Cardiorenal syndromes

McCullough, Peter A.; Ahmad, Aftab

doi:10.4330/wjc.v3.i1.1

Cited by 30 publications

(34 citation statements)

References 49 publications

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“…It is also known that the presence of CKD increases severity, worsens the response to treatment, and is associated with poor cardiac and renal outcomes in cardiorenal syndrome. 4,5 The renin-angiotensin system (RAS) has a critical role in the development of cardiovascular and renal disease in a clinical setting. It has been reported that the role of RAS in congestive heart failure (CHF) and CKD is complex owing to involvement of multiple peptides and receptors.…”

mentioning

confidence: 99%

Impaired post-infarction cardiac remodeling in chronic kidney disease is due to excessive renin release

Ogawa

Suzuki²,

Takayama³

et al. 2012

Laboratory Investigation

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The complex pathophysiological interactions between heart and kidney diseases are collectively known as cardiorenal syndrome. The renin-angiotensin system (RAS) may have a pivotal role in the development of cardiorenal syndrome. The aim of this study was to elucidate the RAS activity responsible for adverse post-infarction remodeling and prognosis in mice with renal failure. To establish the type IV cardiorenal syndrome model, 5/6 nephrectomy (NTX) was performed in a surgical procedure, followed by the induction of myocardial ischemia (MI) by a coronary artery ligation 4 weeks later. NTX and MI resulted in deteriorated left ventricular remodeling and RAS activation, which was improved by an aliskiren that appeared to be independent of renal function and blood pressure (BP). Moreover, MI induced in renin and angiotensinogen double-transgenic (Tg) mice showed comparable effects to MI plus NTX mice, including advanced ventricular remodeling and enhancement of RAS, oxidative stress, and monocytes chemoattractant protein (MCP)-1. Aliskiren suppressed these changes in the MI-induced Tg mice. In in vitro study, Nox2 expression was elevated by the stimulation of plasma from NTX mice in isolated neonatal cardiomyocytes. However, Nox2 upregulation was negated when we administered plasma from aliskiren-treated-NTX mice or isolated cardiomyocytes from AT1-deficient mice. Primary mononuclear cells also showed an upregulation in the expression of Nox2 and MCP-1 by stimulation with plasma from NTX mice. Our data suggest that renal disorder results in ventricular dysfunction and deteriorates remodeling after MI through excessive RAS activation. Moreover, renin inhibition improved the changes caused by cardiorenal syndrome. It is well known that there is a complex relationship between cardiovascular and renal diseases. In fact, end-stage renal disease or decreased estimated glomerular filtration rate correlates with an increased risk of cardiovascular diseases. 1 This clinical condition is known as cardiorenal syndrome. In addition, the presence of chronic kidney disease (CKD) is a relatively frequent complication in patients with advanced heart failure and left ventricular (LV) dysfunction. Its presence is associated with a worse prognosis following cardiovascular diseases. 2 Although preventing this condition includes identification and amelioration of the precipitating factors and connections, 3 the pathophysiological mechanisms of the syndrome remain to be elucidated. It is also known that the presence of CKD increases severity, worsens the response to treatment, and is associated with poor cardiac and renal outcomes in cardiorenal syndrome. 4,5 The renin-angiotensin system (RAS) has a critical role in the development of cardiovascular and renal disease in a clinical setting. It has been reported that the role of RAS in congestive heart failure (CHF) and CKD is complex owing to involvement of multiple peptides and receptors. Increased RAS activity results in the development of CHF by stimulation of cardiac hypertrophy, apopt...

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mentioning

confidence: 99%

Impaired post-infarction cardiac remodeling in chronic kidney disease is due to excessive renin release

Ogawa

Suzuki²,

Takayama³

et al. 2012

Laboratory Investigation

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“…Decreased cardiac output also activates the renin-angiotensin-aldosterone system and the sympathetic nervous system, which in turn causes congestion and constriction in afferent arterioles. These results in further decreases in renal perfusion pressure (34). Theoretically, the above-mentioned pathophysiological mechanism is valid; however, recent studies suggest different mechanisms.…”

Section: Discussionmentioning

confidence: 93%

“…Deterioration of this close interrelation between these two organ systems is known as "cardio-renal syndrome," and studies in HF have clarified the pathophysiological mechanisms behind this syndrome. It has been thought that renal dysfunction in HF is attributable to low cardiac output, which consequently causes reduction in blood flow and renal perfusion pressure (9,34). Decreased cardiac output also activates the renin-angiotensin-aldosterone system and the sympathetic nervous system, which in turn causes congestion and constriction in afferent arterioles.…”

Section: Discussionmentioning

confidence: 99%

Elevated mean pulmonary artery pressure in patients with mild-to-moderate mitral stenosis: a useful predictor of worsening renal functions?

