scholarly journals Acute Kidney Injury in Heart Failure Revisited—The Ameliorating Impact of “Decongestive Diuresis” on Renal Dysfunction in Type 1 Acute Cardiorenal Syndrome: Accelerated Rising Pro B Naturetic Peptide Is a Predictor of Good Renal Prognosis

2017 ◽  
Vol 6 (9) ◽  
pp. 82 ◽  
Author(s):  
Macaulay Onuigbo ◽  
Nneoma Agbasi ◽  
Mohan Sengodan ◽  
Karen Rosario
2019 ◽  
Vol 9 (1) ◽  
pp. 5-22 ◽  
Author(s):  
E. V. Reznik ◽  
I. G. Nikitin

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.


Nephron ◽  
2020 ◽  
Vol 144 (12) ◽  
pp. 629-633 ◽  
Author(s):  
Yoshio Funahashi ◽  
Sheuli Chowdhury ◽  
Mahaba B. Eiwaz ◽  
Michael P. Hutchens

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.


Critical Care ◽  
2014 ◽  
Vol 18 (Suppl 1) ◽  
pp. P364
Author(s):  
W Vandenberghe ◽  
S Gevaert ◽  
H Peperstraete ◽  
I Herck ◽  
J Decruyenaere ◽  
...  

Author(s):  
Dinna N. Cruz ◽  
Anna Giuliani ◽  
Claudio Ronco

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.


2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Hao Phan Thai ◽  
Bao Hoang Bui ◽  
Tien Hoang Anh ◽  
Minh Huynh Van

Background. The presence of acute kidney injury in the setting of acute heart failure (AHF) or acute decompensated heart failure (ADHF) is a very common occurrence and was termed cardiorenal syndrome 1 (CRS1). Neutrophil gelatinase-associated lipocalin (NGAL) in the blood and urine is one of the earliest biomarkers of acute kidney injury due to ischemia or renal toxicity. This study was aimed to evaluate the diagnostic efficacy of plasma NGAL in the diagnosis of CRS1. Methods. There were 139 patients with AHF or ADHF in the department of Cardiovascular Resuscitation and Interventional Cardiology at Ho Chi Minh City 115 People Hospital from September 2018 to March 2019. This was a prospective cohort study. Results. There were 48 cases (rate 34.5%) with CRS1, mean age was 66.12 ± 15.77 and men accounted for 50.4%. There were no significant differences of vital signs at admission, diagnosis, and EF-based heart failure between CRS1 and non-CRS1 groups. The urea, creatinine on first day (creatinine D1) and third day (creatinine D3), NT-proBNP, and NGAL levels were higher in the CRS1 group than the non-CRS1 group, p < 0.05 . The optimal cutoff plasma NGAL for diagnosing CRS1 was >353.23 ng/ml, area under curve (AUC) 0.732 (95% CI 0.65–0.80, p < 0.001 ), sensitivity 74.47%, specificity 68.48%, positive predictive value 54.7%, and negative predictive value 84%. Multivariable logistic regression analysis eGFRCKDEPID1 remained the strongest independent predictor of CRS1. Building the optimal regression model (without eGFRCKDEPID1) by the BMA (Bayesian model average) method with two variables NGAL and Creatinine D1, we had the equation: odds ratio = ey while y = −2.39 + 0.0037 × NGAL + 0.17 × Creatinine D1. The nomogram (without eGFRCKDEPID1) was designed to predict the likelihood of CRS1 with AUC 0.79. Conclusions. The combination of plasma NGAL and creatinine D1 on the first day at admission had a high accuracy of predictive model for CRS1.


2010 ◽  
Vol 31 (22) ◽  
pp. 2791-2798 ◽  
Author(s):  
J. P. E. Lassus ◽  
M. S. Nieminen ◽  
K. Peuhkurinen ◽  
K. Pulkki ◽  
K. Siirila-Waris ◽  
...  

2016 ◽  
Vol 7 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Jun Zhang ◽  
Mohammad Kazem Fallahzadeh ◽  
Peter A. McCullough

Background: Although there are some animal models for biomarkers of contrast-induced acute kidney injury (CI-AKI), for cardiorenal syndrome (CRS) and for acute renal failure, the interplay between CI-AKI and CRS has yet to be evaluated. Insight into the pathogenesis of CRS is urgently needed from animal models in order to foster the discovery and implementation of novel biomarkers for this disease. Specially designed animal models for type 1 and 3 CRS, particularly CI-AKI, have not yet emerged. Summary: We hypothesize that the aging male spontaneously hypertensive rat (SHR) is likely to be a suitable model. The SHR model is able to mimic risk factors for preclinical CRS that appears in the clinical setting, specifically hypertension, age, preexisting damage and dysfunction of the heart and kidney, endothelial dysfunction, increased level of reactive oxygen species, decreased level and bioavailability of nitric oxide (NO), impairment of the L-arginine-NO pathway, and insulin resistance. In the SHR, CI-AKI results in a different profile of AKI biomarkers than is seen with preexisting chronic kidney injury. Key Messages: The SHR model can be used to evaluate the interaction between CI-AKI and CRS type 1 and 3 and to verify neutrophil gelatinase-associated lipocalin (NGAL) as a reliable CI-AKI biomarker for clinical application. Further research is warranted with a large number of aging male SHRs to prove NGAL as a sensitive, specific, highly predictive, early biomarker for CI-AKI.


