Active clinical trials for "Kidney Diseases"

Background: A low amount of red blood cells in the blood of patients with limited kidney function is a well known problem. Besides the lack of substances in the blood like iron or erythropoietin the shortened survival of red blood cells leads to the low red blood cell count. Red blood cells of patients on kidney replacement therapy (dialysis) die earlier than those of healthy persons. They live only about 70 days compared to 120 days in healthy humans. Today little is known about the causes for the shorter survival of the red blood cells in patients on dialysis. Because inflammation leads to a shorter life of the red blood cells in people suffering from several diseases leading to inflammation we would like to learn about the role of inflammation in the shortened life of red blood cells of dialysis patients. When red blood cells are dying the content is broken down to several substances. One of these substances is the gas carbon monoxide (CO). The carbon monoxide is exhaled with the breath. The more red blood cells die the more CO is exhaled. That's why we can calculate the lifespan of the red blood cells when we measure the amount of CO in breath at the same time as the red blood cell count in the blood. Aim of the study: We aim to learn about the influence of inflammation of on red blood cell survival in dialysis patients. To look for factors with effect on inflammation or red blood cell survival, for example type of dialysis access, medication or kind of dialysis treatment. Study procedures: Over the course of the 18 month study, 6 observational assessments will take place. If the patient experiences a situation with increased inflammation during the study period (for example any kind of infection or intervention) up to two more study visits will take place. Each study visit will include blood sampling, performed without the need for an extra needle stick, and a breath sampling in order to calculate the red blood survival and to measure markers for inflammation in the blood. The breath sample will be taken using the easy to use GaSampler device developed by a company called Quintron especially for medical breath sampling. In order to get a sample of air at the patient's home for calculation of carbon monoxide produced in the body we will ask the patients to take home an open empty plastic bottle before each study visit. The bottle should be kept overnight on a table or sideboard in the apartment. Before leaving home for hemodialysis or in clinic visit the patient will seal the plastic bottle with the top, take it to the dialysis center and hand it to the research staff. Risks: The amount of the additional blood drawn is 30 ml; this is the amount 2 tablespoons, at each study visit. This does not harm the patient. The breath sampling does not imply any risk.

Proteinuria is not only a marker of chronic kidney disease (CKD) progression, but also a marker of cardiovascular disease and death. In previous studies, active vitamin D deficiency is associated with cardiovascular risk factors such as albuminuria, diabetes mellitus, and lower glomerular filtration rate (GFR). And calcitriol was shown to have a preventive effect in progressive glomerular damage in a renal ablation model. Calcitriol, an active form of vitamin D (1,25-dihydroxyvitamin-D3), is commonly used for the treatment of secondary hyperparathyroidism in patients with advanced chronic kidney diseases. Therefore, the objective of this study is to evaluate the anti-proteinuric effect of calcitriol in non-diabetic kidney disease patients. They will be treated with calcitriol and placebo for 24 weeks and observed for 24 weeks after treatment. Proteinuria, renal function, serum and urinary inflammatory markers, and adverse event will be monitored.

Diabetes is the most common metabolic disease of childhood. Vascular disease is a leading complication of diabetes, and attempts to maintain close glycemic control do not prevent the sequelae that claim the lives and quality of life of millions of diabetics each year. Up to forty percent of patients with diabetes mellitus ultimately develop diabetic nephropathy, the most common cause of end-stage renal disease requiring dialysis in the US. Flavonoid-rich diets are a promising intervention to prevent the endothelial dysfunction that apparently leads to this deadly complication. The mechanisms are still unclear but probably involve nitric oxide synthesis. The investigators hypothesize that early maintenance of the integrity of renal vasculature will significantly improve the lifelong prognosis for patients with diabetes. Flavonoids with anti-inflammatory and antioxidant activities could be used to protect endothelial function, and together with good glycemic control, prevent the development and progression of nephropathy. The investigators aims are to: compare endothelial function by studying reactive hyperemia, nitric oxide, and proinflammatory factors in adolescents (12-21 years old) with diabetes versus healthy sex- and age-matched control subjects. identify early markers in urine for vascular endothelial injury. examine the effects of flavonoids on vascular function, urine nitric oxide, and proinflammatory factors in patients with diabetes mellitus.

Objective: To examine the effects of three commonly applied treatments of disordered phosphorus homeostasis on biochemical markers and vascular characteristics in patients with moderate and advanced non-dialysis dependent chronic kidney disease.

The objective of this study was to observe the safety of paricalcitol utilization in pediatric participants (ages 0 to 16 years old) being treated for secondary hyperparathyroidism (SHPT). Participants were to be followed for a minimum of 3 months and up to approximately 36 months to monitor the incidence of hypercalcemia (high calcium levels in blood).

