View clinical trials related to Proteinuria.
Filter by:Background: - Membranous nephropathy is associated with damage to the walls of the glomeruli, the small blood vessels in the kidneys that filter waste products from the blood. This damage causes leakage of blood proteins into the urine and is associated with low blood protein levels, high blood cholesterol values, and swelling of the legs. These problems can decrease or go away without treatment in about 25 percent of patients, but if they persist, some patients may experience impaired (or loss of) kidney function, blood vessel and heart disease, and a risk of forming blood clots in veins. - Kidney biopsies that show that antibodies have been deposited along the glomeruli suggest that specialized cells of the immune system, called B and T cells, are causing damage to the kidneys through their increased activity. To suppress the action of B and T cells and to decrease the harmful deposits in the kidneys, drug treatments are required. - Patients with membranous nephropathy are often treated with immunosuppressive drugs such as cyclosporine or cytoxan plus steroids that attempt to reduce or suppress the activity of the immune system, decrease antibody production, and reduce antibody deposits in the kidney. However, not everyone responds to these medications and the kidney disease can return in some patients when the drugs are stopped. Also, there are side effects associated with long term usage of these medications. Rituximab, a different immunosuppressant, has also been used for this purpose. Although cyclosporine and Rituximab have been used separately, they have not been tried in combination as a possible treatment for membranous nephropathy. Objectives: - To determine the safety and effectiveness of combining rituximab and cyclosporine to treat membranous nephropathy. Eligibility: - Individuals 18 years of age and older who have been diagnosed with membranous nephropathy based on a kidney biopsy done within the preceding 24 months, and who have had excess levels of protein in the urine for at least 6 months based on urine and blood tests. Design: - Potential participants will be screened with an initial clinic evaluation and full medical history. - Before the treatment, there will be a run-in period that will last up to 2 months. During this time, participants will be placed on a blood pressure lowering medication and will not take any other immunosuppressant medications. - Participants will visit the NIH clinical center for a baseline evaluation, four intravenous infusions of rituximab, and also at 1- to 6-month intervals throughout the study. - Active treatment period will involve a 6-month course of cyclosporine and a total of four doses of rituximab. Participants will take cyclosporine tablets twice daily, and have two infusions of rituximab given 2 weeks apart, After 6 months, the cyclosporine dose will slowly be decreased over several weeks and then completely discontinued. Participants will then receive another course (two doses 2 weeks apart) of rituximab, depending on results of blood work. - Participants will have frequent blood and urine tests performed to monitor the results of treatment and reduce the chance of side effects.
Study Hypothesis: Reduction in albuminuria has been shown to decrease progression of diabetic nephropathy. In diabetic nephropathy patients treated with maximal antihypertensive doses with dual RAAS blockade (total daily dose valsartan 320 mg and either enalapril 40 mg or benazepril 40 mg daily, or losartan 100mg), persistent albuminuria reflects further additional RAAS activation. Microvascular renal disease due to increased RAAS activation may be more effectively treated with triple blockade by the addition of a direct renin inhibitor (DRI) Aliskiren.
The purpose of this study is to analyze the clinical effects and adverse reactions of tripterygium glycosides (TW) and CTX in LN-V patients with gross proteinuria.
Diabetic nephropathy (DN) is the most important complication of diabetes mellitus (DM) and the most common cause of end-stage renal disease (ESRD). Diabetic nephropathy is a clinical syndrome characterized by persistent albuminuria (> 300 mg/d or > 200 mcg/min) that is confirmed on at least 2 occasions 3 to 6 months apart, a relentless decline in the glomerular filtration rate (GFR), and elevated arterial blood pressure. In addition to the renal hemodynamic alterations, patients with overt diabetic nephropathy (dipstick-positive proteinuria and decreasing GFR) generally develop systemic hypertension. Hypertension is an adverse factor in all progressive renal diseases and seems especially so in diabetic nephropathy. The deleterious effects of hypertension are likely directed at the vasculature and microvasculature. Use of angiotensin converting enzyme (ACE) inhibitors and/or angiotensin receptor blockers (ARBs), strict glycemic control and use of antilipidemic drugs may improve progression of DN. TNF-like weak inducer of apoptosis (TWEAK, TNFSF12) is a member of the TNF superfamily of structurally related cytokines. The human TWEAK gene encodes a 249-amino acid type II transmembrane glycoprotein (30 kD). TWEAK may be expressed as a full-length, membrane-bound protein and as a 156-amino acid, 18-kD soluble protein, (sTWEAK) that results from proteolysis of TWEAK. TWEAK gene is expressed in many tissues, including brain, kidney, heart, arterial wall, monocytes and macrophages. Reduced soluble TNF-like weak inducer of apoptosis (sTWEAK) plasma levels have been reported both in patients with subclinical atherosclerosis and chronic kidney disease (CKD). Long pentraxin 3 (PTX3) is a multimeric inflammatory mediator. Increased serum PTX3 levels have been reported among end-stage renal disease patients. Moreover, PTX3 has been suggested to represent a novel mortality risk factor, and elevated PTX3 levels have been shown to accompany increased albuminuria among patients with chronic kidney disease (CKD). There is no data about the effects of Renin angiotensin system blockage (RAS), calcium channel blocker and combined drugs on TWEAK and PTX3 levels in diabetic proteinuric patients with hypertension. The aim of this study was to find out whether the beneficial effects of RAS blockage, calcium channel blocker and combined drugs in diabetic hypertensive proteinuric patients has any relation with the alteration of TWEAK and PTX3 levels. The investigators searched for the effects of angiotensin II (AII) receptor blocker (Valsartan 160 mg), calcium channel blocker (Amlodipine 10 mg) and AII receptor blocker plus calcium channel blocker (Valsartan 160 mg + Amlodipine 10 mg) on the clinical and laboratory parameters of diabetic hypertensive proteinuric patients.
