View clinical trials related to Renal Insufficiency, Chronic.
Filter by:This study consists of a 4 week run-in period with a Ca based phosphate binder and 12 weeks treatment period by MCI-196 or placebo, (both on Ca based phosphate binder). During the treatment period, MCI-196 or placebo will be titrated every 3 weeks.
The primary objectives of this study are the following: 1. To test if the proportion of participants achieving a hemoglobin value greater than or equal to 10.0 g/dL at any time point after the first dose during the study is greater than 0.8 when administered de novo darbepoetin alfa once a week (QW) for treatment of anemia in pediatric patients with chronic kidney disease receiving and not receiving dialysis, and 2. To test if the proportion of participants achieving a hemoglobin value greater than or equal to 10.0 g/dL at any time point after the first dose during the study is greater than 0.8 when administered de novo darbepoetin alfa every 2 weeks (Q2W) for treatment of anemia in pediatric patients with chronic kidney disease receiving and not receiving dialysis.
An important subgroup of protein-bound toxins are generated as a result of protein fermentation in the colon. P-cresol is a fermentation metabolite of tyrosine. In renal failure, the colonic generation rate of p-cresol is markedly elevated. After absorption, the majority of p-cresol is conjugated to form p-cresyl sulphate. There is clear evidence, both in vitro and in vivo, that accumulation of conjugated fermentation metabolites is correlated with clinical important endpoints. Free p-cresol is an independent predictor for mortality in hemodialysis patients. Moreover, in renal failure patients, neither hemodialysis nor peritoneal dialysis is capable of normalising the clearly elevated serum concentrations of p-cresyl sulphate. Removal is at least partially diminished by the important protein binding of p-cresol. Besides adaptation of renal replacement therapies to improve removal of protein bound solutes, another approach is to lower the generation of uremic toxins. The mechanisms underlying colonic carbohydrate and protein fermentation, responsible for the generation of p-cresol, are only partially understood. On the one hand, the ratio of fermentable carbohydrates to proteins has been shown to be an important determinant of protein fermentation. On the other hand, changes in the colonic bacterial flora influence the generation of p-cresol in dogs and in healthy human individuals. The effect of antibiotic therapy on bacterial protein fermentation and thus on the generation of p-cresol is not known. A reanalysis of data abstracted from a recent longitudinal study in peritoneal dialysis (PD) patients suggests that antibiotic therapy may lower p-cresol levels substantially. The current study aims at confirming these data in a prospective manner.
This 2 arm study will compare 'time and motion' (provider time spent on anemia management) and effect on hemoglobin (Hb) levels, of methoxy polyethylene glycol-epoetin beta (Mircera) and epoetin alfa, in anemic patients with chronic kidney disease (CKD) on hemodialysis. Patients stable on intravenous (iv) epoetin alfa will be randomized either to receive standard of care therapy (epoetin alfa (iv) 3 times weekly), or to receive Mircera 120-360 micrograms (iv), monthly. After a titration period, average time spent on anemia treatment over a 3 month period will be evaluated. The anticipated time on study treatment is 3-12 months, and the target sample size is 100-500 individuals.
The ATIC study is a randomised, double- blind, placebo-controlled trial in which the effects of oxidative stress-lowering treatment on vascular function and structure are studied in patients with chronic non-diabetic renal failure who are free from manifest arterial occlusive disease. Participants in the trial were randomised to active treatment consisting of add-on therapy with pravastatin, vitamin E and homocysteine-lowering therapy, or to placebo. Subjects not using angiotensin converting enzyme inhibitors (ACE-inhibitors) or angiotensin receptor blockers (ARBs) at inclusion were put on ACE-inhibitors for at least two weeks before the baseline measurement and randomisation. Those who were on ARBs continued their ARBs. We excluded individuals with diabetes mellitus (ADA criteria), active vasculitis, nephrotic syndrome (>3gr/24hr urine protein), renal transplantation, fasting total cholesterol > 7 mmol/L, cholesterol-lowering therapy within three months prior to inclusion or known ischemic cardiac, cerebrovascular or peripheral arterial disease. Ninety-three patients (out of 118 eligible patients) took part in the study and written informed consent was obtained from all participants.
Although ionizing radiations have been proposed for the prevention of intimal hyperplasia in coronary and peripheral arteries, information is lacking on how irradiation may prevent neointimal smooth-muscle cell proliferation and restenosis on prosthetic haemodialysis vascular access. We will assess the preventive effect of one dose of radiations (14 Gy) administered transcutaneously one day after dilatation of stenosis on prosthetic haemodialysis vascular access in a randomized controlled trial with a standardized clinical and ultrasonographic one-year follow-up.
Patients with chronic kidney disease (CKD) and those with end-stage renal disease (ESRD) undergoing renal replacement therapies show elevated serum phosphate levels which predispose them to cardiovascular calcifications and high risks of death from cardiovascular diseases. However, in certain patients hyperphosphatemia is not related to dialysis insufficiency, excessive daily dietary phosphorus intake or high serum parathyroid hormone (PTH) levels, suggesting that other mechanisms could be involved. Transgenic mice lacking the klotho gene showed a phenotype which resembles that of dialyzed ESRD patients, in the sense that they have hyperphosphatemia, vascular calcifications, and a short lifespan. This study will analyze whether functional polymorphisms or variants in the human klotho gene are associated with hyperphosphatemia in these patients.
The purpose of this study was to evaluate the long term safety and tolerability of peginesatide for the maintenance of hemoglobin in participants with chronic kidney disease (CKD) who had received at least 24 weeks of peginesatide treatment in an earlier study.
The substantially increased cardiovascular morbidity and mortality rates in chronic kidney disease (CKD) patients cannot be sufficiently explained by traditional coronary risk factors. It is apparent that inflammation of the vessel wall plays an essential role in the pathophysiology of atherosclerosis, and the strong association between elevated inflammatory biomarkers and cardiovascular death further supports this mechanism. Approximately 50% of the mortality in this population of patients is attributable to cardiovascular disease. Insulin resistance is also a common problem in uremic patients. It has been shown that insulin resistance may contribute to atherosclerotic cardiovascular disease. An intriguing observation in CKD patients with advanced uremia is that the metabolic profile of these patients is characterized by persistent low-grade inflammation, a state of insulin resistance, and significantly increased prevalence of atherosclerosis. It is possible that these metabolic derangements can be the inciting factors for development and progression of uremic atherosclerosis. Peroxisome proliferator-activated receptor gamma (PPAR-gamma) is a ligand-activated nuclear transcription factor found in cells of the immune system and the vasculature, where it exerts an overall protective effect on the development of atherosclerosis, in part through modulation of inflammation. The agonists for PPAR-gamma improve not only the insulin resistance, but also have profound beneficial effects on inflammation, oxidative stress, endothelium, and lipid metabolism. In this proposal, the investigators hypothesize that short-term administration of a PPAR-gamma agonist (pioglitazone) will improve the inflammatory state, insulin resistance, and endothelial dysfunction in chronic kidney disease patients with advanced uremia.
Treatment of anemia associated with chronic kidney disease (CKD) during 36 weeks with safety follow up phase of 52 weeks