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 Acute kidney injury in cardiorenal syndrome type 1: a meta-analysis

Critical Care ◽  
2014 ◽  
Vol 18 (Suppl 1) ◽  
pp. P364
Author(s):  
W Vandenberghe ◽  
S Gevaert ◽  
H Peperstraete ◽  
I Herck ◽  
J Decruyenaere ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Meta Analysis ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Syndrome Type

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.

Acute kidney injury

2021 ◽  
pp. 895-911
Author(s):  
Sofie A Gevaert ◽  
Eric Hoste ◽  
John A Kellum
Keyword(s):  
Intensive Care Unit ◽  
Acute Kidney Injury ◽  
Cardiac Output ◽  
Intensive Care ◽  
Renal Replacement Therapy ◽  
Replacement Therapy ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Cardiac Care ◽  
Syndrome Type

Acute kidney injury is a serious condition, occurring in up to two-thirds of intensive care unit patients, and 8.8-55% of patients with acute cardiac conditions. Renal replacement therapy is used in about 1.5-15% of intensive care unit patients. The term cardiorenal syndrome refers to combined heart and kidney failure; three types of acute cardiorenal syndrome have been described: acute cardiorenal syndrome or cardiorenal syndrome type 1, acute renocardiac syndrome or cardiorenal syndrome type 3, and acute cardiorenal syndrome type 5 (cardiac and renal injury secondary to a third entity such as sepsis). Acute kidney injury replaced the previously used term 'acute renal failure' and comprises the entire spectrum of the disease, from small changes in function to the requirement of renal replacement therapy. Not only failure, but also minor and less severe decreases, in kidney function are of clinical significance both in the short and long-term. The most recent definition for acute kidney injury is proposed by the Kidney Disease: Improving Global Outcomes clinical practice guidelines workgroup. This definition is a modification of the RIFLE and AKIN definitions and staging criteria, and it stages patients according to changes in the urine output and serum creatinine (see Tables 68.1 and 68.2). Acute kidney injury is a heterogeneous syndrome with different and multiple aetiologies, often with several insults occurring in the same individual. The underlying processes include nephrotoxicity, and neurohormonal, haemodynamic, autoimmune, and inflammatory abnormalities. The most frequent cause for acute kidney injury in intensive cardiac care patients are low cardiac output with an impaired kidney perfusion (cardiogenic shock) and/or a marked increase in venous pressure (acute decompensated heart failure). Predictors for acute kidney injury in these patients include: baseline renal dysfunction, diabetes, anaemia, and hypertension, as well as the administration of high doses of diuretics. In the intensive cardiac care unit, attention must be paid to the prevention of acute kidney injury: monitoring of high-risk patients, prompt resuscitation, maintenance of an adequate mean arterial pressure, cardiac output, and intravascular volume (avoidance of both fluid overload and hypovolaemia), as well as the avoidance or protection against nephrotoxic agents. The treatment of acute kidney injury focuses on the treatment of the underlying aetiology, supportive care, and avoiding further injury from nephrotoxic agents. More specific therapies have not yet demonstrated efficacy. Renal replacement therapy is indicated in life-threatening changes in fluid, electrolyte, and acid-base balance, but there are also arguments for more early initiation.

Acute kidney injury in heart failure

2015 ◽  
Author(s):  
Dinna N. Cruz ◽  
Anna Giuliani ◽  
Claudio Ronco
Keyword(s):  
Heart Failure ◽  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Volume Overload ◽  
Bioelectrical Impedance ◽  
Impedance Analysis ◽  
Cardiorenal Syndrome ◽  
Renal Diseases ◽  
Consensus Definition ◽  
Short And Long Term

Acute kidney injury (AKI) occurring during heart failure (HF) has been labelled cardiorenal syndrome (CRS) type 1. CRS is defined as a group of ‘disorders of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the other’. This consensus definition was proposed by the Acute Dialysis Quality Initiative, with the aim to standardize those disorders where cardiac and renal diseases coexist. Five subtypes have been proposed, according to which organ is affected first (cardiac vs renal) and whether the dysfunction is acute or chronic. Another subtype which includes systemic conditions leading to both heart and kidney dysfunction is also described.The term ‘worsening renal function’ has been regularly used to describe the acute and/or subacute changes that occur in the kidneys following HF. However, the AKI classification according to the current consensus definition better represents the entire spectrum of AKI in the setting of HF.The pathophysiology of heart–kidney interaction is complex and still poorly understood. Factors beyond the classic haemodynamic mechanisms appear to be involved: neurohormonal activation, venous congestion, and inflammation have all been implicated.Diuretics are still a cornerstone in the management of HF. Intravenous administration by bolus or continuous infusion appears to be equally efficacious. Biomarkers and bioelectrical impedance analysis can be helpful in estimating the real volume overload and may be useful to predict and avoid AKI. The role of ultrafiltration remains controversial, and it is currently recommended only for diuretic-resistant patients as it has not been associated with better outcomes. The occurrence of AKI during HF is associated with substantially greater short- and long-term mortality.

scholarly journals MP298BIOMARKERS IN EARLY DIAGNOSTIC OF ACUTE KIDNEY INJURY IN PATIENTS WITH ACUTE CARDIORENAL SYNDROME

2017 ◽  
Vol 32 (suppl_3) ◽  
pp. iii535-iii536
Author(s):  
Kurmanov Maxim ◽  
Efremovtseva Maria ◽  
Avdoshina Svetlana ◽  
Villevalde Svetlana ◽  
Kobalava Zhanna
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Early Diagnostic

scholarly journals CARDIORENAL SYNDROME IN PATIENTS WITH CHRONIC HEART FAILURE AS A STAGE OF THE CARDIORENAL CONTINUUM (PART I): DEFINITION, CLASSIFICATION, PATHOGENESIS, DIAGNOSIS, EPIDEMIOLOGY

