scholarly journals Insights of Worsening Renal Function in Type 1 Cardiorenal Syndrome: From the Pathogenesis, Biomarkers to Treatment

2021 ◽  
Vol 8 ◽  
Author(s):  
Kang Fu ◽  
Yue Hu ◽  
Hui Zhang ◽  
Chen Wang ◽  
Zongwei Lin ◽  
...  
Keyword(s):  
Renal Function ◽  
Poor Prognosis ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Therapeutic Strategies ◽  
Diagnostic Efficiency ◽  
Independent Predictive Factor ◽  
Worsening Renal Function ◽  
Renal Safety

Type-1 cardiorenal syndrome refers to acute kidney injury induced by acute worsening cardiac function. Worsening renal function is a strong and independent predictive factor for poor prognosis. Currently, several problems of the type-1 cardiorenal syndrome have not been fully elucidated. The pathogenesis mechanism of renal dysfunction is unclear. Besides, the diagnostic efficiency, sensitivity, and specificity of the existing biomarkers are doubtful. Furthermore, the renal safety of the therapeutic strategies for acute heart failure (AHF) is still ambiguous. Based on these issues, we systematically summarized and depicted the research actualities and predicaments of the pathogenesis, diagnostic markers, and therapeutic strategies of worsening renal function in type-1 cardiorenal syndrome.

scholarly journals Determination of renal function and injury using near-infrared fluorimetry in experimental cardiorenal syndrome

2017 ◽  
Vol 312 (4) ◽  
pp. F629-F639 ◽  
Author(s):  
Mizuko Ikeda ◽  
Rumie Wakasaki ◽  
Katie J. Schenning ◽  
Thomas Swide ◽  
Jeong Heon Lee ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Function ◽  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Filtration Rate ◽  
Near Infrared ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Syndrome Type

Cardiorenal syndrome type 1 causes acute kidney injury but is poorly understood; animal models and diagnostic aids are lacking. Robust noninvasive measurements of glomerular filtration rate are required for injury models and clinical use. Several have been described but are untested in translational models and suffer from biologic interference. We developed a mouse model of cardiorenal syndrome and tested the novel near-infrared fluorophore ZW800-1 to assess renal and cardiac function. We performed murine cardiac arrest and cardiopulmonary resuscitation followed by transthoracic echocardiography, 2 and 24 h later. Transcutaneous fluorescence of ZW800-1 bolus dispersion and clearance was assessed with whole animal imaging and compared with glomerular filtration rate (GFR; inulin clearance), tubular cell death (using unbiased stereology), and serum creatinine. Correlation, Bland-Altman, and polar analyses were used to compare GFR with ZW800-1 clearance. Cardiac arrest and cardiopulmonary resuscitation caused reversible cardiac failure, halving fractional shortening of the left ventricle ( n = 12, P = 0.03). Acute kidney injury resulted with near-zero GFR and sixfold increase in serum creatinine 24 h later ( n = 16, P < 0.01). ZW800-1 biodistribution and clearance were exclusively renal. ZW800-1 t1/2 and clearance correlated with GFR ( r = 0.92, n = 31, P < 0.0001). ZW800-1 fluorescence was reduced in cardiac arrest, and cardiopulmonary resuscitation-treated mice compared with sham animals 810 s after injection ( P < 0.01) and bolus time-dispersion curves demonstrated that ZW800-1 fluorescence dispersion correlated with left ventricular function ( r = 0.74, P < 0.01). Cardiac arrest and cardiopulmonary resuscitation lead to experimental cardiorenal syndrome type 1. ZW800-1, a small near-infrared fluorophore being developed for clinical intraoperative imaging, is favorable for evaluating cardiac and renal function noninvasively.

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.

Impact of Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Blockers on Renal Function in Type 1 Cardiorenal Syndrome

2021 ◽  
pp. 107424842110226
Author(s):  
Daniel T. Ilges ◽  
Morgan L. Dermody ◽  
Caitlyn Blankenship ◽  
Valerie Mansfield ◽  
Joseph S. Van Tuyl
Keyword(s):  
Renal Function ◽  
Angiotensin Converting Enzyme ◽  
Enzyme Inhibitor ◽  
Angiotensin Receptor Blockers ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Converting Enzyme ◽  
Angiotensin Receptor ◽  
Converting Enzyme Inhibitors

Introduction: Angiotensin-converting enzyme inhibitor (ACE-I) and angiotensin receptor blocker (ARB) discontinuation during acute heart failure (AHF) is associated with increased mortality following hospitalization. Although the etiology of acute kidney injury (AKI) in type 1 cardiorenal syndrome (CRS) has been linked to renal venous congestion, ACE-I/ARB withdrawal (AW) theoretically promotes renal function recovery. ACE-I/ARBs are dose-reduced or withheld in approximately half of patients with CRS, but the subsequent impact on renal function remains largely uninvestigated. This study compared AW to ACE-I/ARB continuation (AC) during CRS. Methods: This was a retrospective, single-center chart review. Patients aged 18-89 years admitted from April 2018 to August 2019 with AHF and AKI were identified using discharge ICD-10 codes. All patients were treated with an ACE-I/ARB before admission. Key exclusion criteria included shock, pregnancy, and end-stage renal disease. The primary endpoint was change in serum creatinine (SCr) from admission through 72 hours. Data were analyzed utilizing chi-square and Mann-Whitney U tests with SPSS software. Results: A total of 111 admissions were included. AW occurred in 68 patients upon admission. AW patients presented with a higher blood urea nitrogen ( P = 0.034), higher SCr ( P = 0.021), and lower ejection fraction ( P = 0.04). Median SCr change from admission to 72 hours did not differ between groups (AW −0.1 mg/dL vs AC 0.0 mg/dL, P = 0.05). There was no difference in SCr reduction ≥0.3 mg/dL at 72 hours, 30-day readmissions, or ACE-I/ARB prescription at discharge. Conclusions: In patients with type 1 CRS, AW was not associated with improved renal function at 72 hours. A larger sample size is necessary to confirm these results.

