View clinical trials related to Renal Insufficiency, Chronic.
Filter by:The goal of this pilot clinical trial is to evaluate a culturally tailored computerized education program in hospitalized African-American patients with advanced chronic kidney disease (CKD). The main question it aims to answer are: does computerized adaptive education (CAE) increase patients' knowledge about CKD self-care and renal replacement therapy (RRT) options compared to usual care (UC) and will CAE will be increase patients' intent to participate in CKD self-care and RRT preparation compared to UC
In chronic kidney disease (CKD), hypertension is characterized by the phenomenon of sodium-sensitivity, i.e., the disproportionate increase in blood pressure (BP) due to an increase in dietary sodium consumption to maintain homeostasis through urinary sodium excretion. Impaired renal circulation, blunt suppression of renin-angiotensin-aldosterone system, sympathetic nervous system overactivity, paradoxically reduced levels of atrial natriuretic peptide and hyperinsulinemia represent the main pathophysiologic mechanisms. Accumulated evidence has suggested that uromodulin plays a central role in the development of sodium-sensitive hypertension. Uromodulin is a kidney-specific glycoprotein which is exclusively produced by the epithelial cells lining the thick ascending limb and early distal convoluted tubule. It is currently recognized as a multifaceted player in kidney physiology and disease, with discrete roles for intracellular, urinary, interstitial and serum uromodulin. Among these, urinary uromodulin modulates renal sodium handling through regulating tubular transporters that reabsorb sodium and are targeted by diuretics, i.e., the loop diuretic-sensitive Na+-K+-2Cl- cotransporter type 2 (NKCC2) and the thiazide-sensitive Na+/Cl- cotransporter (NCC). Given these roles, the contribution of uromodulin to sodium-sensitive hypertension has been proposed. In preclinical models, uromodulin deficiency causes decreased BP that is resistant to dietary salt, while uromodulin overexpression causes hypertension due to increased tubular sodium reabsorption that is responsive to furosemide. Genetic human studies have identified robust associations of specific UMOD gene variants with sodium sensitivity and incident hypertension risk, while comprehensive Mendelian randomization studies have affirmed these associations by highlighting the causal relationship between UMOD variants, urinary uromodulin levels and hypertension. Furthermore, clinical studies in both healthy individuals and hypertensive patients have indicated a link between sodium sensitivity and uromodulin, directly affecting mean BP levels and BP response to salt intake. With regards to CKD population, solid data on the link of uromodulin with sodium sensitivity are currently missing from the literature. There is only a pediatric study in the setting of CKD (stages 2-3), which failed to show an association between urinary uromodulin levels indexed to urinary creatinine (UMOD/uCr) and either 24-hour or office BP; however, this study has several limitations, and its results should be interpreted with caution. To best of our knowledge, there is no study up to date investigating the effect of dietary sodium intake on 24-hour ambulatory blood pressure depending on urinary uromodulin levels in adult CKD patients.
This study will evaluate the safety, tolerability, pharmacokinetics, and CRP-lowering effect of quarterly and monthly subcutaneous administration of TOUR006 in participants with chronic kidney disease and elevated hs-CRP.
To demonstrate safety and performance of AquaPass System for improving fluid balance in hemo-dialysis patients, by increasing fluid loss via the skin.
It has been shown that excretion of sodium and water through the skin in the form of sweat represents a regulatory mechanism of electrolyte- and fluid balance. Since patients with chronic kidney disease (CKD) exhibit increased skin sodium content, we investigated the feasibility of sweat testing as a novel experimental tool to a more complete assessment of fluid- and sodium homeostasis. In this cross-sectional feasibility study, we applied pilocarpine iontophoresis to induce sweat testing in 58 patients across various stages of CKD including patients after kidney transplantation as well as a healthy control cohort (n=6) to investigate possible effects of CKD and transplantation status on sweat rate and sodium concentration. Due to non-linear relationships, we modeled our data using polynomial regression. Decline of kidney function showed a significant association with lower sweat rates: adj R²= 0.2278, F(2, 61) = 10.29, p = 0.000141. Sweat sodium concentrations were increased in moderate CKD, however this effect was lost in end stage renal disease: adj R² = 0.3701, F(4, 59) = 10.26, p = 2.261e-06. We observed higher sweat weight in males compared to females. Diagnostic sweat analysis represents an innovative and promising noninvasive option for more thorough investigation of sodium- and fluid homeostasis in CKD patients. Lower sweat rates and higher sweat sodium concentrations represent a unique feature of CKD patients with potential therapeutic implications.
Phase III, multicentre, double-blind, randomised, parallel, equivalence clinical trial to determine the efficacy, safety and immunogenicity of Megalabs® recombinant human alfa epoetin for subcutaneous use, compared to Eprex® (Janssen-Cilag Farmacêutica Ltda.), in the treatment of anaemia in participants with chronic renal disease, dependent on haemodialysis
A fundamental strategy to improve adherence to nutritional treatment in patients with chronic kidney disease is the implementation of educational programs. The aim of this study is to evaluate the effect of a multidisciplinary educational program on dietary adherence, nutritional knowledge, nutritional status, metabolic control and quality of life in patients with chronic kidney disease, predialysis, peritoneal dialysis and hemodialysis. A randomized clinical trial will be carried out, in which patients who meet the inclusion criteria will be randomly assigned to three possible groups: predialysis educational intervention, dialysis educational intervention and control group. At the initial visit, the nutritional status will be evaluated by means of anthropometric parameters, screening and dynamometry, the biochemical parameters of interest will be extracted from the clinical record, nutritional knowledge and quality of life will be evaluated, and the diet will be explained. In the second visit, adherence to the diet will be evaluated and the food registry will be carried out. In the intervention groups, the educational program will begin with a duration of five months. Patients will come twice a month to the hospital to participate in the educational sessions and attend group psychology sessions. After completion of the educational program, the same measurements as at the beginning of the study will be carried out in the three groups.
