Stitt-Cavanagh Erin, MacLeod Laura, Kennedy Chris
Kidney Research Centre, Chronic Disease Program, Ottawa Hospital Research Institute, University of Ottawa, Ontario, Canada.
ScientificWorldJournal. 2009 Oct 14;9:1127-39. doi: 10.1100/tsw.2009.133.
Approaching epidemic levels, diabetic kidney disease (DKD) is now the leading cause of end-stage renal disease (ESRD). Microalbuminuria is an early clinical marker of DKD that results from damage to the glomerular filtration barrier at the level of the highly differentiated glomerular podocyte cells. Injury to these epithelial cells, podocytopathies, includes cellular hypertrophy, foot process effacement, detachment from the glomerular basement membrane, and apoptosis. Here we review the role of a number of recently identified factors that contribute to podocytopathies in DKD. These factors include members of the renin-angiotensin system (RAS), including angiotensin-converting enzyme (ACE) types 1 and 2, prorenin and its receptor, reactive oxygen species (ROS), prostanoids, peroxisome proliferator-activated receptors (PPAR), advanced glycation end-products (AGEs) and their receptors (RAGE), adiponectin, and microRNAs. As the number of therapeutic options that slow, but do not halt, the progression of DKD to ESRD remains limited, a more comprehensive understanding of the signaling events that contribute to this increasingly prevalent disease may identify novel avenues for treatment and prevention.
糖尿病肾病（DKD）正接近流行程度，现已成为终末期肾病（ESRD）的主要病因。微量白蛋白尿是DKD的早期临床标志物，它是由高度分化的肾小球足细胞水平的肾小球滤过屏障受损所致。这些上皮细胞损伤，即足细胞病变，包括细胞肥大、足突消失、与肾小球基底膜脱离以及凋亡。在此，我们综述了一些最近发现的导致DKD中足细胞病变的因素的作用。这些因素包括肾素 - 血管紧张素系统（RAS）的成员，包括1型和2型血管紧张素转换酶（ACE）、肾素原及其受体、活性氧（ROS）、前列腺素、过氧化物酶体增殖物激活受体（PPAR）、晚期糖基化终产物（AGEs）及其受体（RAGE）、脂联素和微小RNA。由于减缓但不能阻止DKD进展为ESRD的治疗选择仍然有限，对导致这种日益普遍疾病的信号事件有更全面的了解可能会为治疗和预防找到新途径。