The study is designed to test if the combination of two potent antioxidant nutritional supplements, N-acetylcysteine and the milk thistle extract silibin, is capable of correcting the shedding of urine protein, the oxidative stress, and the inflammation in patients with type 2 diabetes mellitus and diabetic kidney disease.
To understand the urine analysis of athletes
In recent years, diabetic nephropathy, which may lead to dialysis treatment, is the most prevalent underlying disease of people in developed countries. A wide range of studies have been carried out, from various points of view, to understand the progress of renal dysfunction in diabetic nephropathy. The endogenous nitric oxide synthase (NOS) inhibitor asymmetric dimethylarginine (ADMA) is elevated in patients with chronic kidney disease (CKD) and may have a role in the cardiovascular mortality and morbidity of these patients. In diabetic nephropathy, high ADMA levels were related to progression of diabetic nephropathy. The Fas (CD95) antigen is a cell surface polypeptide belonging to the tumor necrosis factor receptor (TNF-R) family (type I membrane protein) that transduces a death signal after interaction with its ligand. Apoptotic cells are then recognized and removed by phagocytes. Recent studies suggest that, in uremic patients, peripheral blood mononuclear cells undergo accelerated apoptosis and this correlates with Fas levels. There is no data about the effects of Renin angiotensin system blockage (RAS) on CD95 and ADMA levels in diabetic patients with proteinuria. The aim of this study was to find out whether the beneficial effects of RAS blockage in diabetic proteinuria has any relation with the alteration of ADMA and CD95levels. The investigators searched for the effects of ACE inhibitor ramipril on the clinical and laboratory parameters of diabetic patients with proteinuria.
This study is a multicenter, prospective, interventional study. It does not have a control group. All participants will receive 160 mg valsartan for 8 weeks. Among them, the patients with persistent proteinuria (defined as proteinuria more than 1 g/g after 8 weeks treatment of valsartan) will receive 320 mg valsartan for further 16 weeks. Participants who did not receive any ACEI or ARB previously will have a titration period for 4 weeks (80 mg for 4 weeks, 160 mg for 4 weeks, and then 320 mg for 16 weeks). The investigators will evaluate the change of urinary angiotensinogen excretion between at baseline, at 8 weeks, and 24 weeks.
The purpose of this study is to evaluate the safety of several dose levels of CCL2-LPM in patients with IgA Nephropathy who have high levels of protein in the urine.
Patients with chronic kidney disease (CKD) have higher blood pressures than the general population. They also tend to have protein leaking into the urine (proteinuria). CKD, high blood pressure and proteinuria independently and together increase the risk of developing atherosclerosis (hardening) of the arteries that leads to diseases such as heart attack and stroke. Although there are a number of drugs available that lower blood pressure, these are not always fully effective. Furthermore, there are even fewer drugs that simultaneously lower blood pressure, reduce proteinuria, and slow down kidney damage in CKD. Recent research has shown that drugs like sitaxsentan not only lower blood pressure but also reduce proteinuria and potentially slow down the progression of CKD [1,2]. Before sitaxsentan can become freely available to individuals with CKD it is important to look at the effects this drug could have on proteinuria and blood pressure. 1. Goddard J, Johnston NR, Hand MF, et al. Endothelin-A receptor antagonism reduces blood pressure and increases renal blood flow in hypertensive patients with chronic renal failure: a comparison of selective and combined endothelin receptor blockade. Circulation 2004;109:1186-1193. 2. Krum H, Viskoper RJ, Lacourciere Y et al. The effect of an endothelin receptor antagonist, bosentan, on blood pressure in patients with essential hypertension. New Engl J Med 1998;338:784-790.