2019 ◽  
Vol 9 (1) ◽  
pp. 5-22 ◽  
Author(s):  
E. V. Reznik ◽  
I. G. Nikitin
Keyword(s):  
Heart Failure ◽  
Acute Kidney Injury ◽  
Chronic Heart Failure ◽  
Impaired Renal Function ◽  
Prognostic Value ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Syndrome Type ◽  
Patients With Heart Failure

The combination of heart failure and renal failure is called cardiorenal syndrome. It is a stage of the cardiorenal continuum and, possibly, a small link of the cardiorenal-cerebral-metabolic axis. Despite the fact that the phrase “cardiorenal syndrome” and its five types have become a part of the medical lexicon, many aspects of this problem are still not clear. Cardiorenal syndrome can be diagnosed in 32-90.3% of patients with heart failure. Cardiorenal syndrome type 1 or 2 develops in most cases of heart failure: cardiorenal syndrome presents with the development ofchronic kidney disease in patients with chronic heart failure and acute kidney injury in patients with acute heart failure. Impaired renal function has an unfavorable prognostic value. It leads to an increase in the mortality of patients with heart failure. It is necessary to timely diagnose the presence of cardiorenal syndrome and take into account its presence when managing patients with heart failure. Further researches are needed on ways toprevent the development and prevent the progression of kidney damage in patients with heart failure, to which the efforts of the multidisciplinary team should be directed. The first part of this review examines the currently definition, classification, pathogenesis, epidemiology and prognosis of cardiorenal syndrome in patients with heart failure.

scholarly journals Enhancing acute kidney injury regeneration by promoting cellular dedifferentiation in zebrafish

2018 ◽  
Author(s):  
Lauren Brilli Skvarca ◽  
Hwa In Han ◽  
Eugenel B. Espiritu ◽  
Maria A. Missinato ◽  
Elizabeth R. Rochon ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Injury ◽  
Cardiac Injury ◽  
Kidney Injury ◽  
Acute Injury ◽  
Cardiomyocyte Proliferation ◽  
Deacetylase Inhibitor ◽  
Summary Statement ◽  
Renal Tubular ◽  
Kidney Injury Molecule 1

ABSTRACTAcute kidney injury (AKI) is a serious disorder for which there is no approved pharmaceutical treatment. Following injury, native nephrons display limited regenerative capabilities, relying on the dedifferentiation and proliferation of renal tubular epithelial cells (RTECs) that survive the insult. Previously, we identified 4-(phenylthio)butanoic acid (PTBA), a histone deacetylase inhibitor (HDI) that enhances renal recovery and showed that PTBA treatment increased RTEC proliferation and reduced renal fibrosis. Here, we investigated the regenerative mechanisms of PTBA in zebrafish models of larval renal injury and adult cardiac injury. With respect to renal injury, we showed that delivery of PTBA using an esterified prodrug (UPHD25) increases the reactivation of the renal progenitor gene Pax2a, enhances dedifferentiation of RTECs, reduces Kidney injury molecule-1 expression, and lowers the number of infiltrating macrophages. Further, we find that the effects of PTBA on RTEC proliferation depend upon retinoic acid signaling and demonstrate the therapeutic properties of PTBA are not restricted to the kidney but also increase cardiomyocyte proliferation and decrease fibrosis following cardiac injury in adult zebrafish. These studies provide key mechanistic insights into how PTBA enhances tissue repair in models of acute injury and lay the groundwork for translating this novel HDI into the clinic.SUMMARY STATEMENTMortality associated with acute kidney injury (AKI) is in part due to limited treatments available to ameliorate kidney injury. We identified a compound that enhances AKI recovery by promoting cellular dedifferentiation.

scholarly journals Kidney injury associated with antitumor therapy: focus on the adverse events of modern immuno-oncological drugs

2021 ◽  
Vol 93 (6) ◽  
pp. 649-660
Author(s):  
Elena S. Kamyshova ◽  
Irina N. Bobkova ◽  
Marina I. Sekacheva
Keyword(s):  
Adverse Events ◽  
Cytotoxic T Lymphocyte ◽  
Checkpoint Inhibitors ◽  
Kidney Injury ◽  
Inhibitory Effect ◽  
Immune System Activation ◽  
Programmed Death ◽  
Programmed Death Protein 1 ◽  
System Activation ◽  
New Generation

Immune checkpoint inhibitors (ICIs), including cytotoxic T-lymphocyte associated antigen 4 (CTLA-4) and programmed death protein 1 (PD-1) or its ligand (PD-L1), are a new generation of immuno-oncological drugs that to date have demonstrated efficacy in a number of malignancies. The mechanism of ICT inhibitors action consist in the potentiation of the immune response by eliminating the tumor cells inhibitory effect on the T-lymphocytes activation. However, excessive immune system activation can cause the development of a special class of immune-related adverse events (irAEs) involved a wide variety of organs and systems, including the kidneys. Despite the fact that immuno-mediated kidney injury caused by ICI therapy develops quite rarely, it can be serious and determine the patient's prognosis, which necessitates early diagnosis and timely start of treatment. In this regard, awareness of the manifestations of ICI-associated renal irAEs is particularly relevant not only for oncologists and for nephrologists, but for doctors of other specialties. In this review, we elucidated the main variants of immuno-mediated kidney injury caused by ICI therapy, discussed possible predictors and mechanisms of their development, and considers the general principles of diagnosis and management of patients according to the severity of irAEs.

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