View clinical trials related to Renal Insufficiency, Chronic.
Filter by:To assess the performance of the Nova Max Creatinine and eGFR assay in the hands of CLIA-Waived Point-of-Care users in at least three (3) distinct Point-of-Care clinical settings on venous, and capillary blood and compare the performance characteristics to a traceable laboratory reference method (the Siemens EXL creatinine determination). To assess the Ease of Use of the Nova Max Creatinine and eGFR Meter System in the hands of the intended CLIA-Waived Point-of-Care users.
This study will assess the safety and efficacy of once daily dosing of vadadustat for the treatment of pediatric participants with anemia of chronic kidney disease (CKD) naive to erythropoiesis-stimulating agent (ESA) treatment.
This study will assess the safety and efficacy of once daily dosing of vadadustat for the treatment of pediatric participants with anemia of Chronic Kidney Disease (CKD) after conversion from an Erythropoiesis Stimulating Agent (ESA).
This is a prospective, descriptive, observational research study designed to observe and document the clinical practice by domain experts, and how the knowledge of new findings that are published in the medical literature affect clinical decision making. The study will evaluate risk factors and co-variants, including genetic variants that are associated with disease progression such as pain, inflammation, organ dysfunction, disability and quality of life.
Because the atherosclerosis process partly occur in the intercellular space of the vessel wall, the determination of the constitution of lipoproteins in the interstitial fluid may expand the knowledge about the atherosclerosis process and lead to a better understanding of what constitutes the increased risk of developing cardiovascular disease in patients with chronic diseases. The investigators hypothesize that the apoB-containing particles in T2D patients are more susceptible to be retained or consumed in the intercellular compartment, which in turn could be one explanation for the elevated risk of atherosclerosis. The investigators hypothesise that with the progression of chronic kidney disease this process is further increased. Patients undergoing dialysis are known to have a very high risk of cardiovascular disease. The investigators now want to study the cholesterol metabolism in interstitial fluid in subjects undergoing hemodialysis because of diabetic nephropathy and in subjects undergoing hemodialysis because of chronic kidney disease of other causes.
The proposed studies will examine the effect of fisetin on adipose tissue-derived mesenchymal stem/stromal cell function, kidney function, markers of inflammation, and physical function in individuals with advanced chronic kidney disease.
The fibroblast growth factor-23-bone-kidney axis is part of newly discovered biological systems linking bone to other organ functions through a complex endocrine network that is integrated with the parathormone/vitamin D axis and which plays an equally important role in health and disease . Most of the known physiological function of fibroblast growth factor 23 to regulate mineral metabolism can be accounted for by actions of this hormone on the kidney.In a recent experimental study, fibroblast growth factor-23 was shown to cause pathological hypertrophy in rat cardiomyocytes by "calcineurin-nuclear factor of activated T cells" and treatment with fibroblast growth factor -blockers reduced left ventricular hypertrophy in experimental models of chronic renal failure.The current hypothesis is that, in healthy individuals, iron deficiency stimulates increased production of fibroblast growth factor23. At the same time, iron is thought to be the cofactor of enzymes taking part in the degradation of intact fibroblast growth factor-23 and thought to have a role in the excretion of degraded FGF-23 parts .Studies speculated that Angiotensin Converting Enzyme inhibitors may exert their anti-proteinuria effects at least in part by reducing serum fibroblast growth factor-23 levels although it is difficult from the results of this study to understand which comes first and brings about the other; decrease in proteinuria or fibroblast growth factor-23. Available evidence points to the deleterious effects of increased fibroblast growth factor-23 level in proteinuria, but the precise molecular mechanism still remains to be explored. An intricate and close association exists among parathormone, phosphorus, active vitamin D with FGF23, but the independent role of the latter on proteinuria is the least explored. Elaborately conducted studies that control effects of confounding factors adequately are needed to demonstrate the independent pathogenic role of FGF23.
The transition from chronic kidney disease (CKD) to end-stage renal disease ESRD is a vulnerable and challenging period of time for patients and providers. Suboptimal control of blood pressure is known to be common in patients with the advanced stages of CKD, and may contribute to their elevated risk of progression to ESRD, cardiovascular morbidity, and mortality. This proposal is a pilot randomized controlled trial designed to test whether intensive blood pressure lowering is feasible and safe in patients with advanced CKD as they transition to ESRD.
The Heparin form a complex with a plasma protein, antithrombin III (ATIII), which is an endogenous anticoagulant. This complex inhibits the formation of thrombin and accelerates its destruction. Moreover, heparin and other proteases ATIII inactivate the clotting cascade, especially the anti-activated factor X. The end result of these actions is the inhibition of biochemical training and synthesis of certain clotting factors that activators of critical functions in the genesis of a blood clot. Patients with chronic renal failure (CRF) who use the treatment of hemodialysis need a system of anticoagulation with the direct thrombin inhibitor and / or heparinóides to prevent thrombosis. Based on clinical studies, to control the level of plasma heparin in patients with CRF is essential. Evidence of clotting as APTT, TP, ACT and proof of the activity of anti-factor Xa should be used as a substrate of protection for those patients on hemodialysis.
The uremic syndrome is mainly related to the retention of a host of compounds, due to altered glomerular filtration and other factors of renal dysfunction, e.g. tubular secretion. Uremic retention solutes are arbitrarily subdivided in three different categories according to their physicochemical characteristics and their subsequent behaviour during dialysis: (i) the small, water-soluble, non-protein bound compounds, (ii) the larger middle molecules, mainly peptides and (iii) the small protein-bound compounds (1). Although direct proof is lacking, several lines of evidence indicate that albumin is the most important carrier protein. Removal of protein bound uremic retention solutes is limited. The Prometheus® system fractionates blood into plasma and cellular components, using an albumin-permeable polysulfon filter (AlbuFlow®) with a specially designed sieving coefficient curve (1.0 for 2-microglobulin, >0.6 for albumin, <0.3 for IgG, <0.1 for fibrinogen and <0.01 for IgM). Due to the high sieving coefficient of the filter for large molecules (i.e. cut-off at about 250 kD) molecules up to the size of albumin (69 kD) easily pass from blood into the secondary circuit which is filled with isotonic sodium chloride solution, whereas larger molecules like fibrinogen (340 kD) cannot pass through the filter. In the secondary circuit the filtered plasma with the albumin-bound toxins flows through one or two adsorbers in a row with maximized adsorption capacity for putative liver toxins that are directly adsorbed (`fractionated plasma separation and adsorption' or FPSA). The purified plasma is then returned to the blood side of the albumin filter. In order to eliminate water-soluble toxins, blood thereafter undergoes hemodialysis using a conventional high-flux dialyser. We hypothesise that removal of protein bound uremic retention solutes can be improved by FPSA as compared to standard hemodialysis.