Komers R
Klinika diabetologie a experimentální terapie IKEM, Praha.
Cas Lek Cesk. 1996 Mar 6;135(5):135-9.
The early stages of diabetes mellitus are in some patients associated with renal haemodynamic changes resulting in increased glomerular filtration. This "diabetic hyperfiltration" is considered to be one of pathophysiological mechanisms and risk factors for the development of diabetic nephropathy. The aim of this paper is to review some contemporary views on pathophysiological mechanisms leading to this disorder with emphasis on the role impaired activity of humoral factors influencing renal haemodynamics. In addition to poor metabolic control due to insulinopenia there is a convincing experimental evidence suggesting the role of atrial natriuretic factor and endothelium-derived nitric oxide in mediating renal haemodynamic changes in diabetes. Enhanced renal activity of angiotensin I converting enzyme resulting in local overproduction of angiotensin II and accelerated degradation of kinins may be another factor contributing to the genesis of diabetic hyperfiltration. Hyperglycaemia induces changes in cellular signalling of these vasoactive systems. Furthermore, diabetes is a state of decreased capability of renal vascular bed to autoregulate blood flow likely due to altered activity of tubuloglomerular feedback and ion channels.
在一些糖尿病患者的早期阶段，会出现与肾血流动力学变化相关的情况，导致肾小球滤过增加。这种“糖尿病性超滤过”被认为是糖尿病肾病发生发展的病理生理机制和危险因素之一。本文旨在综述关于导致这种病症的病理生理机制的一些当代观点，重点关注影响肾血流动力学的体液因子活性受损所起的作用。除了因胰岛素缺乏导致的代谢控制不佳外，有令人信服的实验证据表明，心房利钠因子和内皮衍生的一氧化氮在介导糖尿病患者肾血流动力学变化中发挥作用。血管紧张素I转换酶的肾活性增强，导致局部血管紧张素II过度产生以及激肽加速降解，可能是促成糖尿病性超滤过发生的另一个因素。高血糖会引起这些血管活性系统细胞信号传导的变化。此外，糖尿病可能是由于肾小管-肾小球反馈和离子通道活性改变，导致肾血管床自身调节血流的能力下降的一种状态。
