Active clinical trials for "Diabetic Nephropathies"

The aim of this study is to evaluate the prevalence of secondary hyperparathyroidism among patients with diabetic nephropathy.

The main objective is to study the epigenetic contribution to the pathophysiology of diabetic nephropathy in Qatari population.

Cells damaged by hyperglycemia are unable to downregulate glucose entrance in presence of high extracellular glucose resulting in intracellular activation of deleterious biochemical pathways. Expression of GLUT-1, the major glucose transporter in mesangial cells, is increased and participates in the induction of diabetic nephropathy. Variants in the gene encoding GLUT-1 (SLC2A1) have been associated to this diabetic complication. The aim of this study was to test whether polymorphisms in SLC2A1 confer susceptibility to diabetic nephropathy in Brazilian type 1 diabetes patients.

Kidney disease in diabetes (diabetic nephropathy) tends to run in families. It is likely, therefore, that there are genes that predict or are associated with either getting or not getting diabetic nephropathy. The GoKinD Study will provide clinical information and DNA for investigators to look for these genes. Evaluation will be performed and DNA obtained from approximately 1100 diabetic persons with kidney disease and 1000 diabetic persons without kidney disease. In some cases, samples for DNA will also be obtained from the parents of these subjects. Clinical information and DNA will be coded so that individuals cannot be identified, but the DNA can be linked to the clinical data from the individual. Multiple investigators will be able to use this genetic material to test hypotheses about the genetics of kidney disease in diabetes.

Diabetes mellitus is one of the most prevalent health problems worldwide. Diabetic nephropathy has become the leading cause of end-stage kidney disease worldwide and is associated with an increased cardiovascular risk. Traditionally, metabolic and hemodynamic factors are the main causes of renal lesions in patients with type two diabetes mellitus and diabetic nephropathy , both considered non-immune diseases. Serial researches has demonstrated that diabetic nephropathy is a metabolic and hemodynamic disorder, with inflammation playing a vital role in the process.

A multicentre real life study is proposed. The study has as its goal primary to compare the levels of ketonemia measured in patients with albuminuria and patients normo albuminurici to evaluate a possible correlation between ketone level and alteration of renal function in the diabetic patient, comparing the eGFR values of patients with ketonemia high and of patients with low ketonemia. In these patients, the lack of insulin causes one imbalance between ketogenesis and ketolysis, with increased production and reduced body clearance ketones. Several studies explore the effects of ketone bodies on cell function and lesions diabetic complications: ketonemia induces oxidative stress and increases the risk and the progression of complications, moreover, the increase in ketone levels may have pro-inflammatory effects. However, ketonemia levels between normal and DKA are poorly studied and their effects are still unknown. It is hypothesized that in diabetic patients with DKD the level of ketones may be high; Increased ketone levels may promote an alteration of renal function. We want to evaluate the relationship between ketone levels and renal function, because the kidneys, as well as the heart, are among the main organs in which the ketone bodies are oxidized to produce energy and DKD has a high morbidity and mortality in diabetes. The main objectives for being able to demonstrate the hypothesis in question are: Evaluate the level of ketones in albuminurate patients with diabetes and in patients with renal function altered; Evaluate the association between ketone level and decline of renal function in the diabetic patient e therefore the impact of ketonemia on the progression of renal function loss.

The purpose of the study is to detect the effect of treatment of hyperuricemia on eGFR (Estimated Glomerular Filtration Rate) as an objective criterion for assessment of progression of diabetic nephropathy in patients with Type 2 Diabetes Mellitus.

The study will be conducted at Assiut University Hospital. Eligible subjects will be screened for vascular calcification by Doppler ultrasound examination. A correation between the level of serum Osteopontin (OPN) level and the extent of vascular calcification will be evaluated.

It is well understood that hypertension, dyslipidemia, and diabetes mellitus are the major risks of chronic kidney disease. Current guidelines recommend screening kidney estimated glomerular filtration function with serum creatinine. But it is not the utmost effective method and the GFR would be underestimated. Since good correlation was noticed between serum creatinine and chronic kidney disease, urinary microalbumin levels is better for patients with risks of chronic kidney diseases. With adequate and early education, or antihypertensive agents with angiotensin converting enzyme inhibitors (ACEi) or angiotensin II receptor blockers (ARB), all could alleviate renal function deterioration and the severity of proteinuria. As a result, high sensitive methods is urgent and needed for early screening and diseases following up under medication with ACEi and ARB in chronic kidney disease patients. In this project, the investigators are going to include the patients with typy II diabetes mellitus combining with hypertension who are treated with antihypertensive agents. Such volunteers will be treated with Candesartan 8-16mg/ day and maintain systolic blood pressure <130 mm/Hg, diastolic blood pressure < 80 mm/ Hg as the goal. Therefore, this project would make effort on correlation with urinary microalbumin and other biomarkers changes under Candesartan treatment- one of ARB medication for 12 weeks, and further exploration of new biomarkers that may be related to renal parenchymal injuries.

The heart and vessels are surrounded by layers of adipose tissue, which is a complex organ composed of adipocytes, stromal cells, macrophages, and a neuronal network, all nourished by a rich microcirculation. The layers of adipose tissue surrounding the heart can be subdivided into intra- and extra-pericardial fat. Their thicknesses and volumes can be quantified by echocardiography and computed tomography or magnetic resonance imaging, respectively. The term extrapericardial fat defines thoracic adipose tissue external to the parietal pericardium. It originates from primitive thoracic mesenchymal cells and thus derives its blood supply from noncoronary sources. Intrapericardial fat is further subdivided into epicardial and pericardial fat. Anatomically, epicardial and pericardial adipose tissues are clearly different. Epicardial fat is located between the outer wall of the myocardium and the visceral layer of pericardium.