Active clinical trials for "Renal Insufficiency, Chronic"

The purpose of the study is to investigate whether a high phosphorous containing meal causes acute changes in p-phosphate levels in patients with dialysis-dependent kidney failure.

Almost 15% of Americans have chronic kidney disease (CKD), with an even higher rate in Veterans due to common risk factors such as high blood pressure and diabetes. People with CKD have a high risk of cardiovascular (CV) diseases, such as heart attacks, heart failure, and strokes. Extra fluid in the body, called volume overload, may lead to CV disease in people with CKD. It is unknown if volume overload develops in the earliest stages of CKD, when treating it with common, inexpensive medicines called diuretics may improve long-term CV outcomes. This study will lay important groundwork to answer this question in Veterans with early CKD by comparing two ways to measure volume overload and studying the change in common symptoms like fatigue and short-term CV function after treatment with diuretic medicines.

Worldwide, diabetic kidney disease (DKD) is the most common cause of chronic and end stage kidney disease. Large-sized prospective randomized clinical trials indicate that intensified glucose and blood pressure control, the latter especially by using agents that interfere with the renin-angiotensin-aldosterone system (RAS), halts the onset and (particularly) the progression of DKD, in both type 1 Diabetes Mellitus (T1DM) and type 2 Diabetes Mellitus (T2DM) patients. However, despite the wide use of angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), a considerable amount of patients develop DKD (20-40%), indicating an unmet need for renoprotective therapies as DKD largely causes the increased mortality risk from cardiovascular disease (CVD) in people with diabetes. Sodium-glucose linked transporters (SGLT-2) inhibitors are a relatively novel glucose-lowering drug for the treatment of T2DM as they lower plasma glucose levels by blocking renal glucose reabsorption. In addition, these agents exert pleiotropic actions beyond glucose control. As such, SGLT-2 inhibitors decrease proximal sodium reabsorption, reduce blood pressure, body weight and uric acid. In large trials and likely through these pleiotropic effects, SGLT2 inhibitors reduce cardiovascular mortality, hospitalization for heart failure and reduce end stage kidney disease. At this point in time, the renoprotective mechanisms involved with SGLT-2 inhibition still remain speculative, though a consistent finding is that SGLT-2 inhibitors reduce estimated eGFR after first dosing, which is reversible after treatment cessation. This "dip" indicates a renal hemodynamic phenomenon reminiscent of the RAS blockers and is thought to reflect a reduction in intraglomerular pressure. The mechanisms of this observation have only been partially investigated by us and others. From studies in peolpe with T1DM it is hypothesized that SGLT-2 inhibition increases sodium chloride delivery to the macula densa, which in turn augments the afferent arteriolar resistances, known as tubuloglomerular feedback (TGF), consequently reducing glomerular (hyper)filtration and hydrostatic pressure. Recently a trial has been conducted in humans with T2DM to investigate if this also holds true in these patients. Suprisingly, this study showed that the renohemodynamic actions of SGLT-2 inhibition in T2DM are not due to afferent vasoconstriction but rather efferent vasodilation [van Bommel/van Raalte Kidney International 2019 in press]. The investigators realized that the SGLT-2 associated dip in eGFR remains insufficient understood. The increase in sodium excretion following SGLT-2 inhibition peaks at day 2-3 after which it normalizes. It is unknown whether this drop in eGFR is related to this peak in sodium excretion, as the drop remains after normalization of sodium excretion. Therefore it might be possible that glucosuria, by inducing osmotic diuresis, is the main driver of the reduction in intraglomerular pressure more than sodium, since SGLT-2 inhibitors cause persisting glucosuria. Furthermore, it is known that SGLT-2 induced glucosuria and possibly sodium excretion is dependent of renal function and HbA1c and consequently is diminished in people with CKD or without T2DM. However, the renoprotective effects in T2DM are also observed in patients with impaired kidney function and seem statistically independent of glucose levels. Until now it has not been investigated whether or not the SGLT-2 induced eGFR alterations occur in people with CKD with or without T2DM. It is clinically relevant to understand the renal hemodynamics of SGLT-2 inhibitors in these populations since then it is possible to interpret the results from the ongoing trials in people with CKD without T2DM, such as EMPA-KIDNEY and DAPA-CKD. Recently, potential mediators of renal arterole tone, such as adenosine, have been measured to gain more insight into mechanisms of SGLT-2 inhibitor-induced changes in renal hemodynamics. Adenosine is known to augment preglomerular arteriolar resistance. Adenosine was significantly increased after SGLT-2 inhibition, as was also observed in patients with type 1 diabetes. However, it can also induce postglomerular vasodilation via A2aR activation in the presence of RAS blockade. One study in T1DM rats has shown that increased adenosine generation by the macula densa in response to SGLT-2 inhibition suppresses hyperfiltration, as the improvements in preglomerular arteriolar resistance were abolished after adenosine antagonist administration. To date, this has not been investigated in T2DM humans. Therefore, this trial will assess TGF responses with and without adenosine blockade by caffeine.