Zorkun

Amioglu²,

Bektaşoğlu³

et al. 2013

Anadolu Kardiyol Derg

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Elevated mean pulmonary artery pressure in patients with mild-tomoderate mitral stenosis: a useful predictor of worsening renal functions?Hafif ve orta derecede mitral darlığı bulunan hastalarda artmış ortalama pulmoner arter basıncı bozulan böbrek fonksiyonlarını göstermede yararlı bir belirteç olabilir mi?Address ABSTRACTObjective: Renal dysfunction commonly accompanies the course of cardiac disorders and strongly associates with increased morbidity and mortality. Elevated central venous pressure is related to worsening renal function in patients with heart failure. However, predictors of worsening renal function in mitral stenosis-whose pathophysiologic process is similar to heart failure with regard to right heart dysfunction-are unknown. This study aimed to evaluate whether clinical and echocardiographic parameters might predict worsening renal function in patients with mild-to-moderate mitral stenosis. Methods:The current study has a prospective cohort design. Sixty consecutive patients (9 male, 51 female, mean age 50±13 years) with mildto-moderate mitral stenosis were followed up for 34±13 months (range 1-60) and their renal functions were monitored. Worsening renal function was defined as a decline in glomerular filtration rate of ≥ 20% on follow-up. In order to presence or absence of worsening renal functions, study patients divided into two groups. Statistical analysis was performed using the Chi-square, Independent samples t / Mann-Whitney U tests, univariate and multivariate Cox proportional hazards analyses, receiver operating characteristic (ROC) and Kaplan-Meier curve analyses.Results: Worsening renal function was observed in 14 patients (23%). In univariate analysis, male gender, mean pulmonary artery pressure (mPAP), peak tricuspid regurgitation velocity, systolic pulmonary artery pressure, digitalis and antiplatelet usage, right atrial size, and TEI index were determined to be predictors of worsening renal function. In a multivariate Cox proportional hazards model, mPAP (HR=1.136, 95% CI: 1.058-1.220, p<0.001) and male gender (HR=4.110, 95% CI: 1.812-9.322, p=0.001) were associated with increased risk of worsening renal function during the follow-up period. In ROC curve analysis, the optimal cut-off value of mPAP to predict worsening renal function was measured as more than 21 mmHg, with 78.6% sensitivity and 58.7% specificity (AUC 0.725, 95% CI 0.595-0.838). According to the Kaplan-Meier curve, a significant difference was found between those who had mPAP of >21 mmHg, and those who did not have, in terms of worsening renal function (p=0.006), and the difference between the groups increased after 30 months of follow-up. Conclusion: Elevated mean pulmonary artery pressure at the time of initial evaluation, in patients with mild-to-moderate mitral stenosis, might help to predict worsening renal function. (Anadolu Kardiyol Derg 2013; 13: 457-64) Key words: Mean pulmonary artery pressure, mitral stenosis, worsening renal function, Cox proportional regression analysis, survival Original Investigati...

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“…Siderocalin has been shown to be elevated in patients with ADHF predicting the need for renal replacement therapies and or death [72]. It is unknown at present whether or not NGAL could serve as a therapeutic target either via infusion of recombinant protein or molecular mimicry with the intent of reducing oxidative stress results in cell dysfunction, accelerated apoptosis, and cell death, and fibrosis [73]. One such molecular approach, using an NGAL-like agent to bind available tissue catalytic iron is with the mild iron chelator oral deferiprone, is an attractive therapeutic target from a conceptual standpoint.…”

Section: Non-hemodynamic Factorsmentioning

confidence: 99%

Type 4 Cardiorenal Syndrome: Myocardial Dysfunction, Fibrosis, and Heart Failure in Patients with Chronic Kidney Disease

Narala¹

2012

J Clinic Experiment Cardiol

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Cardiorenal syndromes

Cited by 30 publications

References 49 publications

Impaired post-infarction cardiac remodeling in chronic kidney disease is due to excessive renin release

Impaired post-infarction cardiac remodeling in chronic kidney disease is due to excessive renin release

Elevated mean pulmonary artery pressure in patients with mild-to-moderate mitral stenosis: a useful predictor of worsening renal functions?

Type 4 Cardiorenal Syndrome: Myocardial Dysfunction, Fibrosis, and Heart Failure in Patients with Chronic Kidney Disease

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