Pathogenesis of diabetic nephropathy

Abstract

As the increasing prevalence of diabetes reaches epidemic proportions worldwide, diabetic nephropathy and associated end‐stage renal failure will be an unavoidable major health burden to not only individuals with diabetes and their families, but also to the health systems both in developed and developing countries. Over the past decade, a large body of research has focused on diabetic nephropathy ranging from studies in molecular signaling, hemodynamic regulation and pharmaceutical intervention to clinical outcomes. It is likely that the pathophysiology of diabetic nephropathy involves a multifactorial interaction between metabolic and hemodynamic factors. Metabolic factors involve glucose‐dependent pathways, such as advanced glycation end‐products and their receptors. Hemodynamic factors include various vasoactive hormones, such as components of the renin–angiotensin system. It is likely that these metabolic and hemodynamic factors interact through shared molecular and signaling pathways, such as nuclear factor kappa‐light‐chain‐enhancer of activated B cells and protein kinase C with associated reactive oxygen species generation. It is likely that these contributing factors cause pathological damage not only to the glomerulus, in particular podocytes, but also to the tubulointerstitium. Specific inhibitors of the various pathways are now available and these emerging pharmaceutical interventions might have potential implications for the prevention and treatment of diabetic nephropathy. The mainstay of therapy remains the achievement of optimal glycemic and blood pressure control in order to slow the progression of diabetic nephropathy. Agents that interrupt the renin–angiotensin system have been shown to be particularly useful as renoprotective agents in both hypertensive and normotensive type 1 and type 2 diabetic subjects. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2011.00131.x, 2011)

Studies on the Antidiabetic Activities ofCordyceps militarisExtract in Diet-Streptozotocin-Induced Diabetic Sprague-Dawley Rats

“…Diabetes patients suffer with a series of metabolic disorders in carbohydrate, fat, and proteins [1]. Noninsulin-dependent diabetes mellitus (NIDDM), caused by insulin resistance, is known as the most common form of diabetes (type 2 diabetes) [2]. According to statistics, till 2025, 8 billion people in the whole world will suffer with type 2 diabetes.…”

Salidroside ameliorates diabetic nephropathy in rats by activating renal AMPK/SIRT1 signaling pathway

“…Nonetheless, oxidative stress and apoptosis are two linked pathways which considered major hallmarks of DN and are believed to be the leading causes of most of the adverse‐related renal and clinical manifestations (Cao & Cooper, ; Habib, ; Lee et al, ). Herein, Salidroside nephroprotective effect was also associated with antioxidant and an anti‐apoptotic mechanisms as evident by the significantly reduction in the levels ROS, lipid peroxidation (MDA), cleaved caspase‐3, and Bax and the higher levels of GSH, ATP, and Bcl‐2, as well as in the levels and activity of MnSOD in the kidneys of T1DM‐treated rats.…”

Drug Related Problems Diabetic Nephropathy Patients in a Tertiary Hospital in Malaysia

“…Gliclazide was not appropriate for patients who had renal impairment. 16 Third, the patients received the right type of drug, but it was inapproriate for patients condition. Irbesartan 300mg can only be used in T2DM patients who had a serum creatinine > 300 mg/ml.…”