View clinical trials related to Renal Insufficiency, Chronic.
Filter by:To understand how AKI (Acute Kidney Injury) leads to chronic kidney disease so therapies can be found to alter the progression of events thereby significantly impacting the long-term outcomes of children who develop AKI.
This is a randomized, dose-ranging, efficacy and tolerability study in chronic kidney disease patients with hyperphosphatemia on hemodialysis. Patient participation in the study is approximately 10 weeks in duration.
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?
The purpose of this study is to learn more about why most patients with early stages of kidney disease have high blood pressure. We know the body produces natural substances that cause blood vessels to open wider to carry more blood when needed. An example is during exercise. Other natural substances cause blood vessels to get smaller and slow down blood flow when needed. An example is when people are cold. The balance between these substances is important. People with kidney disease and high blood pressure do not have the normal balance of these substances. This study will include 3 groups of people, people with normal blood pressure, people with high blood pressure and people with kidney disease. - Subjects will have a screening physical examination, including an ECG and laboratory tests - Subjects with high blood pressure may not take their regular blood pressure medication for 3 weeks prior to the inpatient GCRC study - Subjects will be given intra-arterial medications that will cause changes in the blood vessels during the in-patient study. The study will then compare the responses of the three groups. A GFR test will be done to confirm the renal function of the group with chronic kidney disease. These studies will provide insight into the mechanisms of the pathogenesis of enhanced α1 vasoreactivity in subjects with progressive renal disease. This will lay the groundwork for new strategies in the treatment and prevention of vascular disease among the rapidly growing group of individuals with CKD.
Asymmetric dimethylarginine, ADMA, in plasma, is significantly elevated in patients with renal disease and associated with cardiovascular morbidity and mortality. We found that whole blood (WB) possesses the metabolic pathways required for both the generation and elimination of ADMA and we have developed ex vivo methods to assess the WB accumulation of ADMA in humans. The over-arching hypothesis is that dysregulation of ADMA metabolic pathways leads to greater ADMA whole blood content and greater capacity to accumulate ADMA, which 1) is not reflected by plasma levels and 2) is a better predictor of cardiovascular outcome than plasma levels in end-stage renal disease (ESRD). The following specific aims will be pursued to characterize whole blood ADMA in ESRD: 1. Compare and contrast baseline free plasma ADMA and total whole blood (free plus protein-incorporated) ADMA concentrations in ESRD patients, matched hypertensive controls and a normal population. 2. Determine the capacity of WB to accumulate (the net balance of generation and elimination) ADMA in ESRD patients, matched hypertensive controls and a normal population. We will use state-of-the-art, high performance liquid chromatography techniques to measure ADMA levels in plasma and whole blood. Samples for ADMA measurements will be obtained from subjects with end-stage renal disease immediately before their dialysis treatments. Samples will also be obtained from volunteers without kidney disease. This group will be matched to the end-stage renal volunteers by age, gender and ethnicity. These volunteers will also be matched for the presence of hypertension and diabetes. The third group will consist of a normal population to measure the normal levels of ADMA and compare to the other two groups. There is growing evidence to support a pathological role of ADMA in humans. These experiments will enhance our understanding of how ADMA is processed in the human body and how it is associated with kidney disease. Potentially, these results will lay the groundwork for new insights into the link between ADMA and the high cardiovascular disease burden in patients with kidney disease.
The purpose of this study is to evaluate the effects of cinacalcet (cinacalcet HCl or Sensipar®/Mimpara®) on cardiovascular events and death in chronic kidney disease (CKD) patients with secondary hyperparathyroidism (HPT) who are receiving dialysis.
The prevention of contrast-mediated nephropathy (CMN), which accounts for considerable morbidity and mortality, remains a vexing problem. Contrast induced renal vasoconstriction is believed to play a pivotal role in the CMN mechanism. The aim of this study is to examine the efficacy of the prostacyclin analogue iloprost (dose 1ng/kg/min) in preventing CMN in high-risk patients undergoing a coronary procedure.
This study, done in collaboration with Johns Hopkins University School of Public Health in Baltimore, Maryland, will examine the role of genes in the development of atherosclerotic cardiovascular disease (CVD) in patients undergoing kidney dialysis. The rate of illness and death from CVD among patients on dialysis is extraordinarily high, accounting for about 50 percent of deaths. Blood levels of inflammatory markers are elevated in these patients, strongly predicting illness and death from CVD. The discovery of gene variants related to the inflammatory process in atherosclerotic CVD may lead to better medical treatments and improved survival in patients with end-stage kidney disease. Participants of John's Hopkins University's CHOICE (Choices for Healthy Outcomes in Caring for End-Stage Renal Disease) program are included in this study. Blood samples previously collected from these patients will be analyzed in the laboratory for genes that might be associated with the inflammatory process and atherogenesis.
The purpose of this study is to assess disability in anemic patients over the age of 65 who have kidney disease and are receiving weekly PROCRIT® (Epoetin Alfa, a glycoprotein that stimulates red blood cell production).
The primary goal of the trial was to evaluate whether the optimal antiproteinuric doses of benazepril (an ACE inhibitor) or losartan (an ARB), as compared with their conventional doses, can safely improve the long-term renal outcome in nondiabetic patients with proteinuria and chronic renal insufficiency. The second aim was to compare the long-term renal protection between benazepril and losartan at similar clinical setting.