Department of Physiology and Biophysics, University of Miami Miller School of Medicine, FL, USA.
Am J Kidney Dis. 2011 Oct;58(4):637-46. doi: 10.1053/j.ajkd.2011.03.035. Epub 2011 Jun 29.
Diabetic nephropathy (DN) represents a major public health cost. Tight glycemic and blood pressure control can dramatically slow, but not stop, the progression of the disease, and a large number of patients progress toward end-stage renal disease despite currently available interventions. An early and key event in the development of DN is loss of podocyte function (or glomerular visceral epithelial cells) from the kidney glomerulus, where they contribute to the integrity of the glomerular filtration barrier. Recent evidence suggests that podocytes can be the direct target of circulating hormones, lipids, and adipokines that are affected in diabetes. We review the clinical and experimental evidence implicating novel endocrine and metabolic pathways in the pathogenesis of podocyte dysfunction and the development of DN.
糖尿病肾病（DN）是一项重大的公共卫生成本。严格的血糖和血压控制可以显著减缓疾病的进展，但不能阻止疾病的进展，尽管目前有多种干预措施，但仍有大量患者进展为终末期肾病。DN 发展过程中的一个早期和关键事件是肾脏肾小球中足细胞功能（或肾小球内脏上皮细胞）的丧失，足细胞有助于肾小球滤过屏障的完整性。最近的证据表明，足细胞可能是循环激素、脂质和脂肪因子的直接靶标，这些物质在糖尿病中受到影响。我们回顾了涉及新的内分泌和代谢途径在足细胞功能障碍和 DN 发病机制中的临床和实验证据。
