scholarly journals The Role of Congestion in Cardiorenal Syndrome Type 2: New Pathophysiological Insights into an Experimental Model of Heart Failure

2015 ◽  
Vol 6 (1) ◽  
pp. 61-72 ◽  
Author(s):  
Annalisa Angelini ◽  
Chiara Castellani ◽  
Grazia Maria Virzì ◽  
Marny Fedrigo ◽  
Gaetano Thiene ◽  
...  
Keyword(s):  
Heart Failure ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Heart Tissue ◽  
Heart Cell ◽  
Tubular Damage ◽  
Syndrome Type ◽  
Neutrophil Gelatinase Associated Lipocalin

Background: In cardiorenal syndrome type 2 (CRS2), the role of systemic congestion in heart failure (HF) is still obscure. We studied a model of CRS2 [monocrotaline (MCT)-treated rats] secondary to pulmonary hypertension and right ventricular (RV) failure in order to evaluate the contribution of prevalent congestion to the development of kidney injury. Methods: Ten animals were treated with MCT for 4 weeks until they developed HF. Eleven animals were taken as controls. Signs of hypertrophy and dilatation of the right ventricle demonstrated the occurrence of HF. Brain natriuretic peptide (BNP), serum creatinine (sCreatinine), both kidney and heart neutrophil gelatinase-associated lipocalin (NGAL), matrix metallopeptidase 9 (MMP9), serum cytokines as well as kidney and heart cell death, as assessed by TUNEL, were studied. Results: Rats with HF showed higher BNP levels [chronic HF (CHF) 4.8 ± 0.5 ng/ml; controls 1.5 ± 0.2 ng/ml; p < 0.0001], marked RV hypertrophy and dilatation (RV mass/RV volume: CHF 1.46 ± 0.31, controls 2.41 ± 0.81; p < 0.01) as well as pleural and peritoneal effusions. A significant increase in proinflammatory cytokines and sCreatinine was observed (CHF 3.06 ± 1.3 pg/ml vs. controls 0.54 ± 0.23 pg/ml; p = 0.04). Serum (CHF 562.7 ± 93.34 ng/ml vs. controls 245.3 ± 58.19 ng/ml; p = 0.02) as well as renal and heart tissue NGAL levels [CHF 70,680 ± 4,337 arbitrary units (AU) vs. controls 32,120 ± 4,961 AU; p = 0.001] rose significantly, and they were found to be complexed with MMP9 in CHF rats. A higher number of kidney TUNEL-positive tubular cells was also detected (CHF 114.01 ± 45.93 vs. controls 16.36 ± 11.60 cells/mm2; p = 0.0004). Conclusion: In this model of CHF with prevalent congestion, kidney injury is characterized by tubular damage and systemic inflammation. The upregulated NGAL complexed with MMP9 perpetuates the vicious circle of kidney/heart damage by enhancing the enzymatic activity of MMP9 with extracellular matrix degradation, worsening heart remodeling.

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 Reduced Albuminuria and Potassemia Indicate Early Renal Repair Processes after Resynchronization Therapy in Cardiorenal Syndrome Type 2

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Agnieszka Gala-Błądzińska ◽  
Janusz Romanek ◽  
Danuta Mazur ◽  
Tomasz Stepek ◽  
Marcin Braun ◽  
...  
Keyword(s):  
New York ◽  
Renal Function ◽  
Nyha Class ◽  
Kidney Injury ◽  
Heart Association ◽  
Cardiorenal Syndrome ◽  
Syndrome Type ◽  
Class Iii ◽  
Resynchronization Therapy

