Departments of Metabolism, Endocrinology, and Molecular Medicine Osaka City University Graduate School of Medicine, Osaka, Japan; Departments of Nephrology, Osaka City University Graduate School of Medicine, Osaka, Japan.
Departments of Nephrology, Osaka City University Graduate School of Medicine, Osaka, Japan.
Diabetes Res Clin Pract. 2014 Jul;105(1):40-6. doi: 10.1016/j.diabres.2014.04.019. Epub 2014 Apr 28.
The renin-angiotensin system (RAS) plays an important role in the pathogenesis of diabetic nephropathy. The aim of the present study was to investigate intrarenal RAS activity in patients with type 2 diabetes (T2DM).
We measured urinary angiotensinogen, a reliable biomarker of intrarenal RAS activity, in 14 controls without T2DM, 25 T2DM patients without nephropathy, 11 chronic kidney disease (CKD) patients without T2DM and 46 CKD patients with T2DM. Associations between urinary angiotensinogen and clinical parameters were examined.
Compared with the controls, urinary [angiotensinogen:creatinine] were significantly higher in T2DM patients without nephropathy (4.70 ± 2.22 vs. 8.31 ± 5.27 μg/g, p=0.037). Age, hemoglobin A1c (HbA1c) and fasting plasma glucose correlated significantly and positively with the log{urinary [angiotensinogen:creatinine]} (r=0.632, p=0.007; r=0.405, p=0.027; r=0.583, p=0.003, respectively) in T2DM patients without nephropathy. In contrast, the urinary [angiotensinogen:creatinine] were not significantly different between CKD patients with and without T2DM (22.7 ± 27.8 vs. 33.5 ± 40.8 μg/g, p=0.740); although they were significantly higher when compared with non-CKD patients. In the CKD patients with T2DM systolic blood pressure, serum creatinine, estimated glomerular filtration rate and urinary [albumin:creatinine] correlated significantly with the log{urinary [angiotensinogen:creatinine]} (r=0.412, p=0.004; r=0.308, p=0.037; r=-0.382, p=0.001; r=0.648, p<0.001, p<0.001, respectively).
Our findings indicate that poor glycemic control is significantly associated with intrarenal RAS activity in T2DM patients without nephropathy, and that decreased renal function is significantly associated with intrarenal RAS activity in CKD patients with T2DM.
肾素-血管紧张素系统（RAS）在糖尿病肾病的发病机制中起着重要作用。本研究旨在探讨 2 型糖尿病（T2DM）患者的肾内 RAS 活性。
我们测量了 14 名无 T2DM 的对照组、25 名无肾病的 T2DM 患者、11 名无 T2DM 的慢性肾脏病（CKD）患者和 46 名有 T2DM 的 CKD 患者的尿血管紧张素原，这是肾内 RAS 活性的可靠生物标志物。检查尿血管紧张素原与临床参数之间的关系。
与对照组相比，无肾病的 T2DM 患者的尿[血管紧张素原：肌酐]显着升高（4.70±2.22 vs. 8.31±5.27μg/g，p=0.037）。年龄、糖化血红蛋白（HbA1c）和空腹血糖与无肾病的 T2DM 患者的 log{尿[血管紧张素原：肌酐]}显着正相关（r=0.632，p=0.007；r=0.405，p=0.027；r=0.583，p=0.003）。相比之下，有和没有 T2DM 的 CKD 患者的尿[血管紧张素原：肌酐]没有显着差异（22.7±27.8 vs. 33.5±40.8μg/g，p=0.740）；尽管与非 CKD 患者相比，它们显着更高。在有 T2DM 的 CKD 患者中，收缩压、血清肌酐、估计肾小球滤过率和尿[白蛋白：肌酐]与 log{尿[血管紧张素原：肌酐]}显着相关（r=0.412，p=0.004；r=0.308，p=0.037；r=-0.382，p=0.001；r=0.648，p<0.001，p<0.001，分别）。
我们的研究结果表明，血糖控制不佳与无肾病的 T2DM 患者的肾内 RAS 活性显着相关，而肾功能下降与有 T2DM 的 CKD 患者的肾内 RAS 活性显着相关。
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