scholarly journals POS-011 THE EFFECT IN RENAL FUNCTION AND VASCULAR DECONGESTION IN TYPE 1 CARDIORENAL SYNDROME TREATED WITH TWO STRATEGIES OF DIURETICS, A RANDOMIZED CLINICAL TRIAL

2021 ◽  
Vol 6 (4) ◽  
pp. S5
Author(s):  
J. Chavez Iñiguez ◽  
A. De la Torre-Quiroga ◽  
A. Aranda G de Quevedo ◽  
A. Romero-Muñoz ◽  
J. Gómez-Fregoso ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Renal Function ◽  
Randomized Clinical Trial ◽  
Cardiorenal Syndrome

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 Oxidative Stress: Dual Pathway Induction in Cardiorenal Syndrome Type 1 Pathogenesis

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Grazia Maria Virzì ◽  
Anna Clementi ◽  
Massimo de Cal ◽  
Alessandra Brocca ◽  
Sonya Day ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Syndrome Type ◽  
Copper Zinc Superoxide Dismutase ◽  
Stress Markers ◽  
Oxidative Stress Pathway ◽  
Significant Augmentation ◽  
Copper Zinc

Cardiorenal Syndrome Type 1 (Type 1) is a specific condition which is characterized by a rapid worsening of cardiac function leading to acute kidney injury (AKI). Even though its pathophysiology is complex and not still completely understood, oxidative stress seems to play a pivotal role. In this study, we examined the putative role of oxidative stress in the pathogenesis of CRS Type 1. Twenty-three patients with acute heart failure (AHF) were included in the study. Subsequently, 11 patients who developed AKI due to AHF were classified as CRS Type 1. Quantitative determinations for IL-6, myeloperoxidase (MPO), nitric oxide (NO), copper/zinc superoxide dismutase (Cu/ZnSOD), and endogenous peroxidase activity (EPA) were performed. CRS Type 1 patients displayed significant augmentation in circulating ROS and RNS, as well as expression of IL-6. Quantitative analysis of all oxidative stress markers showed significantly lower oxidative stress levels in controls and AHF compared to CRS Type 1 patients (P<0.05). This pilot study demonstrates the significantly heightened presence of dual oxidative stress pathway induction in CRS Type 1 compared to AHF patients. Our findings indicate that oxidative stress is a potential therapeutic target, as it promotes inflammation by ROS/RNS-linked pathogenesis.

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 Poor prognosis of heart failure patients with in‐hospital worsening renal function and elevated BNP at discharge

2020 ◽  
Vol 7 (5) ◽  
pp. 2912-2921
Author(s):  
Toshitaka Okabe ◽  
Tadayuki Yakushiji ◽  
Takehiko Kido ◽  
Taro Kimura ◽  
Yu Asukai ◽  
...  
Keyword(s):  
Heart Failure ◽  
Renal Function ◽  
Poor Prognosis ◽  
Heart Failure Patients ◽  
Worsening Renal Function

scholarly journals Determinants of Monocyte Apoptosis in Cardiorenal Syndrome Type 1

2018 ◽  
Vol 8 (3) ◽  
pp. 208-216 ◽  
Author(s):  
Andrea Breglia ◽  
Grazia Maria Virzì ◽  
Silvia Pastori ◽  
Alessandra Brocca ◽  
Massimo de Cal ◽  
...  
Keyword(s):  
Gene Expression ◽  
Caspase 3 ◽  
Kidney Injury ◽  
Annexin V ◽  
Cardiorenal Syndrome ◽  
Pathophysiological Mechanism ◽  
Syndrome Type ◽  
Caspase 9 ◽  
Apoptotic Pathway

Background: Cardiorenal syndrome type 1 (CRS type 1) is characterized by a rapid worsening of cardiac function leading to acute kidney injury (AKI). Its pathophysiology is complex and not completely understood. In this study, we examined the role of apoptosis and the caspase pathways involved. Material and Methods: We enrolled 40 acute heart failure (AHF) patients, 11 of whom developed AKI characterizing CRS type 1. We exposed the human cell line U937 to plasma from the CRS type 1 and AHF groups and then we evaluated apoptotic activity by annexin-V evaluation, determination of caspase-3, -8 and -9 levels, and BAX, BAD, and FAS gene expression. Results: We observed significant upregulation of apoptosis in monocytes exposed to CRS type 1 plasma compared to AHF, with increased levels of caspase-3 (p < 0.01), caspase-9 (p < 0.01), and caspase-8 (p < 0.03) showing activation of both intrinsic and extrinsic pathways. Furthermore, monocytes exposed to CRS type 1 plasma had increased gene expression of BAX and BAD (intrinsic pathways) (p = 0.010 for both). Furthermore, strong significant correlations between the caspase-9 levels and BAD and BAX gene expression were observed (Spearman ρ = – 0.76, p = 0.011, and ρ = – 0.72, p = 0.011). Conclusion: CRS type 1 induces dual apoptotic pathway activation in monocytes; the two pathways converged on caspase-3. Many factors may induce activation of both intrinsic and extrinsic apoptotic pathways in CRS type 1 patients, such as upregulation of proinflammatory cytokines and hypoxia/ischemia. Further investigations are necessary to corroborate the present findings, and to better understand the pathophysiological mechanism and consequent therapeutic and prognostic implications for CRS type 1.

Sign in / Sign up

Export Citation Format

Share Document