Background. Patients with chronic cardiorenal syndrome type 2 (T2-CRS) who qualify for resynchronization therapy (CRT) are exposed perioperatively to potentially nephrotoxic factors including contrast agents and blood loss. Methods. The objective of this prospective interventional study was to assess the effects of CRT on renal function in patients with T2-CRS within the first 48 hours following implantation. Initially, 76 patients (15% female; aged 69 ± 9.56 years) with heart failure (New York Heart Association classes II–IV), ejection fraction ≤ 35%, and QRS > 130 ms were included in the study. During CRT implantation, a nonionic contrast agent (72.2 ± 44.9 mL) was administered. Prior to and 48 hours following implantation, renal function was evaluated using the following serum biomarkers: creatinine (sCr), estimated glomerular filtration rate (using the Chronic Kidney Disease Epidemiology Collaboration equation [eGFRCKD-EPI]), and the electrolyte and urine biomarkers albumin (uAlb), albumin/creatinine ratio (UACR), and neutrophil gelatinase-associated lipocalin (uNGAL). Results. Before CRT, patients classified as NYHA class III or IV had higher uNGAL levels in comparison to uNGAL levels after CRT (43.63 ± 60.02 versus 16.63 ± 18.19; p=0.041). After CRT implantation, uAlb, UACR, and potassium levels were reduced (p<0.05), and uNGAL, sCr, and eGFRCKD-EPI were unchanged. The contrast medium volume did not correlate with the test biomarkers (p>0.05). Conclusions. In patients with T2-CRS, uNGAL is a biomarker of kidney injury that correlates with the NYHA classes. A stable uNGAL value before and after CRT implantation confirms the lack of risk of contrast-induced nephropathy. Reduced albuminuria and blood potassium are biomarkers of improving T2-CRS in the early post-CRT period.

scholarly journals Peritoneal Dialysis for Chronic Congestive Heart Failure

2015 ◽  
Vol 40 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Karlien François ◽  
Claudio Ronco ◽  
Joanne M. Bargman
Keyword(s):  
Heart Failure ◽  
Peritoneal Dialysis ◽  
Clinical Symptoms ◽  
Positive Impact ◽  
Cardiorenal Syndrome ◽  
Current Evidence ◽  
Chronic Congestive Heart Failure ◽  
Syndrome Type ◽  
Fluid Removal

Maladaptive responses between a failing heart and the kidneys ultimately lead to permanent chronic kidney disease, referred to as cardiorenal syndrome type 2. In this narrative review, we discuss the pathophysiological pathways in the progression of cardiorenal failure and review the current evidence on peritoneal dialysis as a treatment strategy in cardiorenal syndrome type 2. A patient with heart failure can present with clinical symptoms related to venous congestion even in the absence of end-stage renal disease. Diuretics remain the cornerstone for the treatment of fluid overload related to heart failure. However, with chronic use, diuretic resistance can supervene. When medical therapy is no longer able to relieve congestive symptoms, ultrafiltration might be needed. Patients with heart failure tolerate well the gentle rate of fluid removal through peritoneal dialysis. Recent publications suggest a positive impact of starting peritoneal dialysis in patients with cardiorenal syndrome type 2 on the hospitalisation rate, functional status and quality of life.

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 The Role of Cell-Free Plasma DNA in Patients with Cardiorenal Syndrome Type 1

2021 ◽  
pp. 1-8
Author(s):  
Grazia Maria Virzì ◽  
Anna Clementi ◽  
Sabrina Milan Manani ◽  
Chiara Castellani ◽  
Giovanni Giorgio Battaglia ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Syndrome Type ◽  
Plasma Dna ◽  
Apoptosis And Inflammation ◽  
Factor Α ◽  
Clinical Conditions

<b><i>Background:</i></b> Recent research highlighted the potential role of circulating cell-free DNA (cfDNA), resulted by apoptosis or cell necrosis, as a prognostic marker in the setting of different clinical conditions. Cardiorenal syndrome type 1 (CRS type 1) is characterized by a rapid worsening of cardiac function leading to acute kidney injury (AKI). Apoptosis of renal epithelial cells is proposed as a mechanism involved in CRS type 1. In this study, we investigated cfDNA levels in patients with acute heart failure (AHF) and CRS type 1 and the possible correlation between cfDNA levels and inflammatory and apoptotic parameters. <b><i>Methods:</i></b> We enrolled 17 AHF patients and 15 CRS type 1 who exhibited AKI at the time of admission (caused by AHF) or developed AKI during the first 48 h from admission. cfDNA was extracted from plasma and quantified by real-time polymerase chain reaction. Plasma levels of NGAL, tumor necrosis factor-α, interleukin (IL)-6, IL-18, and caspase-3 were measured. <b><i>Results:</i></b> We observed significantly higher levels of cfDNA in patients with CRS type 1 than patients with AHF. Caspase-3, IL-6, IL-18, and NGAL levels resulted significantly increased in patients with CRS type 1. Moreover, a positive correlation between cfDNA levels and caspase-3 levels was found, as well as between cfDNA levels and IL-6 and renal parameters. <b><i>Conclusion:</i></b> Our study explores the premise of cfDNA as a marker for apoptosis and inflammation in CRS type 1 patients. cfDNA could potentially serve as an index for noninvasive monitoring of tissue damage and apoptosis in patients with AKI induced by AHF.

