Bilous R W, Mauer S M, Sutherland D E, Najarian J S, Goetz F C, Steffes M W
Department of Laboratory Medicine, University of Minnesota Medical School, Minneapolis.
N Engl J Med. 1989 Jul 13;321(2):80-5. doi: 10.1056/NEJM198907133210204.
The microvascular complications of diabetes mellitus may be caused, in part, by poor glycemic control. Diabetic patients who have received renal allografts may have new glomerular lesions that are manifested structurally by increases in mesangial and glomerular volume. Successful pancreas transplantation produces long-term normoglycemia and provides a unique opportunity to evaluate the impact of the normalization of the blood glucose level on the development of the renal lesions typical of diabetes mellitus in transplanted kidneys. We obtained biopsy specimens from the functioning renal allografts of 12 patients with insulin-dependent (Type I) diabetes before successful pancreas transplantation (performed one to seven years after renal transplantation) and repeated the biopsy at least 1.9 years later. In renal biopsy specimens obtained before pancreas transplantation, the mesangial volume was normal or modestly increased and the glomerular basement membrane was moderately thickened. At follow-up, no progression could be detected in any structural measure in the glomerulus. Furthermore, the recipients of pancreas transplants had smaller glomerular volumes than 13 matched diabetic patients who were recipients of renal allografts but who did not undergo pancreas transplantation (mean +/- SD, 1.80 +/- 0.55 vs. 2.47 +/- 0.73 x 10(6) microns 3; P = 0.02) and showed markedly less mesangial expansion (mesangial-volume fraction, 0.19 +/- 0.07 vs. 0.31 +/- 0.10 microns 3 per cubic micrometer; P = 0.004). We conclude that successful pancreas transplantation is associated with significantly less severe diabetic glomerulopathy in kidneys previously transplanted into diabetic patients. These data support the hypothesis that normoglycemia can prevent the progression of diabetic glomerulopathy in humans.
糖尿病的微血管并发症可能部分由血糖控制不佳引起。接受肾移植的糖尿病患者可能会出现新的肾小球病变,其结构表现为系膜和肾小球体积增加。成功的胰腺移植可产生长期正常血糖,并提供了一个独特的机会来评估血糖水平正常化对移植肾中典型糖尿病肾病病变发展的影响。我们从12例胰岛素依赖型(I型)糖尿病患者成功进行胰腺移植前(肾移植后1至7年进行)的功能正常的移植肾中获取活检标本,并在至少1.9年后重复活检。在胰腺移植前获取的肾活检标本中,系膜体积正常或略有增加,肾小球基底膜中度增厚。随访时,未检测到肾小球的任何结构指标有进展。此外,胰腺移植受者的肾小球体积小于13例匹配的接受肾移植但未进行胰腺移植的糖尿病患者(均值±标准差,1.80±0.55对2.47±0.73×10⁶立方微米;P = 0.02),且系膜扩张明显较少(系膜体积分数,每立方微米0.19±0.07对0.31±0.10立方微米;P = 0.004)。我们得出结论,成功的胰腺移植与先前移植给糖尿病患者的肾脏中糖尿病肾小球病的严重程度显著降低相关。这些数据支持正常血糖可预防人类糖尿病肾小球病进展的假说。