The study aims to determine if use of physical activity trackers coupled with provider feedback will increase awareness of young adults of their physical fitness and improve blood pressure levels. The goal of this pilot study is feasibility, with a secondary goal of examining potential effect sizes for planning purposes for a larger randomized controlled trial.

Diabetes control is often assessed by tests of glucose levels over time, such as the glycosylated hemoglobin A1c (HbA1c) and fructosamine. In the later stages of chronic kidney disease (CKD) there is limited data available on the utility of these tests. There are reasons to believe that the tests may be less accurate in this population. Continuous glucose monitoring (CGM) offers an effective method for understanding the totality of glucose exposure and incidence of both hyperglycemic and hypoglycemic excursions.

This study was planned to determine the effects of upper extremity functional capacity, physical activity level and physical functions of patients receiving hemodialysis treatment.

The medium cut-off dialysis (MCO) membrane has been developed to improve middle molecule removal compared to standard high-flux dialysis filters. The aim of this study is to compare levels of middle molecules after 12 weeks of MCO hemodialysis, compared to 12 weeks of hemodiafiltration using standard high-flux filter.

Hyperphosphatemia is a severe complication to chronic kidney disease (CKD) and is associated with increased risk of vascular calcification, cardiovascular morbidity and mortality. Early dietary intervention and improvement in dietary therapy might optimally reduce cardiovascular complications. For this purpose the investigators investigated patients with CKD stage 3-4, the participants dietary habits, developed a New Nordic Renal Diet and investigated the short term effect on phosphorus homeostasis.

This open-labeled, multicenter study is designed to evaluate the efficacy, safety and PK/PD of roxadustat in ESA-naïve and ESA-treated pediatric patients with CKD Stages 3, 4, and 5, as well as end-stage renal disease (ESRD) who are receiving either hemodialysis (HD) or peritoneal dialysis (PD). The study will enroll patients between the ages of 2 to <18 years in two sequential cohorts, with the older cohort of ages 12 to <18 years enrolled first. Approximately 30 patients will be enrolled in each age-based cohort.

The purpose of the study is to learn more about how treatment with vitamin D can affect iron metabolism and blood levels of hepcidin (hormone controlling iron levels) in people with chronic kidney disease (CKD). Iron is an essential mineral which is a major component of proteins that carry oxygen in the blood. Problems with iron metabolism can lead to low blood levels (anemia), which can commonly happen in people with CKD. New research over the last decade has uncovered a new hormone called 'hepcidin', which is made in the liver and released into the blood. Hepcidin controls how much iron is in the blood by preventing the absorption of iron from food. Blood levels of hepcidin C are found to be high in people with CKD, and a recent small study in people with normal kidney function showed that treatment with vitamin D decreased hepcidin levels. In this study, investigators would like to examine the effects of vitamin D (Ergocalciferol) on iron metabolism and blood levels of hepcidin in individuals with CKD.