions, autophagy facilitates cellular adaptation; however, activation of autophagy in response to renal injury may be insufficient to provide protection, especially under dysregulated conditions. Kidney-specific deletion of Atg genes in mice has consistently demonstrated worsened acute kidney injury (AKI) outcomes supporting the notion of a pro-survival role of autophagy. Recent studies have also begun to unfold the role of autophagy in progressive renal disease and subsequent fibrosis. Autophagy also influences tubular cell death in renal injury. In this review, we reported the current understanding of autophagy regulation and its role in the pathogenesis of renal injury. In particular, the classic mammalian target of rapamycin (mTOR)-dependent signaling pathway and other mTOR-independent alternative signaling pathways of autophagy regulation were described. Finally, we summarized the impact of autophagy activation on different forms of cell death, including apoptosis and regulated necrosis, associated with the pathophysiology of renal injury. Understanding the regulatory mechanisms of autophagy would identify important targets for therapeutic approaches.

scholarly journals Advances in the Pathogenesis of Cardiorenal Syndrome Type 3

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Anna Clementi ◽  
Grazia Maria Virzì ◽  
Alessandra Brocca ◽  
Massimo de Cal ◽  
Silvia Pastori ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cardiac Injury ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Electrolyte Imbalance ◽  
Immune System Activation ◽  
Cellular Apoptosis ◽  
System Activation ◽  
Acute Cardiac Event ◽  
Type 3

Cardiorenal syndrome (CRS) type 3 is a subclassification of the CRS whereby an episode of acute kidney injury (AKI) leads to the development of acute cardiac injury or dysfunction. In general, there is limited understanding of the pathophysiologic mechanisms involved in CRS type 3. An episode of AKI may have effects that depend on the severity and duration of AKI and that both directly and indirectly predispose to an acute cardiac event. Experimental data suggest that cardiac dysfunction may be related to immune system activation, inflammatory mediators release, oxidative stress, and cellular apoptosis which are well documented in the setting of AKI. Moreover, significant derangements, such as fluid and electrolyte imbalance, metabolic acidosis, and uremia, which are typical features of acute kidney injury, may impair cardiac function. In this review, we will focus on multiple factors possibly involved in the pathogenesis issues regarding CRS type 3.

scholarly journals The Role of Imaging in the Management of Cardiorenal Syndrome

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Sajid Melvin George ◽  
Kambiz Kalantarinia
Keyword(s):  
Clinical Utility ◽  
Imaging Techniques ◽  
Obstructive Uropathy ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Renal Ultrasound ◽  
Resonance Imaging ◽  
Contrast Enhanced ◽  
And Function

Imaging of the kidney and the heart can provide valuable information in the diagnosis and management of cardiorenal syndromes. Ultrasound- (US-) based imaging (echocardiogram and renal US) is an essential component in the initial diagnostic workup of CRS. Echocardiography provides information on the structure and function of heart, and renal ultrasound is useful in differentiating between acute and chronic kidney disease and excluding certain causes of acute kidney injury such as obstructive uropathy. In this paper we overview the basic concepts of echocardiogram and renal ultrasound and will discuss the clinical utility of these imaging techniques in the management of cardiorenal syndromes. We will also discuss the role of other imaging modalities currently in clinical use such as computerized tomography and magnetic resonance imaging as well as novel techniques such as contrast-enhanced ultrasound imaging.

scholarly journals Plasma Lipopolysaccharide Concentrations in Cardiorenal Syndrome Type 1

2019 ◽  
Vol 9 (5) ◽  
pp. 308-315
Author(s):  
Grazia Maria Virzì ◽  
Andrea Breglia ◽  
Ghada Ankawi ◽  
Chiara Bolin ◽  
Massimo de Cal ◽  
...  
Keyword(s):  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Syndrome Type ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Significant Difference ◽  
Renal Markers ◽  
Neutrophil Gelatinase ◽  
Time Of Admission

Background: Cardiorenal syndrome (CRS) type 1 is characterized by a rapid worsening of cardiac function that leads to acute kidney injury (AKI). This study evaluated the role of lipopolysaccharide (LPS) in the development of AKI in patients with acute heart failure (AHF) and its relationship with renal parameters, to enable a better comprehension of the pathophysiology of CRS type 1. Methods: We enrolled 32 AHF patients, 15 of whom were classified as having CRS type 1. Eight of these 15 exhibited AKI at the time of admission (caused by AHF) and the other 7 developed AKI during their stay in hospital (in the first 48 h). We evaluated the plasmatic LPS concentrations as well as conventional (serum creatinine [sCr] and urea) and unconventional (neutrophil gelatinase-associated lipocalin [NGAL] and cystatin C) renal markers. Results: LPS levels were significantly higher in the CRS type 1 patients. No significant difference in LPS level was found in patients who were admitted with AKI and those developed AKI in hospital, but there was a tendency towards a higher level of LPS in CRS type 1 patients admitted with AKI. The LPS concentrations at admission were similar in CRS type 1 survivors (n = 12) and nonsurvivors (n = 3) (p = 0.22). We observed a positive correlation between LPS level and NGAL, Scr at admission and peak Scr during hospitalization and urea at admission. Conclusion: CRS type 1 patients present with an increased level of LPS and there is a direct correlation between LPS and renal parameters. This pilot research is the first study to explore the premise of LPS as novel pathophysiological factor in CRS type 1.

scholarly journals Toll-like receptors and damage-associated molecular patterns: novel links between inflammation and hypertension

2014 ◽  
Vol 306 (2) ◽  
pp. H184-H196 ◽  
Author(s):  
Cameron G. McCarthy ◽  
Styliani Goulopoulou ◽  
Camilla F. Wenceslau ◽  
Kathryn Spitler ◽  
Takayuki Matsumoto ◽  
...  
Keyword(s):  
Immune System ◽  
Innate Immune System ◽  
Cell Injury ◽  
Receptor Activation ◽  
Innate Immune ◽  
Immune System Activation ◽  
System Activation ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns

Low-grade systemic inflammation is a common manifestation of hypertension; however, the exact mechanisms that initiate this pathophysiological response, thereby contributing to further increases in blood pressure, are not well understood. Aberrant vascular inflammation and reactivity via activation of the innate immune system may be the first step in the pathogenesis of hypertension. One of the functions of the innate immune system is to recognize and respond to danger. Danger signals can arise from not only pathogenic stimuli but also endogenous molecules released following cell injury and/or death [damage-associated molecular patterns (DAMPs)]. In the short-term, activation of the innate immune system is beneficial in the vasculature by providing cytoprotective mechanisms and facilitating tissue repair following injury or infection. However, sustained or excessive immune system activation, such as in autoimmune diseases, may be deleterious and can lead to maladaptive, irreversible changes to vascular structure and function. An initial source of DAMPs that enter the circulation to activate the innate immune system could arise from modest elevations in peripheral vascular resistance. These stimuli could subsequently lead to ischemic- or pressure-induced events aggravating further cell injury and/or death, providing more DAMPs for innate immune system activation. This review will address and critically evaluate the current literature on the role of the innate immune system in hypertension pathogenesis. The role of Toll-like receptor activation on somatic cells of the vasculature in response to the release of DAMPs and the consequences of this activation on inflammation, vasoreactivity, and vascular remodeling will be specifically discussed.

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