Powrie J K, Watts G F, Ingham J N, Taub N A, Talmud P J, Shaw K M
Division of Medicine, United Medical School, Guy's Hospital, London.
BMJ. 1994 Dec 17;309(6969):1608-12. doi: 10.1136/bmj.309.6969.1608.
To ascertain which factors determine the progression from very low rates of albumin excretion to persistent microalbuminuria in patients with insulin dependent diabetes mellitus.
A 10 year prospective study of a cohort of diabetic patients.
Outpatient department of the Portsmouth District Hospitals.
97 patients with insulin dependent diabetes mellitus who were initially free of microalbuminuria and hypertension.
Urinary albumin: creatinine ratio.
Eight of the 97 patients had developed microalbuminuria (urinary albumin:creatinine ratio > 3 mg/mmol in three consecutive early morning samples) by the 10 year follow up. The group who developed microalbuminuria had higher baseline log10 plasma glucose concentrations (mean (SD), 1.210 (0.122) v 0.984 (0.196) mmol/l, P < 0.001) and glycated haemoglobin concentrations (1.112% (0.069%) v 0.997% (0.076%), P < 0.001) and a younger age at onset of diabetes (10.0 (5.5) v 15.6 (7.8) years, P < 0.05). There was no difference in baseline duration of diabetes, smoking, sex, insulin dose, body mass index, serum creatinine concentration, or systolic, diastolic, or mean arterial blood pressure between the two groups. Multiple linear regression analysis showed that urinary albumin:creatinine ratio at 10 years was influenced by initial albumin:creatinine ratio (P = 0.006), initial glycated haemoglobin concentration (P = 0.002), and duration of diabetes (P = 0.045). Genotype for angiotensin converting enzyme was not related to the development of microalbuminuria nor, in a larger group of patients, the presence of any degree of diabetic nephropathy.
In patients with insulin dependent diabetes mellitus the progression of minimal albuminuria and the development of microalbuminuria is determined primarily by poor long term glycaemic control. There is a weaker relation with longer duration of disease and younger age at onset of diabetes, but blood pressure does not seem to be implicated. Gene polymorphism for angiotensin converting enzyme is not linked to the development of microalbuminuria or established diabetic nephropathy.
确定哪些因素决定胰岛素依赖型糖尿病患者从极低的白蛋白排泄率进展为持续性微量白蛋白尿。
对一组糖尿病患者进行为期10年的前瞻性研究。
朴茨茅斯地区医院门诊部。
97例最初无微量白蛋白尿和高血压的胰岛素依赖型糖尿病患者。
尿白蛋白：肌酐比值。
在10年随访中，97例患者中有8例出现了微量白蛋白尿（连续3次清晨样本的尿白蛋白：肌酐比值>3mg/mmol）。出现微量白蛋白尿的组基线log10血浆葡萄糖浓度较高（均值（标准差），1.210（0.122）对0.984（0.196）mmol/L，P<0.001）和糖化血红蛋白浓度较高（1.112%（0.069%）对0.997%（0.076%），P<0.001），且糖尿病发病年龄较小（10.0（5.5）对15.6（7.8）岁，P<0.05）。两组之间在糖尿病基线病程、吸烟、性别、胰岛素剂量、体重指数、血清肌酐浓度或收缩压、舒张压或平均动脉血压方面无差异。多元线性回归分析显示，10年时的尿白蛋白：肌酐比值受初始白蛋白：肌酐比值（P=0.006）、初始糖化血红蛋白浓度（P=0.002）和糖尿病病程（P=0.045）影响。血管紧张素转换酶基因型与微量白蛋白尿的发生无关，在更大一组患者中，也与任何程度的糖尿病肾病的存在无关。
在胰岛素依赖型糖尿病患者中，微量白蛋白尿的进展和微量白蛋白尿的发生主要由长期血糖控制不佳决定。与疾病病程较长和糖尿病发病年龄较小的关系较弱，但血压似乎未涉及其中。血管紧张素转换酶基因多态性与微量白蛋白尿的发生或已确诊的糖尿病肾病无关。
