Allograft diabetic nephropathy may progress to end-stage renal disease
Allograft diabetic nephropathy may progress to end-stage renal disease
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DOI：
10.1111/j.1399-3046.2004.00182.x
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发表时间：
2004-08-01
影响因子：
1.3
通讯作者：
Friedman, EA
中科院分区：
文献类型：
--
作者：
Salifu, MO;Nicastri, AD;Friedman, EA
糖尿病肾病的系膜扩张和肾小球基底膜增厚特征在非糖尿病供体的同种异体肾移植的糖尿病受者中复发，但进展为肾衰竭的记录很少。本文报告三位女性肾移植受者（年龄分别为40岁、62岁及73岁），因复发性糖尿病肾病（两名患者）及新发糖尿病（一名患者）而发展为终末期肾病（ESRD）。分析蛋白尿、未控制的高血压、氮质血症、移植肾病理结果和血液透析的需要。没有一个肾脏供体（一个尸体，两个活体亲属）在移植前患有已知的糖尿病或葡萄糖代谢紊乱。这三名患者患有不同类型的糖尿病; 1型，2型和移植后新发糖尿病（NODAT）。在每例受试者中，在移植后平均8.3年（范围8-9）时通过试纸检测到蛋白尿，并增加至肾病范围（3.7-4.8 g/天），诱导低白蛋白血症和氮质血症。根据肾小球基底膜增厚、结节性和弥漫性毛细血管间肾小球硬化、小动脉硬化和肾小管萎缩伴晚期糖尿病肾病特征性肾小管基底膜增厚，平均11.7年（范围10-14年）对同种异体移植糖尿病肾病进行组织病理学诊断。所有三名患者均出现尿毒症并恢复血液透析。2例患者在2个月内死于败血症，1例患者在恢复维持性血液透析后2.5年死亡。我们推断，无论是否患有糖尿病，肾移植后复发或新发糖尿病肾病的临床病程均长达10年。由于糖尿病移植受者的生存期较短，慢性移植物功能障碍患者很少进行肾活检，因此，由于移植物糖尿病肾病（ADN）导致的终末期肾病的报告有限。然而，在一些但不是所有患者中发生同种异体移植糖尿病肾病表明个体遗传变异调节疾病表达。
Mesangial expansion and glomerular basement membrane thickening characteristic of diabetic nephropathy recur in diabetic recipients of renal allografts from non-diabetic donors but progression to renal failure is minimally documented. Three female renal allograft recipients (aged 40, 62 and 73 yr), who developed end-stage renal disease (ESRD) due to recurrent diabetic nephropathy (two patients) and de novo diabetes (one patient) are reported. Onset of proteinuria, uncontrolled hypertension, azotemia, renal allograft pathologic findings and the need for hemodialysis were analyzed. None of the kidney donors (one cadaver, two living related) had known diabetes or perturbed glucose metabolism pre-transplantation. The three patients presented had different varieties of diabetes; type 1, type 2 and new onset diabetes after transplantation (NODAT). In each subject, proteinuria was detected by dipstick at a mean of 8.3 yr (range 8-9) post-transplantation and increased to the nephrotic range (3.7-4.8 g/day) inducing hypoalbuminemia and azotemia. A histopathologic diagnosis of allograft diabetic nephropathy was made in a mean of 11.7 yr (range 10-14), based on glomerular basement membrane thickening, nodular and diffuse intercapillary glomerulosclerosis, arteriolosclerosis, and tubular atrophy with marked tubular basement membrane thickening characteristic of advanced diabetic nephropathy. All three patients manifested uremia and resumed hemodialysis. Two patients died from sepsis within 2 months and one patient died 2.5 yr later after resumption of maintenance hemodialysis. We infer that recurrent or de novo diabetic nephropathy in renal allografts follows a clinical decade-long course irrespective of diabetes. Reports of ESRD due to allograft diabetic nephropathy (ADN) have been limited because of shorter survival of diabetic transplant recipients and few kidney biopsies performed in patients with chronic allograft dysfunction. The occurrence of allograft diabetic nephropathy in some, but not all patients, however, suggests that individual genetic variability modulates disease expression.