Contrast induced nephropathy (CIN) is a term applied to acute renal failure associated with intravascular injection of iodinated contrast agents typically used for cardiac angiography. CIN occurs in about 15% of those who have had cardiac angiography, with dialysis required by about 0.5% of cases. The development of CIN is associated with other adverse outcomes including major adverse cardiovascular events (MACE) and death. The mechanism underlying the association with MACE and death is unclear and it is largely unknown whether measures reducing the frequency or severity of CIN also reduce these associated adverse events. The cause of CIN in humans is not known, but many preventive therapies have been tested based on our understanding of the mechanism underlying CIN from animal models. Despite multiple studies, no one drug or therapy has been proven to consistently prevent CIN at this time. Prophylactic fluid therapy is uniformly recommended as a component of preventive approaches for CIN. However, the optimal type, dose and duration of fluid therapy remain unclear. Existing studies suggest a role for isotonic saline[3] or bicarbonate[4]. Initial use of hypotonic fluid followed by isotonic fluid might allow a more rapid and sustained increase in tubular fluid flow by suppression of ADH. This should assist in reducing tubular fluid viscosity and the potential for injury by contrast medium. The aim of this research program is to design and test strategies for the prevention of CIN in patients undergoing elective cardiac angiography or percutaneous coronary intervention (PCI). The primary purpose of this pilot study will be to determine the biological plausibility of using a hypotonic solution for CIN prophylaxis. Specific Objectives: Primary To compare the effects of two fluid prophylaxis strategies for CIN on urine output, urine pH, urine composition (urine metabolic profiling), a novel marker of renal injury (NGAL) and urine osmolality Secondary To assess the relative sensitivity of definitions of CIN based on changes in serum creatinine or cystatin C within 72 hours post contrast. To determine the feasibility of a future multicenter randomized trial of a hypotonic fluid prophylaxis strategy for the prevention of radiocontrast nephropathy.

Cyclosporin decreases proteinuria and improve renal function in patients with idiopathic membranous nephropathy, but has a risk of side effects such as nephrotoxicity. The investigators plan to the study to evaluate whether mycophenolate mofetil (MMF) could be a reasonable alternative with fewer side effect.

This is a multicenter, randomized, double-blind, placebo-controlled clinical trial to investigate the renoprotective efficacy of combined pentoxifylline (PTX) and angiotensin receptor blockers (valsartan), compared with placebo and valsartan in 700 patients with Chronic Kidney Disease (CKD) stages 3 and 4. The effect on cardiovascular comorbidity will also be observed. The observation period will be 3 years. The primary endpoints consists of doubling of serum creatinine, end stage renal disease (ESRD), and death from any cause. The secondary endpoints include changes of microalbuminuria or proteinuria, serum and urinary levels of TNF-a(tumor necrosis factor-alpha ), MCP-1(monocyte chemotactic protein), TGF-beta1(transforming growth factor ), collagens III (amino terminal peptide of procollagen III) and IV, and fibronectin, urinary N-acetyl-beta-glucosaminidase, as well as serum fibrinogen and high-sensitive CRP(C reactive protein), and development of heart failure, nonfatal myocardial infarction, and stroke or transient ischemic attack.

This study is design to compare two different strategies aiming to lessen the degree of the ongoing process of allograft injury either by removing tacrolimus from the maintenance immunosuppressive protocol or by reducing tacrolimus dose. The primary goal is to assess the change in renal function at 6 and 12 months after conversion using creatinine levels and calculated creatinine clearance. The study will include two groups: The study group of 30 patients and a matched control group with creatinine levels at similar range.

Arterial calcification within the coronaries and other vessels is greatly accelerated among patients with chronic or end-stage kidney disease. The mechanisms leading to increased calcification are unknown, but include hyperphosphatemia, hyperparathyroidism and altered vitamin D metabolism. Moreover, recent data demonstrates that circulating carboxy fragments of PTH (7-84) are physiologic antagonists of intact PTH (1-84) and may directly contribute to vascular calcification. Current PTH assays no not distinguish between intact and carboxy PTH fragments leading to an overestimation of intact PTH levels. Because second generation PTH assays detect both 1-84 and 7-84 PTH fragments, the use of vitamin D analogues to treat secondary hyperparathyroidism could lead to excessive suppression of 1-84 and a preponderance of carboxy PTH fragments. Moreover, increased administration of vitamin D analogues amy contribute to vascular calcifications. To investigate these questions, we plan to investigate the effect of managing new ESRD patients using conventional and third generation PTH assays on vitamin D administration and the development of coronary calcification. Hypothesis #1: Clinical management of secondary hyperparathyroidism in new hemodialysis patients using the Scantibodies 1-84/7-84 PTH ratio for one year will reduce the amount of Vitamin D administration resulting in reduced coronary calcification compared to patients in which PTH management is accomplished by conventional, second generation PTH assay.