Providence Health Care, Spokane, Washington.
University of Washington School of Medicine, Seattle, Washington.
Clin J Am Soc Nephrol. 2017 Dec 7;12(12):2032-2045. doi: 10.2215/CJN.11491116. Epub 2017 May 18.
Diabetic kidney disease develops in approximately 40% of patients who are diabetic and is the leading cause of CKD worldwide. Although ESRD may be the most recognizable consequence of diabetic kidney disease, the majority of patients actually die from cardiovascular diseases and infections before needing kidney replacement therapy. The natural history of diabetic kidney disease includes glomerular hyperfiltration, progressive albuminuria, declining GFR, and ultimately, ESRD. Metabolic changes associated with diabetes lead to glomerular hypertrophy, glomerulosclerosis, and tubulointerstitial inflammation and fibrosis. Despite current therapies, there is large residual risk of diabetic kidney disease onset and progression. Therefore, widespread innovation is urgently needed to improve health outcomes for patients with diabetic kidney disease. Achieving this goal will require characterization of new biomarkers, designing clinical trials that evaluate clinically pertinent end points, and development of therapeutic agents targeting kidney-specific disease mechanisms (, glomerular hyperfiltration, inflammation, and fibrosis). Additionally, greater attention to dissemination and implementation of best practices is needed in both clinical and community settings.
糖尿病肾病在约 40%的糖尿病患者中发展，是全球 CKD 的主要病因。尽管终末期肾病（ESRD）可能是糖尿病肾病最明显的后果，但大多数患者实际上在需要肾脏替代治疗之前，死于心血管疾病和感染。糖尿病肾病的自然病程包括肾小球高滤过、进行性白蛋白尿、肾小球滤过率（GFR）下降，最终导致 ESRD。与糖尿病相关的代谢变化导致肾小球肥大、肾小球硬化和肾小管间质炎症和纤维化。尽管目前有多种治疗方法，但糖尿病肾病的发病和进展仍存在较大的残余风险。因此，迫切需要广泛创新，以改善糖尿病肾病患者的健康结果。实现这一目标需要对新的生物标志物进行特征描述，设计评估临床相关终点的临床试验，并开发针对肾脏特异性疾病机制（肾小球高滤过、炎症和纤维化）的治疗药物。此外，还需要在临床和社区环境中更加重视最佳实践的传播和实施。
