Active clinical trials for "Diabetic Nephropathies"

The purpose of this study is to determine the safety and effect of green tea (epigallocatechin gallate) in albuminuria in diabetic patients and nephropathy.

There is considerable evidence that increased blood glucose results in the generation of reactive oxygen species, ultimately leading to increased oxidative stress in a variety of tissues. This may lead to the activation of stress-sensitive intracellular signaling pathways, causing cellular damage and late complications of diabetes including renal injury. Although the investigators understanding of how hyperglycemia-induced oxidative stress ultimately leads to tissue damage has advanced considerably in recent years, effective therapeutic strategies to prevent or delay the development of this damage remain limited. The flavonoid complex silymarin, an extract from the milk thistle, and its major pharmacological active component silibinin are free radical scavengers and potent membrane stabilizers by preventing lipid peroxidation. Furthermore, during early stages of diabetes, flavonoids minimize oxidative stress, and inflammation which represent important factors in the development of diabetic nephropathy. In this study the investigators plan to evaluate the renoprotective effect of milk thistle extract on type II diabetic patients with kidney disease.

The study objective is to investigate the effects of three low doses of atrasentan on urinary albumin/creatinine ratio (UACR) levels in subjects with Type 2 diabetic nephropathy. Patients with Type 2 diabetes with nephropathy must be receiving a renin-angiotensin system inhibitor, such as an Angiotensin converting enzyme inhibitor (ACEi) or an Angiotensin II Receptor Blocker (ARB) for participation in this study. ACEi and ARB treatment are the standard of care for the management of proteinuria in Chronic Kidney Disease (CKD) patients.

To determine the effects of three different doses of bardoxolone methyl administered orally on the kidney function (glomular filtration rate) in patients with diabetic nephropathy.

Plasma adiponectin concentration is inversely associated with renal function. There is little literature on adiponectin levels and regulation by antihypertensive medication with an angiotensin II-receptor blocker (ARB), especially in subjects with type 2 diabetes in different stage of chronic kidney disease (CKD).

The purpose of this study is to determine whether oral sevelamer carbonate binds advanced glycation end products (AGEs) in the gastrointestinal (GI) tract of patients with diabetic nephropathy leading to decrease body AGE load and therefore decreases the inflammation and oxidative stress in these patients.

Diabetic nephropathy has become the single most frequent cause of end-stage renal disease. On a molecular level, at least five major pathways have been implicated in glucose-mediated vascular and renal damage and all of these could reflect a single hyperglycaemia-induced process of overproduction of reactive oxygen species. Recent studies have shown that inflammation, and more specifically pro-inflammatory cytokines play a determinant role in the development of micro- vascular diabetic complications, most of the attention has been focused on the implications of TNF-α in the setting of diabetic nephropathy. Glutathione is the most abundant low-molecular-weight thiol, and Glutathione/ glutathione disulfide is the major redox couple in animal cells. N-acetylcysteine is effective precursors of cysteine for tissue Glutathione synthesis. Not only does N-acetylcysteine exhibit antioxidant properties, but it may also counteract the glycation cascade through the inhibition of oxidation. N-acetylcysteine can also reduce the apoptosis elicited by reactive oxygen species . Indeed, N-acetylcysteine has been shown to inhibit reactive oxygen species induced mesangial apoptosis and to be able to protect cells from glucose-induced inhibition of proliferation.

Evaluation of several olmesartan dosages compared to losartan on proteinuria, renal function and inflammatory markers in patients with diabetic nephropathy

The aim of this study is to compare the preventive effect of Telmisartan(Micardis) versus placebo control on the transition to overt nephropathy in patients with diabetic nephropathy manifesting microalbuminuria associated with type II diabetes, and to evaluate the efficacy and safety of Telmisart (Micardis, Gliosartan, Kinzal, Kinzalmono, Predxal, Pritor, Samertan, Telmisartan) for diabetic nephropathy patients.

Background The relationship between long-term heavy lead exposure and chronic interstitial nephropathy is well recognized in the previous literatures. Several epidemiological studies have demonstrated a positive association between blood lead levels and the age related decreases of renal function in the general population and suggested that environmental low-level lead exposure may accelerate the progression of renal function in the healthy persons. In addition, previous our works suggest environmental lead exposure may correlate to progressive renal insufficiency and lead chelation therapy or repeated lead chelation may improve and slow the progressive renal insufficiency in non-diabetic patients with chronic renal diseases. However, Diabetes mellitus is increasing in prevalence worldwide and is currently estimated to affect more than 6.5 percent of the population of the United States. In addition, diabetes is the most common cause of end-stage renal disease in many countries, accounting for about 40 percent of cases. It is still unknown that the relationship between long-term environmental lead exposure and the progressive renal insufficiency in patients with type II diabetes and diabetic nephropathy. Methods Ninety patints with type II diabetes and diabetic nephropathy (serum creatinine levels between 1.5 mg per deciliter and 3.9 mg per deciliter) who have a normal body lead burden and no history of exposure to lead or other metals will be observed for 24 months. Then, about 50 subjects with high normal body lead burdens (at least 80 μg but less than 600 μg) will be randomly assigned to the study and control groups. For three months, the 25 patients in the study group will receive lead-chelation therapy with calcium disodium EDTA weekly until the body lead burden fallsl below 50 μg, and the 25 control group receive weekly placebo. During the ensuing 12 months, the renal function will be regularly followed up every 3 months and EDTA mobilization tests will be assessed every 6 months. If body lead burden of the study group patients increase more than 60μg, the chelation therapy will be performed again until their body burden are less than 60 μg. The primary end point is an increase in the serum creatinine level to 2 times the base-line value during the observation period. A secondary end point is the change in renal function during the follow up period.