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近年来大量的研究阐明了糖尿病肾病的发展阶段,由此产生了一系列防治措施。以试图延缓或阻止其进展。目前比较一致的看法认为糖尿病肾病发展阶段包括:(1)肾脏肥大和高滤过状态(OFR≥150ml/分);(2)正常自蛋白尿(UAE<20μg/分或<30mg/24h);(3)早期糖尿病肾病。其特征为持续而逐渐增加的微量白蛋白尿(UAE20～200μg/分或30～300mg/24h),血压逐渐升高,肾小球滤过率(GFR)从正常高值开始下降;(4)显性糖尿病肾病,以持续蛋白尿为特征(尿蛋白>0.5克/24h,约UAE>200μg/分);(5)肾功能衰竭的终末阶段。约30％的胰岛素依赖性糖尿病(IDDM)患者最终可发展为糖尿病肾病。发病高峰约在糖尿病后15年,最常见死于尿毒症。大量的研究表明糖尿病肾脏受累中尿自蛋白排泌率(UAE)和肾小球滤过率是基本的标志。基于上述认识,进行了各种干预性治疗试验,取得了令人乐观的结果。控制代谢一些研究发现在糖尿病肾病早期予以严格控制血糖使许多病例的微量白蛋白尿和肾小球高滤过正常化,虽尚无组织损害逆转的证据。然而,在糖尿病鼠,严格控制血糖可见功能及组织学变化。
In recent years, a large number of studies have clarified the stage of development of diabetic nephropathy, resulting in a series of prevention and treatment measures. In an attempt to delay or prevent its progress. The current consensus is that the stages of development of diabetic nephropathy include: (1) renal hypertrophy and hyperfiltration (OFR ≥ 150 ml / min); (2) normal self-proteinuria (UAE <20 μg / min or <30 mg / (3) early diabetic nephropathy. It is characterized by a sustained and gradual increase in microalbuminuria (UAE 20-200 μg / min or 30-300 mg / 24 h), a gradual rise in blood pressure, and a decrease in glomerular filtration rate (GFR) from normal high values; (4) Dominant diabetic nephropathy characterized by persistent proteinuria (urinary protein> 0.5 g / 24h, about UAE> 200 μg / min); (5) terminal stage of renal failure. About 30% of patients with insulin-dependent diabetes mellitus (IDDM) eventually develop diabetic nephropathy. The peak incidence of about 15 years after diabetes, the most common cause of death from uremia. Numerous studies have shown that urinary urinary excretion of urine from the protein excretion rate (UAE) and glomerular filtration rate are the basic signs. Based on the above understanding, conducted a variety of intervention trials, and achieved encouraging results. Control of Metabolism Some studies have found that strict control of blood glucose in the early stages of diabetic nephropathy normalizes microalbuminuria and glomerular hyperfiltration in many cases, although there is no evidence of reversal of tissue damage. However, in diabetic rats, strict control of blood glucose can be seen functional and histological changes.