Wajchenberg B L, Sabbaga E, Fonseca J A
Acta Diabetol Lat. 1983 Jan-Mar;20(1):1-18. doi: 10.1007/BF02629124.
The authors present a contemporary picture of the pathogenesis and clinical course of diabetic nephropathy in type I diabetics describing the stages of the disease and the possible evidence for reversibility of the kidney damage with tight metabolic control. During the so-called latency period, which is clinically non-detectable, the predominant functional abnormalities (increase in GFR with sub-clinical glomerular proteinuria) can be corrected by strict control although there is no evidence for the regression of the associated anatomical changes such as the enlarged filtration area. As for the described increase in thickness of the glomerular basement membrane, from experimental data and pancreatic transplants in man, delay in its development and to some extent regression of the glomerular lesions can be expected. The problem of how the renal lesions in experimental diabetes mirror the changes in the human kidney is discussed. During the symptomatic period, with intermittent and subsequently constant proteinuria and progressive decline in renal function, which are observed in only about 30% of type I diabetics, the role of arterial hypertension and its effective control is emphasized. Finally, the renal failure period is indicative of irreversible damage to the kidneys. The progression from its early to its late stages is variable between different patients but each individual patient shows a constant rate of deterioration. The evidence for the efficacy of medical treatment in slowing down its progression is very limited at present but much can be done to improve the quality of life by dietary measures, treatment of fluid overload and hypertension. When the end-stage diabetic kidney disease is reached, with serum creatinine above 8 mg/dl, renal transplantation from a living donor offers a good chance for a relatively acceptable quality of life for years. In conclusion, it is stressed that the morbidity of diabetic nephropathy could eventually be reduced through effective control of the metabolic abnormalities of diabetes with the methods presently available.
作者呈现了1型糖尿病患者糖尿病肾病发病机制和临床病程的现代图景，描述了疾病阶段以及通过严格代谢控制使肾脏损伤可逆的可能证据。在所谓的潜伏期，临床上无法检测到，尽管没有证据表明相关解剖学变化（如滤过面积增大）会消退，但主要的功能异常（肾小球滤过率增加伴亚临床肾小球蛋白尿）可通过严格控制得到纠正。至于所描述的肾小球基底膜增厚，从实验数据和人类胰腺移植来看，预计其发展会延迟，并且肾小球病变在一定程度上会消退。文中讨论了实验性糖尿病中的肾脏病变如何反映人类肾脏变化的问题。在症状期，仅约30%的1型糖尿病患者会出现间歇性继而持续性蛋白尿以及肾功能进行性下降，文中强调了动脉高血压的作用及其有效控制。最后，肾衰竭期表明肾脏已发生不可逆损伤。不同患者从早期到晚期的进展各不相同，但每个患者的恶化速率是恒定的。目前，药物治疗减缓其进展的疗效证据非常有限，但通过饮食措施、治疗液体过载和高血压，在改善生活质量方面仍有很多可做的。当达到终末期糖尿病肾病，血清肌酐高于8mg/dl时，活体供肾移植为患者提供了多年相对可接受生活质量的良好机会。总之，文中强调，通过目前可用的方法有效控制糖尿病的代谢异常，最终可降低糖尿病肾病的发病率。
