View clinical trials related to Cardio-Renal Syndrome.
Filter by:The prevalence of renal dysfunction after implantation of the artificial heart is high. The infusion of exogenous B-type natriuretic peptide (BNP) after implantation of the total artificial heart (TAH) improves renal function in a sustained manner. The renal protective and hormone-modulating effects of nesiritide may be enhanced with ventriculectomy compared to heart failure surgery that leaves the native myocardium intact. The goal of this project is to determine the renal protective effects of nesiritide after implantation of a mechanical device.
To advance our understanding of the mechanisms of human cardiorenal syndrome with emphasis upon the interaction of diuretic therapy and the renal-angiotensin-aldosterone -system and cGMP pathway. The belief is that the chronic AT1 receptor blockade in subjects with compensated CHF and renal dysfunction will improve renal function with increased sodium excretion, glomerular filtration rate and effective renal plasma flow and renal function reserve as compared to the response of placebo-treated subjects.
The purpose of this study is to evaluate the ability of a non-invasive monitor that measures how much fluid is in the body as well as various blood tests for their ability to predict worsening kidney function in patients with heart failure.
Rationale: Heart Failure (HF) elevated prevalence in Brasil and the world; 20-30% AHF patients develop CardioRenal Syndrome (CRS) type 1; Worsening Renal Failure (WRF) is a prognostic marker of mortality in Acute HF;NGAL is a novel biomarker of Acute Kidney Injury released in 2 hours, and addressed in several different clinical scenarios(contrast injury, cardiopulmonary bypass, critical illness. Hypothesis: Admission NGAL predicts CRS in AHF patients admitted to the Emergency Room (ER). Primary goal: To evaluate the diagnostic accuracy and the best cutoff value of urinary NGAL to predict the development of CRS type 1 in patients admitted to the Emergency Room. Secondary goals: 1- To evaluate the prognostic impact of NGAL on in-hospital adverse outcomes (length of hospitalization, death, institution of renal replacement therapy, use of vasoactive drugs, mechanical ventilation).2- Evaluate the prognostic impact of NGAL in adverse outcomes in 30 days, 60 days and 6 months (death, rehospitalization, institution of renal replacement therapy).3- Identify clinical and hemodynamic characteristics of Acute HF that can influence the evolutionary behavior of NGAL levels in 48 hours.4- Identify the association of drugs commonly used for HF management, which might influence the evolutionary behavior of NGAL levels in 48 hours.5-Assess the impact of NGAL results in clinical decision making. Methods: Observational, prospective, blinded study. Population: Acute HF patients admitted to the ER of Hospital Pró Cardiaco and Hospital Antonio Pedro - Universidade Federal Fluminense. Statistics: Convenience Sample size (n=180); determination of best cut-off: ROC analysis; Predictive performance of the cut-off: sensibility, specificity, likelihood ratio, predictive value, accuracy; Identification of variables to predict CRS: logistic regression and square-Qui test; Correlations analysis of normally distributed variables: Pearson's linear correlation test; Mean values for normally distributed variables: Mann-Wittney test; Significance on p<0,05; Intra-assay variation analysis. Study chronogram: Recruitment: 12 months; Results analysis and conclusions: 60 days; Manuscript preparation for paper submission: 30 days.
We hypothesize that paricalcitol and calcitriol in dose-dependent manner are effective for the management of chronic allograft dysfunction (CAD), protection and repair of kidney and heart, management of chronic renocardiac syndrome (CRS). We assume that paricalcitol can have some advantages if compare with calcitriol or cholecalciferol due to absence of calcemic and phosphatemic complications alongside with great beneficial potential.
Admission BNP was a useful marker for diagnosing and predicting type IV cardio-renal syndrome type IV in patients with chronic kidney disease admitted to the ICU for acute heart failure in a retrospective study. Therefore, we aim to prospectively investigate the utility of serum BNP in evaluating the treatment adequacy and predicting future cardiac events in patients with type IV CRS.