scholarly journals Acute Cardiorenal Syndrome: Models and Heart-Kidney Connectors

Nephron ◽  
2020 ◽  
Vol 144 (12) ◽  
pp. 629-633 ◽  
Author(s):  
Yoshio Funahashi ◽  
Sheuli Chowdhury ◽  
Mahaba B. Eiwaz ◽  
Michael P. Hutchens
Keyword(s):  
Heart Failure ◽  
Cell Culture ◽  
Acute Kidney Injury ◽  
Renal Function ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Syndrome Type ◽  
Culture Models ◽  
Cell Culture Models

Cardiorenal syndrome type 1 (CRS-1) is an acute kidney injury (AKI) due to acute worsening of cardiac function. More than 20% of patients with acute heart failure develop AKI, and AKI predicts poor outcome. Although a number of potential pathways have been suggested as heart-kidney connectors which might drive the syndrome, there are significant barriers to investigation, such as a paucity of animal models, a lack of specific biomarkers, and an inconsistent temporal and causal relationship between changes in cardiac flow and development of renal dysfunction. Thus, mechanisms of heart-kidney interaction are still unclear, and there is no specific or effective therapy for CRS-1. This review, therefore, focuses on mitigating these challenges in the investigation of CRS-1. We review the available models and focus on mechanistic insights gained from those models. In particular, we focus on non-flow and endocrine mediators of CRS-1 such as heart-derived messengers which alter renal function and which may represent targetable pathways in this syndrome. As precise connectors of heart-kidney interaction remain unclear, the establishment of animal and relevant cell-culture models and further investigation are required.

scholarly journals The role of kidney injury molecule-1 in predicting cardiorenal syndrome type 1 after diuretic treatment

2019 ◽  
Vol 4 (1) ◽  
pp. 208-214
Author(s):  
Adem Atici ◽  
Samim Emet ◽  
Ilkim Deniz Toprak ◽  
Ramazan Cakmak ◽  
Murat Akarsu ◽  
...  
Keyword(s):  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Syndrome Type ◽  
Diuretic Treatment ◽  
Kidney Injury Molecule 1

Biomarkers of renal and hepatic failure

2021 ◽  
pp. 434-444
Author(s):  
Mario Plebani ◽  
Monica Maria Mion ◽  
Martina Zaninotto
Keyword(s):  
Kidney Disease ◽  
Early Identification ◽  
Age Groups ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Disease Epidemiology ◽  
Additional Information ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Paediatric Age

In the last years, major advances have been achieved in the understanding of the molecular and pathophysiological mechanisms which underlie the complex interactions between the heart and the kidney, as well as between the heart and the liver. According to these new insights, innovative biomarkers have been proposed for better evaluating and monitoring patients affected by cardiovascular diseases. In addition, some biomarkers should be used as risk factors and for an early identification and treatment of these severe diseases. This chapter reviews the most important biomarkers for evaluating the 'cardiorenal syndrome', in particular, the measurement of serum creatinine and its use for calculating the glomerular filtration rate which, with the new and more efficient equation, namely Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI), still remains the most widely used biomarker. The role of newer biomarkers will be explored. The measurement of cystatin C, representing additional information, particularly in paediatric age groups and in the early phase of kidney disease, plays an increasing role. Neutrophil gelatinase-associated lipocalin (NGAL) is a recently developed but largely used biomarker for the early diagnosis of acute kidney injury, while the well-known albumin/creatinine ratio has been re-evaluated as a simple and useful tool for an early identification of kidney disease. Regarding liver diseases, a growing body of evidence demonstrates the usefulness of non-invasive makers of hepatic fibrosis that may avoid the need for a liver biopsy in most patients. A promising field of research is represented by the role of non-alcoholic fatty liver disease in the pathogenesis of cardiovascular disease.

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