2017 ◽  
Vol 312 (4) ◽  
pp. F629-F639 ◽  
Author(s):  
Mizuko Ikeda ◽  
Rumie Wakasaki ◽  
Katie J. Schenning ◽  
Thomas Swide ◽  
Jeong Heon Lee ◽  
...  

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.


2015 ◽  
Vol 6 (2) ◽  
pp. 116-128 ◽  
Author(s):  
Wim Vandenberghe ◽  
Sofie Gevaert ◽  
John A. Kellum ◽  
Sean M. Bagshaw ◽  
Harlinde Peperstraete ◽  
...  

Background: We evaluated the epidemiology and outcome of acute kidney injury (AKI) in patients with cardiorenal syndrome type 1 (CRS-1) and its subgroups: acute heart failure (AHF), acute coronary syndrome (ACS) and after cardiac surgery (CS). Summary: We performed a systematic review and meta-analysis. CRS-1 was defined by AKI (based on RIFLE, AKIN and KDIGO), worsening renal failure (WRF) and renal replacement therapy (RRT). We investigated the three most common clinical causes of CRS-1: AHF, ACS and CS. Out of 332 potential papers, 64 were eligible - with AKI used in 41 studies, WRF in 25 and RRT in 20. The occurrence rate of CRS-1, defined by AKI, WRF and RRT, was 25.4, 22.4 and 2.6%, respectively. AHF patients had a higher occurrence rate of CRS-1 compared to ACS and CS patients (AKI: 47.4 vs. 14.9 vs. 22.1%), but RRT was evenly distributed among the types of acute cardiac disease. AKI was associated with an increased mortality rate (risk ratio = 5.14, 95% CI 3.81-6.94; 24 studies and 35,227 patients), a longer length of stay in the intensive care unit [LOSICU] (median duration = 1.37 days, 95% CI 0.41-2.33; 9 studies and 10,758 patients) and a longer LOS in hospital [LOShosp] (median duration = 3.94 days, 95% CI 1.74-6.15; 8 studies and 35,227 patients). Increasing AKI severity was associated with worse outcomes. The impact of CRS-1 defined by AKI on mortality was greatest in CS patients. RRT had an even greater impact compared to AKI (mortality risk ratio = 9.2, median duration of LOSICU = 10.6 days and that of LOShosp = 20.2 days). Key Messages: Of all included patients, almost one quarter developed AKI and approximately 3% needed RRT. AHF patients experienced the highest occurrence rate of AKI, but the impact on mortality was greatest in CS patients.


2020 ◽  
Author(s):  
Shu-Min Lin ◽  
Chih-Hsiang Chang ◽  
Ting-Yu Lin ◽  
Allen Chung-Cheng Huang ◽  
Chiung-Hung Lin ◽  
...  

Abstract Objective: Cardiorenal syndrome type I (CRS I) is defined as the development of acute kidney injury (AKI) following acute decompensated heart failure (ADHF). Note that the clinical significance of endothelial markers in ADHF-associated AKI has yet to be clarified. This study investigated the biological processes linking ADHF and AKI to determine whether plasma markers of endothelial injury and activation could serve as predictors for AKI in patients with ADHF. Methods: The study prospectively recruited 125 consecutive patients admitted to a coronary critical unit due to ADHF. Patients with and without AKI were compared in terms of plasma levels of soluble thrombomodulin (sTM), angiopoietin (Ang)-1 and 2, and baseline characteristics. Results: Among the study population, 14 (11.2%) patients developed CRS within 7 days after admission. The hemoglobin levels (11.4 ± 2.1 vs. 13.3 ± 2.2 g/dL, p =0.003) and baseline eGFR (65.7 ± 34.5 vs. 85.5 ± 35.0 mL/minute/1.73m2, p = 0.048) of patients with CRS were lower than those of patients without CRS. Patients with CRS also presented elevated plasma levels of BNP (1,797.2 ± 1,649.1 vs. 687.8 ± 976.6 pg/mL, p = 0.008), Ang-2 (7,524.7 ± 8,485.5 vs. 3,325.3 ± 4,7409 pg/mL, p = 0.006), and sTM (7,763.8 ± 3,803.7 vs. 4,661.3 ± 1,896.8 ng/mL, p < 0.001) compared to patients without CRS. Areas under the ROC curves (AUROC) revealed that Ang-2 and TM plasma levels had significantly discriminative powers pertaining to the development of CRS (0.704, 95% CI 0.55-0.859, p =0.013; and 0.789, 95% CI 0.675-0.903, p <0.001, respectively). Conclusion: These biomarkers suggest a novel avenue for kidney injury in the context of ADHF and indicate that baseline biomarker profiles could potential be used to identify individuals at risk of developing AKI.


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