Mauer S M, Steffes M W, Goetz F C, Sutherland D E, Brown D M
Department of Pediatrics, University of Minnesota School of Medicine, Minneapolis 55455.
Diabetes. 1983 May;32 Suppl 2:52-5. doi: 10.2337/diab.32.2.s52.
The earliest manifestations of clinical diabetic nephropathy, including proteinuria, hypertension, and declining GFR, represent very advanced diabetic glomerulopathy with especially prominent mesangial expansion. Mesangial expansion, by restricting glomerular capillary filtration surface and lumenal volume, stimulates compensatory mechanisms analogous to those resulting from a marked reduction in nephron number. These compensatory mechanisms involve alterations in glomerular hemodynamics designed to maintain glomerular filtration but which ultimately injure the kidney. These hemodynamic perturbations are not specific to diabetes but represent a final common pathway toward endstage renal failure that also characterizes the remnant kidney. This thesis concludes that the onset of clinical diabetic nephropathy augurs inevitable decline in kidney function, and that only studies and interventions exercised before clinical nephropathy develops can influence understanding and outcome of diabetic nephropathy.
临床糖尿病肾病的最早表现，包括蛋白尿、高血压和肾小球滤过率（GFR）下降，代表了非常严重的糖尿病肾小球病变，伴有特别明显的系膜扩张。系膜扩张通过限制肾小球毛细血管滤过面积和管腔容积，刺激了类似于肾单位数量显著减少所导致的代偿机制。这些代偿机制涉及肾小球血流动力学的改变，旨在维持肾小球滤过，但最终会损害肾脏。这些血流动力学紊乱并非糖尿病所特有，而是终末期肾衰竭的最终共同途径，也是残余肾的特征。本论文的结论是，临床糖尿病肾病的发生预示着肾功能不可避免地下降，只有在临床肾病发生之前进行的研究和干预才能影响对糖尿病肾病的认识和预后。
