Active clinical trials for "Proteinuria"

This study will examine the effectiveness of the drug pirfenidone in treating focal segmental glomerulosclerosis (FSGS). Patients with this disease have kidney fibrosis (scarring) and proteinuria (excessive excretion of protein in the urine). About half of patients with FSGS eventually require kidney dialysis or transplant. Steroids, which are currently used to treat the disease, are effective in only a minority of patients. Other drugs, such as cyclosporin and cyclophosphamide, improve proteinuria in a very small percentage of patients and have serious side effects. Patients with FSGS who wish to participate in this study will undergo pre-study evaluation with blood and urine tests. Patients must be on a stable dose of an ACE inhibitor (a drug that lowers blood pressure and reduces proteinuria) for at list 6 months before starting pirfenidone therapy. (Patients who are not already taking an ACE inhibitor will be started on the drug; those who cannot tolerate ACE inhibitors will be given a different drug.) Patients with elevated cholesterol will take a cholesterol-lowering drug. A diet containing approximately 1 gram of protein per kilogram of body weight per day will be recommended. Patients will take pirfenidone by mouth 3 times a day for 12 months. Blood and urine will be tested once a month, either at NIH or by the patient's local kidney specialist. They will collect two 24-hour urine samples at the beginning of the treatment period, at 2-month intervals throughout the study, and at a 6-month follow-up. Patients will also be asked to give three to five tubes of blood and urine samples for analysis during the study. In animal studies, pirfenidone improved kidney function and proteinuria and reduced kidney scarring in rats with a disease similar to FSGS. In human studies, pirfenidone improved breathing and survival in patients with lung fibrosis.

Introduction: Aldosterone seems to have deleterious effects on the kidneys. Many animal studies and few clinical trials now have shown that suppression of aldosterone by aldosterone receptor blockers ameliorated these effects. Method: In a double-blind, cross over study, 24 patients with diabetic nephropathy who were already receiving either ACE inhibitor(lisinopril 20-40 mg/day ) or ARB( losartan 25-100 mg/day )were given spironolactone( 25 mg during the first month and 50 mg during the second and third month if serum K remained ok) or matching placebo with 1 month of washout in between. All patients were from a single center and exclusively male veterans. Blood pressure, serum creatinine, serum K and spot urine protein/creatinine were measured at the beginning and end of each study period. The study was started in May of 2003 and completed in May 2006.

The main purpose of the study is find whether the addition of statin (Atorvastatin) to dual renin-angiotensin-aldosterone system blockade involving angiotensin converting enzyme inhibitor and AT-1 angiotensin II receptor blocker leads to the reduction of proteinuria, main prognostic marker of chronic kidney disease progression.

The study will look at the effect of 30 days of treatment of 15 diabetics with proteinuria with N-acetylcysteine ( Mucomyst ) at a dose of 1 gm twice a day by mouth. The primary outcome that will be measured is change in the oxidant stress as measurable by changes in the serum level of isoprostane, Glutathione peroxidase, aconitase and Total oxidant stress. Secondary outcomes measured will be changes in proteinuria and kidney function as measured by spot urine pr/cr and estimated GFR by MDRD formula.

This is a prospective open labeled trial examining the efficacy of ACTHar Gel (porcine ACTH) on the level of proteinuria in patients with diabetic nephropathy and nephrotic range proteinuria.

A randomized clinical trial to determine if vitamin D repletion in CKD (Chronic Kidney Disease) patients with low vitamin D levels will decrease proteinuria, a marker of kidney damage.

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.

Objective: To evaluate how rosiglitazone does influence the renal plasma flow, the glomerular filtration rate and the degree of proteinuria in type 2 diabetic patients with renal insufficiency due to overt diabetic nephropathy. Background: Diabetic nephropathy is a world wide public health concern of increasing proportions. It has become the most common single cause of end-stage renal disease in the United States and in Europe. Previous studies have already found agents modifying the renin-angiotensin-system (ACE inhibitors and angiotensin receptor blocker) to retard diabetic nephropathy. These agents are likely to exert multiple effects in the kidney. One of them appear to be their known ability to improve endothelial function and to change renal glomerular hemodynamics. In a previous study we demonstrated an improvement of renal endothelial dysfunction in type 2 diabetic patients without end organ damage after treatment with rosiglitazone. In that study, rosiglitazone significantly reduced glomerular hyperfiltration. This was associated with a reduction of urinary albumin excretion. The observed effects are potentially important in the context of renal protection, provided that a similar beneficial effect of rosiglitazone is demonstrable in overt diabetic nephropathy (renal insufficiency, hypertension, proteinuria). Hypothesis Rosiglitazone decreases proteinuria and improves renal hemodynamic function in patients with chronic renal insufficiency due to overt diabetic nephropathy.

The purpose of this study is to evaluate the effects of Crestor (rosuvastatin) and (Lipitor) atorvastatin on urinary protein excretion over 1 year in non-diabetes with moderate proteinuria and hypercholesterolaemia.

Preeclampsia (PE) is a common disorder of pregnancy that complicates 4-7% of all pregnancies. It is a serious condition with acute proteinuria and hypertension and varying degrees of edema after 20 weeks of gestation. PE leads to a severe risk of low birth weight because of prematurity with inherent complications. The pathogenesis is unknown but is assumed to involve placental ischemia.The primary placental disorder results in renal glomerular injury. Established PE is associated with paradoxical suppression of the renin-angiotensin-aldosterone system, RAAS. Despite suppressed RAAS, patients with PE retain NaCl(sodium chloride) after an intravenous isotonic NaCl overload compared to healthy pregnant women on a low NaCl diet. The investigators believe to have data that provide a possible explanation for the overall relationship between proteinuria, NaCl retension, suppression of RAAS, hypertension and underdevelopment of placenta. Earlier data, which the investigators have confirmed, shows abnormal glomerular loss of the enzyme plasmin/plasminogen from plasma to the urine in PE. Active plasmin in urine from patients with nephrotic syndrome and PE activates the epithelial sodium channel ( ENaC ) in renal collecting duct cells. The investigators hypothesize that loss of plasmin/plasminogen are shared for the diseases with proteinuria, including PE, and that plasmin- driven ENaC (epithelial sodium channel) activation is a causal factor in the pathophysiology of established PE. Hyperactive ENaC causes primary renal sodium retention with secondary suppression of the renin-angiotensin-aldosterone system. Aldosterone is recently established as a placental growth factor. Plasma-aldosterone levels are significant higher in normal pregnant women. PE is characterized by low aldosterone levels (a discovery the investigators have also confirmed) and by placental underdevelopment. Study Aim: To test specific hypothesis regarding established PE´s pathophysiological mechanisms. Study Hypothesis: Excretion of urine proteases (plasmin/plasminogen) in PE leads to an activation of ENaC and hence RAAS is less NaCl sensitive while the blood pressure is more NaCl sensitive compared to healthy pregnant women. The degree of aldosterone suppression in PE determines placental development