The purpose of this study is to determine whether in patients with acute decompensated congestive heart failure and the cardiorenal syndrome, i.e. a state in which therapy directed to improve symptoms is limited by further worsening renal function, fluid removal by ultrafiltration is superior to different pharmacological approaches in acutely relieving congestion and preventing further deterioration in renal function and whether it results in longer admission-free survival 90 days after enrolment
Heart failure (HF) is a major public health problem, which affects about 5 million Americans.HF is when the heart muscle does not pump as much blood as the body needs. As a result of this,the body has difficulties in keeping an optimal fluid status. The fluid status of the body is regulated by both the heart and the kidneys. Due to the strong interaction between the heart and the kidneys, heart failure can result in a slight decreased kidney function as well. It is known that people who primarily suffer from chronic kidney disease (CKD) have a higher risk of developing arterial calcifications. Calcification of the arteries is caused by deposits of calcium within the walls of the blood vessels. Calcifications of the arteries may result in a loss of elasticity of the blood vessels. Recent research studies have shown that people with CKD have stiffer blood vessels which in these people, is associated with a higher chance of developing cardiovascular diseases. However, it is not known whether a decrease in kidney function in people with HF results in arterial calcification as well. In addition, it is not known whether this is also associated with a higher risk of developing cardiovascular diseases (diseases of the heart and blood vessels.) We are asking you to take part in this study because you have HF combined with some decrease in your kidney function. The purpose of this study is to see whether people with HF and a decrease in kidney function do have a higher chance of developing arterial calcifications. We will do this by comparing the results of the following; 1) several blood tests, 2) pictures taken of your heart by echocardiogram and computed tomography (CT) scan, and 3) measurements of the elasticity of your arteries. All of these tests are routinely used in clinical care. However, there have not been any research studies that have compared these results to see how they relate to arterial calcification in people with HF who have a decrease in kidney function. We also want to see whether people with HF and a decreased kidney function are at a higher risk of developing cardiovascular diseases. This study is being performed at Massachusetts General Hospital (MGH), in Boston Massachusetts. We expect to enroll a total of 150 subjects at MGH.
Heart failure is a serious condition in which the heart's ability to pump blood through the body is impaired, often making a person feel weak or fatigued. When a person's condition worsens to the point of hospitalization, that person is said to have acute decompensated heart failure (ADHF). Abnormal kidney function in association with cardiac distress, known as cardiorenal syndrome, is a common complication of heart failure and causes further medical problems and need for hospitalization. While there are various effective treatments for heart failure, more research is needed to determine the best treatment for targeting both ADHF and cardiorenal syndrome. This study will compare the safety and effectiveness of ultrafiltration versus standard medical drug therapy in improving renal function and relieving fluid buildup in people hospitalized with ADHF and cardiorenal syndrome.
Erythropoietin (EPO) treatment in patients with the severe cardiorenal syndrome increases cardiac performance and decreases progression of renal failure by dampening the main driving forces of the cardiorenal syndrome in part via non-erythropoietic pathways. I. Does EPO administration to patients with the severe cardiorenal syndrome increase cardiac performance and decrease progression of renal disease? II. Does EPO treatment affect the main driving forces of the cardiorenal connection, that is, dampen the activated renin-angiotensin system (RAS), attenuate increased reactive oxygen species (ROS), normalize increased sympathetic activity, and decrease inflammation? III. Does EPO treatment positively affect the cell function of patients with the cardiorenal syndrome: 1. are gene expression signatures of leukocytes positively influenced by EPO treatment, 2. does EPO shift the Jak/STAT pathway to a less pro-inflammatory profile in monocytes, and 3. are function and number of endothelial progenitor cells (EPCs) affected by treatment with EPO in the cardiorenal syndrome? IV. Can the direct actions of EPO be differentiated from the effects on hemoglobin levels?