The purpose of the study is to evaluate the efficacy, safety and tolerability of balcinrenone/dapagliflozin compared with dapagliflozin alone on patients with chronic kidney disease (CKD) and albuminuria. This study will evaluate the effect of the balcinrenone/dapagliflozin on urinary albumin-to-creatinine ratio (UACR), compared with dapagliflozin in patients with CKD. This is a dose-finding study aiming to identify an optimal dose of balcinrenone/dapagliflozin for a future Phase III study in patients with CKD.
High blood pressure is a risk factor for end-stage renal disease and is common in patients undergoing maintenance hemodialysis. Intradialytic hypotension is associated with an adverse prognosis. More knowledge is needed to identify patients at high risk for intradialytic hypotension and dialysis-associated hypotensive episodes. The aim of this observational single-center pilot study is to evaluate whether point-of-care ultrasound measurements may predict intradialytic hypotension and orthostatic blood pressure falls, in patients with chronic kidney disease who undergo maintenance hemodialysis.
The vascular endothelium is an organ in its own right, playing, among other things, a primordial role in the control of vascular tone. This vascular tone is ensured by pro-dilator mediators (nitric oxide (NO), prostacyclins (PGI2)), or vasoconstrictors (endothelin, thromboxane A2 or PGH2).Uremic toxin accumulation in chronic kidney disease (CKD) is a well-known factor in endothelial dysfunction, often associated with higher cardiovascular risk. This association is also present for terminal chronic kidney disease characterized by the need to resort to an extra-renal purification technique (in-center hemodialysis (HD), daily home hemodialysis (HDQ), peritoneal dialysis) or to resort to renal transplantation. For HD to be effective, it is essential that the blood flow rate passing through the dialyzer is greater than 300ml/min. This imperative requires that any hemodialysis patient have specific vascular access (dialysis catheter or arteriovenous fistula (AVF)) to ensure these flow rates. The vascular access of choice is the arteriovenous fistula , because it is associated with a lower risk of infection and lower morbidity and mortality. Making an arteriovenous fistula consists of surgically creating an anastomosis between a vein and an artery. Complications of arteriovenous fistula are common. Arteriovenous fistula maturation may be delayed (maturation delay) or even absent. Drainage veins and/or anastomoses can also be the site of stenosis or thrombosis. The pathophysiology of these complications is complex and multifactorial. Among the risk factors for these complications (delay or absence of maturation, stenosis thrombosis), the positivity of antiphospholipid antibodies (aPL) can be cited, as well as endothelial dysfunction. Antiphospholipid syndrome (APS) is an autoimmune disease causing a thrombotic phenotype. This is an acquired thrombophilia. In the general population, the prevalence of antiphospholipid antibodies is around 0.5%; this prevalence is far from rare in hemodialysis, since it represents up to 37% in dialysis patients. In a retrospective study carried out at Brugmann University Hospital in 2023 , on 115 patients with AVF and in whom aPL dosages were available, the prevalence of persistent positivity (2 positive dosages spaced more than 12 weeks apart) was 21%. Interestingly, a third of the cohort presented an antibody profile that did not allow them to be classified according to the classification criteria in force. This group corresponds to patients with a single positive dosage, either not recontrolled or recontrolled negative. This group was called Fluctuating. This fluctuating group was associated with arteriovenous fistula complications in a 2019 study. Endothelial dysfunction is also implicated in the pathophysiology of APS. In clinical practice, the "flow mediated dilation" (FMD) test makes it possible to assess endothelial dysfunction in vivo. It involves the phenomenon of post-occlusive hyperemia which is mainly linked to NO and endothelium-dependent vasodilation. In the brachial artery, NO is the sole mediator of FMD. Endothelial dysfunction according to FMD has been described in populations with advanced chronic kidney disease, as well as patients with cardiovascular diseases. Hemodialysis patients with delayed/absence of arteriovenous fistula maturation have more pathological FMDs compared to dialysis patients without fistula problems. However, the additive role of aPL in this different population has not been studied in terms of endothelial dysfunction by FMD. The objective of this study is to evaluate the weight of antiphospholipid biology on endothelial dysfunction in hemodialysis patients, using the FMD test. 1. Compare endothelial dysfunction by FMD according to the stage of chronic kidney disease and in comparison to a control group without chronic kidney disease. 2. Characterize the FMD pre or post dialysis and according to the duration of the long (for example between Thursday and Sunday) vs. short (between Tuesday and Thursday) inter-dialytic period. 3. Evaluate the relationship between endothelial dysfunction according to FMD, aPL positivity and arteriovenous fistula complications in hemodialysis patients. 4. Evaluate the risk factors associated with endothelial dysfunction according to FMD, and in particular evaluate the impact of antiphospholipid antibodies. 5. Evaluate the correlation between endothelial dysfunction according to FMD and other markers of endothelial dysfunction (urinary NO and metabolites of urinary NO, PGI2, endothelin, PGH2).