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Soluble Urokinase Receptor and the Kidney Response in Diabetes Mellitus 时间:2017-06-16 13:02   来源:未知   作者:admin   点击: 次 Abstract:Diabetic nephropathy (DN) is the leading cause of end-stage renal disease (ESRD) worldwide. DN typically manifests by glomerular hyperfiltration and microalbuminuria; then, the disease progresses to impaired glomerular filtration rate, which leads to ESRD. Treatment options for DN include the strict control of blood glucose levels and pressure (e.g., intraglomerular hypertension). However, the search for novel therapeutic strategies is ongoing. These include seeking specific molecules that contribute to the development and progression of DN to potentially interfere with these “molecular targets” as well as with the cellular targets within the kidney such as podocytes, which play a major role in the pathogenesis of DN. Recently, podocyte membrane protein urokinase receptor (uPAR) and its circulating form (suPAR) are found to be significantly induced in glomeruli and sera of DN patients, respectively, and elevated suPAR levels predicted diabetic kidney disease years before the occurrence of microalbuminuria. The intent of this review is to summarize the emerging evidence of uPAR and suPAR in the clinical manifestations of DN. The identification of specific pathways that govern DN will help us build a more comprehensive molecular model for the pathogenesis of the disease that can inform new opportunities for treatment.
  Diabetes mellitus (DM) is a disorder of glucose metabolism that occurs due to either defect in insulin production by the pancreatic beta cells (type 1 DM) or resistance to insulin in the peripheral tissues (type 2 DM). With the increasing prevalence in obesity and metabolic syndrome, incidence of type 2 DM has been increasing worldwide, including the United States, where approximately 29.1 million people or 9.3% of the population are affected [1]. It is estimated that more than 400 million people will be affected with DM by 2030 [2]. Urinary albumin excretion ranging between 30 and 300 mg/24 h (microalbuminuria) is the earliest sign of diabetic kidney disease (DKD) [3]. Along with microalbuminuria, DN is also characterized by the increased levels of plasma creatinine and the decreased estimated glomerular filtration rate (eGFR) [4] since almost one third of type 2 diabetes patients have renal insufficiency without microalbuminuria [5]. This alone questions the assumption that microalbuminuria could be used as a marker rather than a predictor of DN [6]. Diabetic nephropathy (DN) is the major microvascular complication of diabetes and is one of the leading causes of end-stage renal disease (ESRD) affecting one third of all diabetic individuals in the United States [7]. Persistently high albumin excretion (≥300 mg/24 h), a condition known as macroalbuminuria, increases the chances of progressing to ESRD by 10 times compared to patients with normal urine albumin levels [8]. Many factors including diet, lifestyle, chronic blood glucose levels (HbA1C), blood pressure (BP), smoking, serum cholesterol, and genetic predisposition together play a crucial role in the progression of DN to ESRD.
  Since the renin–angiotensin system (RAS) plays an important role in regulating systemic BP, blockade of its activation by either angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin II type 1 receptor blockers (ARBs) are standard treatments for lowering the BP as well as slowing the progression of DN [9] and chronic renal failure [10]. Cumulative evidence has demonstrated that these first-line agents have represented a significant benefit in regard to partial renal protection in patients with diabetes and proteinuria [11–13]. However, antihypertensive therapy with RAS blockers contributes to the hyperkalemia (high potassium level in the blood) [14] especially when the patients treated with a combined therapy utilizing both an ACE inhibitor and an ARB together [15]. Other concerns of the RAS blockade include the potential long-term adverse effects and the need for dose optimization or individualization [16].