课件：糖尿病肾病DiabeicNehroahy.ppt

β-受体阻滞剂 抑制胰岛素分泌 掩盖低血糖症状 延迟低血糖恢复 减少周围组织血流，加重间歇性跛行 血脂升高 支气管痉挛 ??????使用外源性胰岛素时，对血糖升高的作用可忽略，但应防止低血糖 ?????? ?选择性β1-受体阻滞剂副反应轻 α-肾上腺素能阻滞剂 可提高胰岛素敏感性，对防治高血糖有利 可降低总胆固醇和提高高密度脂蛋白胆固醇 饮 食 治 疗 低蛋白饮食： 0.8克/公斤体重/天 0.6克/公斤体重/天 + α-酮酸 其他治疗措施 调脂治疗：他汀类 醛糖还原酶抑制剂 氨基胍 谢 谢 THANK YOU SUCCESS * * 可编辑 * Angiotensin II: Role in Renal Injury This simplified schema depicts a likely mechanism by which angiotensin II promotes renal glomerulosclerosis and tubulo-interstitial fibrosis. Additional details and explanation can be found on the preceding slide. References: Klahr S and Morrissey JJ. The role of vasoactive compounds, growth factors and cytokines in the progression of renal disease. Kidney Int 2000;57[Suppl 75]:S7-14. * UKPDS Relative Risk Reduction for Intensive vs Less Intensive Glucose Control In the UK Prospective Diabetes Study (UKPDS), a total of 3,867 patients, median age 54 years, with newly diagnosed diabetes and who had a mean of two fasting plasma glucose (FPG) concentrations of 6.1-15.0 mmol/L were randomized to intensive glucose control with sulphonylurea (chlorpropamide or glibenclamide) or insulin (n=2,729), or conventional control with diet (n=1,138). The primary aggregate endpoints were diabetes-related endpoints, death-related to diabetes, and death from all causes. To assess the differences between chlorpropamide, glibenclamide, and insulin, the additional endpoint aggregates of myocardial infarction (fatal and non-fatal) and sudden death; stroke (fatal and non-fatal); amputation or death due to peripheral vascular disease; and microvascular complications (retinopathy requiring photocoagulation, vitreous hemorrhage, and or fatal or non-fatal renal failure) were used. Median follow-up for endpoint analysis was 10 years, and 11.1 years for the comparison of agents. The most significant impact of intensive control was seen in the risk reduction of microvascular complications. In the intensive glucose control group there was a 12% reduction in risk for any dia